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Significant implications of glycogen synthase kinase-3β (GSK-3β) have been reported in various neuronal disorders and malignant cancers. GSK-3β modulates diverse protein targets through phosphorylation, and its aberrant activity leads to neurological complications as well as tumour onset. Therefore, inhibiting GSK-3β activity through active-site fitting molecules may offer a favourable strategy for intercepting these disorders. This comprehensive study used multiple assays in tandem in order to explore the most potent GSK-3β inhibitor. Following structural similarity screening, 135 molecular docking and 135 standard MM-GBSA experiments were performed using AZD1080, a known inhibitor as standard. Among the 32 molecules demonstrating a stronger binding affinity than reference, only the two most potent molecules were chosen and their binding free energy was compared to AZD1080 using the Desmond trajectory clustering and eventual MM-GBSA. Additionally, the interaction status of these molecules and AZD1080 with GSK-3β was explored post-molecular dynamics. The stability of the strongest molecule (most potent) was evaluated in the active site of the above-mentioned kinase keeping its apo-form as reference. Notably, the e-Pharmacophores mapping was performed to address the level of complementarity of the most potent molecule and AZD1080 with the functional site of GSK-3β. Using various techniques, we identified the molecule with PubChem CID: 11167509 as the strongest molecule for obstructing GSK-3β, which may serve as a promising therapeutic after the meticulous evaluation on diverse models. [ABSTRACT FROM AUTHOR]

Ginseng and L-carnitine are natural compounds often used as dietary supplements to enhance athletic performance. However, their combined effects on exercise endurance remain unclear. Objectives: This study aimed to investigate the effects of ginseng extract and L-carnitine supplementation on exercise endurance in a rat model. Methods: Male Wistar rats were divided into 10 groups (n = 5 per group): control, ginseng extract (250 and 500 mg/kg/day), L-carnitine (250 and 500 mg/kg/day), and combined treatment. Half of the groups underwent a 16-day exercise training program of swimming without loading. Exercise endurance was assessed using a tail-suspended forced swimming test. Relative organ weight, glycogen content, blood biochemistry, and gene expression were analyzed. Results: Both ginseng extract and L-carnitine supplementation significantly increased exercise endurance, particularly in the exercise group. Ginseng extract and L-carnitine also increased liver glycogen content and upregulated the expression of AMPKα1 and PGC-1α genes in the liver and muscle. In addition, both supplements reduced oxidative stress by decreasing MDA levels and increasing SOD activity. Conclusions: Ginseng extract and L-carnitine supplementation may enhance exercise endurance by improving energy metabolism, reducing oxidative stress, and upregulating key genes involved in mitochondrial biogenesis. [ABSTRACT FROM AUTHOR]

The bacterial pathogen, lipopolysaccharide (LPS), elicits microglial response and induces cytokine secretion that subsequently activates astrocytes. Recent findings have indicated that LPS-induced activation of postnatal glial cells has led to alterations in synapse formation in hippocampal and cortical neurons, thereby resulting in a prolonged increased risk for seizure or depression. Nevertheless, its mechanisms remain to be fully elucidated. Cellular metabolism has recently gained recognition as a critical regulatory mechanism for the activation of peripheral immune cells, as it supplies the requisite energy and metabolite for their activation. In the present study, we report that LPS did not change the expression of reported astrocyte-derived synaptogenic genes in the postnatal hippocampus; however, it induced upregulation of astrocytic complement component regulator Serping1 within the postnatal hippocampus. As a regulatory mechanism, activation of glycogen degradation (glycogenolysis) governs the expression of a subset of inflammatory-responsive genes including Serping1 through reactive oxygen species (ROS)-NF-κB axis. Our study further demonstrated that glycogenolysis is implicated in neurotoxic phenotypes of astrocytes, such as impaired neuronal synaptogenesis or cellular toxicity. These findings suggested that activation of glycogenolysis in postnatal astrocytes is an essential metabolic pathway for inducing responses in inflammatory astrocytes. [ABSTRACT FROM AUTHOR]

The Na+-K+-ATPase is a critical regulator of ion homeostasis during contraction, buffering interstitial K+ accumulation, which is linked to muscle fatigue during intense exercise. Within this context, we adopted a recently reported methodology to examine exercise-induced alterations in maximal Na+-K+-ATPase activity. Eighteen trained healthy young males completed a repeated high-intensity cycling protocol consisting of three periods (EX1-EX3) of intermittent exercise. Each period comprised 10 × 45-s cycling at ~ 105% Wmax and a repeated sprint test. Muscle biopsies were sampled at baseline and after EX3 for determination of maximal in vitro Na+-K+-ATPase activity. Blood was drawn after each period and in association with a 2-min cycling test at a standardized high intensity (~ 90% Wmax) performed before and after the session to assess plasma K+ accumulation. Further, a 5-h recovery period with the ingestion of carbohydrate or placebo supplementation was implemented to explore potential effects of carbohydrate availability before sampling a final biopsy and repeating all tests. A ~ 12% reduction in maximal Na+-K+-ATPase activity was demonstrated following EX3 compared to baseline (25.2 ± 3.9 vs. 22.4 ± 4.8 μmol·min−1·g−1 protein, P = 0.039), which was sustained at the recovery time point (~ 15% decrease compared to baseline to 21.6 ± 5.9 μmol·min−1·g−1 protein, P = 0.008). No significant effect of carbohydrate supplementation was observed on maximal Na+-K+-ATPase activity after recovery (P = 0.078). In conclusion, we demonstrate an exercise-induced depression of maximal Na+-K+-ATPase activity following high-intensity intermittent exercise, which was sustained during a 5-h recovery period and unrelated to carbohydrate availability under the present experimental conditions. This was shown using a novel NADH coupled assay and confirms previous findings using other methodological approaches. [ABSTRACT FROM AUTHOR]

This investigation aimed to assess whether the alternative method of estimating the maximal accumulated oxygen deficit (MAODalt) can detect changes in energy system contribution in different substrate availabilities. Following a graded exercise test to determine maximal oxygen uptake intensity (iVO2max), 26 recreational runners performed a time to exhaustion effort (TTE) as baseline at 110% iVO2max. The same TTE was performed in fasting state, then, a muscle glycogen depletion protocol was executed. Subsequently, participants received a low-carbohydrate diet and beverages containing high (H-CHO, 10.8±2.1 g·kg− 1), moderate (M-CHO, 5.6±1.1 g·kg− 1), or zero (Z-CHO, 0.24±0.05 g·kg− 1) carbohydrates. Another TTE was performed 24 h later. Each energy system contribution was assessed. Generalized linear mixed models were used for statistical analysis (p<0.05). H-CHO increased relative anaerobic capacity (slope effect [baseline –intervention]x[H-CHO – M-CHO]) due to the relative lactic contribution maintenance (slope effect [baseline – intervention]x[H-CHO – Z-CHO] or [H-CHO – M-CHO]) and increase in relative alactic contribution (6.3±3.5 kJ·min− 1). The aerobic contribution was lower (− 8.7±4.0 kJ·min− 1), decreasing performance (− 34±16 s) for H-CHO. M-CHO and Z-CHO maintained anaerobic capacity due to increase in alactic contribution (slope effect [fasting – intervention]x[M-CHO – H-CHO]; and Z-CHO was 7.3±3.4 kJ·min− 1 higher than baseline). Fasting increased relative alactic (2.9±1.7 kJ·min− 1) but decreased aerobic contribution (− 3.3±2.3 kJ·min− 1), impairing performance (− 17±12 s). In conclusion, MAODalt can detect changes in energy system supply in different nutritional states. Therefore, participantʼs nutritional state must be considered prior to conducting the test. [ABSTRACT FROM AUTHOR]

The objective of this study was to assess the impact of short-term fasting and subsequent re-feeding cycles on compensatory growth performance, blood glucose levels, and digestive enzyme activity in mono-sex juvenile Nile tilapia (Oreochromis niloticus) over a 60-day period. A total of 150 juvenile Nile tilapia (Avg. wt. 9.34 ± 0.97 g) were allocated into five treatment groups: a control group (continuously fed) and four fasting groups—T1 (1-day fasting), T2 (3-day fasting), T3 (5-day fasting), and T4 (7-day fasting). Re-feeding occurred for 7 days in each group immediately following the fasting period in a recurring cycle. The average weight gain, specific growth rate, and feed efficiency ratio significantly (p < 0.05) declined starting from the T3 group. Blood glucose levels during fasting significantly decreased starting from the T2 group, but after re-feeding, they returned to levels comparable to the control group. The liver glycogen levels significantly (p ≤ 0.05) decreased during fasting and completely recovered upon re-feeding, while muscle glycogen levels did not show any significant (p ≤ 0.05) changes throughout the experimental duration. The activities of the digestive enzymes amylase and lipase significantly (p ≤ 0.05) decreased during fasting starting from T1 and T2 groups, respectively, but after re-feeding, they returned to the levels seen in the control group. In contrast, the protease enzyme levels during the fasting period initially increased up to the T2 group and subsequently returned to control levels in the T4 group. The findings of this study indicate that only the groups that experienced very short fasting periods, specifically up to the T2 group, attained body weights like the control group upon re-feeding due to compensatory growth. Therefore, this study concluded that implementing up to 3 days of fasting followed by 7 days of re-feeding in multiple cycles can serve as a strategy for minimizing input costs in tilapia farming. [ABSTRACT FROM AUTHOR]

Purpose: The objective of this study was to develop a new MRI technique for non‐invasive, free‐breathing imaging of glycogen in the human liver using the nuclear Overhauser effect (NOE). Methods: The proposed method, called GraspNOE‐Dixon, uses a novel MRI sequence that combines steady‐state saturation‐transfer preparation with multi‐echo golden‐angle radial stack‐of‐stars sampling. Multi‐echo acquisition enables fat/water‐separated imaging for quantification of water‐specific NOE. Image reconstruction is performed using the improved golden‐angle radial sparse parallel imaging (GRASP‐Pro) technique to exploit spatiotemporal correlations in dynamic images. To evaluate the proposed technique, imaging experiments were first performed on glycogen phantoms, followed by in vivo studies involving healthy volunteers and patients with fatty liver disease. In addition, a comparative assessment of signal changes before and after a 12‐h fasting period was performed. Results: Evaluation experiments on glycogen phantoms showed a robust linear correlation between the NOE signal and glycogen concentration. In vivo experiments demonstrated motion‐robust NOE‐weighted images, with potential for further acceleration. In subjects with varying liver fat content, the fat/water separation approach resulted in distortion‐free Z‐spectra, enabling the quantification of glycogen NOE. An approximately one‐third reduction in the NOE signal was observed following a 12‐h fasting period, consistent with a decrease in glycogen level. Conclusion: This study introduces a clinically feasible imaging technique, GraspNOE‐Dixon, for free‐breathing volumetric multi‐echo imaging of hepatic glycogen at 3 T. The motion robust imaging technique developed here may also have applications in other body areas beyond liver imaging. [ABSTRACT FROM AUTHOR]

Hybridisation is a commonly reported phenomenon in fish. This study focuses on cyprinid species, Cyprinus carpio and Carassius gibelio and their hybrids, including F1, F2 and backcross generations obtained by artificial breeding, to investigate the effect of the various types of crossbreeding representing different genomic contributions of common carp and gibel carp on the health and histoarchitecture of key organs involved in metabolism and immunity – the liver and spleen. Comparative histology revealed no clear trend in the organisation of liver and spleen parenchyma based on the type of crossbreeding. However, there are similarities between certain fish lines, most noticeable in the specific properties of hepatocytes and the pattern of glycogen distribution in their cytoplasm, and in the organisation of splenic fibrous skeleton. Moreover, this study suggests that long-term breeding of wild fish species in artificial conditions can affect their physiology, as we noted extravascular haemolysis affecting parts of the splenic parenchyma and small foci of hepatic necrosis. Compared to gibel carp and hybrid lines, the common carp with a longer history of cultivation showed the mildest forms of the pathologies detected, indicating that it coped best with the conditions of artificial breeding. [ABSTRACT FROM AUTHOR]

Diabetes mellitus is a metabolic syndrome that has grown globally to become a significant public health challenge. Hypothesizing that the plasma membrane protein, transient receptor potential ankyrin-1, is a pivotal target in insulin resistance, we investigated the mechanism of action of cinnamaldehyde (CIN), an electrophilic TRPA1 agonist, in skeletal muscle, a primary insulin target. Specifically, we evaluated the effect of CIN on insulin resistance, hepatic glycogen accumulation and muscle and adipose tissue glucose uptake. Furthermore, the in vitro role of CIN in glucose uptake and intracellular signaling was determined in insulin-resistant rats whose calcium influx was analyzed. Moreover, the serum lipid profile was assessed following short-term CIN treatment in rats, and lipid tolerance was analyzed. The effects of CIN on insulin resistance were mediated by TRPA1, with downstream signaling involving the activation of PI3-K, MAPK, PKC, as well as extracellular calcium and calcium release from intracellular stores. Additionally, cytoskeleton integrity was required for the complete action of CIN on glucose uptake in muscle. CIN also ameliorated the serum lipid profile and improved triglyceride tolerance following acute vivo exposure. [ABSTRACT FROM AUTHOR]

The aim of this study was to elucidate the impact of porcine pancreatic enzymes (Creon® pancrelipase) in comparison to microbial-derived alpha amylase (MD amylase) on the small intestine wall structure, mucosal glycogen accumulation, and enterocyte turnover. The impact of enzyme supplementation on the small intestine was explored in 18 pigs with surgically induced exocrine pancreatic insufficiency (EPI). Four healthy pigs served as the control group. EPI led to reduced villus length, crypt depth, and thickness of the mucosa and muscularis layers compared to those of healthy pigs. All these changes appeared to be reversible after enzyme supplementation. Brush border thickness was decreased in EPI and increased with both enzyme preparations, with MD amylase treatment leading to the highest values in the proximal jejunum. No EPI-induced changes were observed in the goblet cell (GC) population, but significant increases in GC number and area were observed following MD amylase treatment. Glycogen accumulation within the duodenal mucosa was significantly increased in EPI pigs. EPI was also shown to significantly increase apoptotic activity and decrease proliferative activity in comparison to healthy animals, while both enzyme preparations resulted in the complete recovery of both proliferative and apoptotic activity in all investigated intestinal segments. Creon® influenced the morphology of the small intestine. However, supplementation of exogenous microbial amylase alone also affected gut morphology in a similar way to that of the complex host pancreatic enzymes offered orally. These data indicate that in addition to their role in digestion of nutrients in EPI, intraluminal pancreatic enzymes, especially amylase, contribute to gut health through maintenance of the intestinal wall architecture and physiological enterocyte turnover. [ABSTRACT FROM AUTHOR]

Glycogen is a polymer used by bacteria to store excess glucose, playing a crucial role in bacterial growth, stress resistance, biofilm formation, and virulence. In bacteria, the glycoside hydrolase family 13 protein are involved in the synthesis and metabolism of glycogen, respectively. The absence of these enzymes leads to changes in bacterial glycogen content, thereby affecting the growth metabolism of the strain. To date, research on the roles of these glycogen-related glycoside hydrolase genes in the synthesis metabolism and bacterial phenotypes of Klebsiella pneumoniae has been limited. In this study, we characterized the glycogen-related glycoside hydrolase genes glgB and glgX of K. pneumoniae. We found that both enzymes exhibited significant degradation activity against glycogen substrates and were capable of degrading amylopectin, amylose, and pullulan. The optimal temperatures for GlgB and GlgX were both in the range of 35-40°C, with optimal pH values of 7.5 and 7.0, respectively, and they exhibited high stability at 37°C. Subsequently, we deleted the glgB and glgX genes in K. pneumoniae. The deletion of the glgB gene resulted in a decrease in the growth rate of the bacteria and defected glycogen synthesis. In contrast, the deletion of the glgX gene slightly accelerated the growth rate and led to continuous glycogen accumulation. In terms of biofilm formation and virulence, defects in glycogen synthesis impeded biofilm formation and virulence, while continuous glycogen accumulation did not affect biofilm formation but slightly increased virulence. In conclusion, the glgB and glgX genes are essential for the glycogen synthesis and metabolism in K. pneumoniae and further influence the biofilm formation capacity and virulence. [ABSTRACT FROM AUTHOR]

Objective: Impaired skeletal muscle glycogen synthesis contributes to insulin resistance (IR). Aerobic exercise reported to ameliorate IR by augmenting insulin signaling, however the detailed mechanism behind this improvement remains unclear. This study investigated whether aerobic exercise enhances glycogen anabolism and insulin sensitivity via EGR-1/PTP1B signaling pathway in skeletal muscle of rats. Methods: Sprague-Dawley rats fed a high-fat diet (HFD), and performed treadmill exercise training for 6-week. Oral glucose tolerance test was conducted to confirm the IR. Periodic Acid-Schiff (PAS) staining and anthrone colorimetry were used to assess the skeletal muscle glycogen. RT-qPCR, western blot, and immunofluorescence were used to detect the EGR-1/PTP1B pathway and associated signaling molecules. Results: We found that exercise training significantly decreased blood glucose, insulin, and homeostasis model assessment for IR (HOMA-IR) against HFD-induced elevation. Decreased muscle glycogen content due to HFD was significantly restored after exercise training. Exercise training promoted mRNA expressions of Irs1, Akt, and Glut4, while inhibited Gsk-3β expression against HFD. Next, the decreased IRS1 (phosphorylated/total), AKT (phosphorylated/total), and GLUT4, and increased GSK-3β proteins with HFD were significantly reversed by exercise. Furthermore, HFD-induced overexpression of EGR-1 and PTP1B evidenced by mRNA, protein, and immunofluorescence intensity, were substantially inhibited by exercise, which may contribute to promote insulin sensitivity and glycogen anabolism. Conclusions: Aerobic exercise training promotes insulin sensitivity and skeletal muscle glycogen synthesis in HFD-fed rats. The beneficial effects of exercise might be mediated by EGR-1/PTP1B signaling pathway in skeletal muscle, however further studies are necessary to confirm this mechanism. [ABSTRACT FROM AUTHOR]

Probing regional glycogen metabolism in humans non-invasively has been challenging due to a lack of sensitive approaches. Here we studied human muscle glycogen dynamics post-exercise with a spatial resolution of millimeters and temporal resolution of minutes, using relayed nuclear Overhauser effect (glycoNOE) MRI. Data at 5T showed a homogeneous distribution of glycogen in resting muscle, with an average concentration of 99 ± 13 mM. After plantar flexion exercise following fasting with recovery under fasting conditions, the calf muscle showed spatially heterogeneous glycogen depletion and repletion kinetics that correlated with the severity of this depletion. Three types of regional glycogen kinetics were observed: (i) single exponential repletion (type a); (ii) biphasic recovery of rapid repletion followed by additional depletion (type b); (iii) biphasic recovery where continued depletion is followed by an exponential recovery (type c). The study of the complex patterns of glycogen kinetics suggests that glycogen breakdown may be quantitatively important during the initial recovery. The non-invasive spatial measurement of glycogen in humans has been challenging due to a lack of sensitive approaches. Here, the authors characterize regional glycogen dynamics in human muscle under exercise using MRI, providing insights into the complex patterns of muscle energy consumption and recovery. [ABSTRACT FROM AUTHOR]

This study aimed to evaluate the effects of adding chromium-methionine (Cr-meth) chelate in extruded diets containing reduced protein content on growth performance, carcass composition, nutrient retention, and hematobiochemical responses in Nile tilapia juveniles. The fish were fed with two control diets (no Cr-meth): positive control (311 g kg−1 of crude protein, estimated 258 g kg−1 of digestible protein) and negative control (255 g kg−1 of crude protein, estimated 207 g kg−1 of digestible protein). Another five experimental diets (mean 251 g kg−1 of crude protein, mean estimated 204 g kg−1 of digestible protein) were supplemented with 0.2, 0.4, 0.6, 0.8, and 1.0 mg Cr-meth kg diet−1. Juveniles (34.31 g) were organized in a randomized design (seven treatments in triplicate) in 21 tanks (250 L) and fed until apparent satiety. The experiment lasted 9 weeks. Fish fed 0.8 and 1.0 mg Cr-meth kg diet−1 showed zootechnical variables similar to the positive control. The reduced protein diets showed lower costs, and supplementation with 0.91 mg kg−1 of chromium matched the profitability observed in the positive control diet. Carcass gross energy and energy retention, plasma cholesterol (total and LDL), and triglycerides values were higher in fish fed 0.6 mg Cr-meth kg diet−1 than in the positive control. Treatments with dietary Cr-meth (mainly between 0.4 and 0.8 mg kg−1) decreased carcass Cr, selenium, and copper retention and increased carcass nitrogen retention and muscle glycogen levels compared to the positive control. This treatment (positive control) also had lower values for total leukocytes and monocytes, respectively, than fish fed 0.2 and 0.4 mg Cr-meth kg diet−1 and for eosinophils and lymphocytes than fish fed 0.8 mg Cr-meth kg diet−1. In conclusion, we recommend supplementation with 0.8 mg Cr-meth kg diet−1 for diets with low protein content, as it produces a dietary protein-sparing effect, reducing costs, improving immune defense, muscle glycogen, and nitrogen retention without compromising growth performance, physiology, and fish metabolism. [ABSTRACT FROM AUTHOR]

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Purpose of review: Women in Africa bear the burden of the HIV epidemic, which has been associated with the high prevalence of bacterial vaginosis (BV) in the region. However, little progress has been made in finding an effective cure for BV. Drawing on advances in microbiome-directed therapies for gastrointestinal disorders, similar live-biotherapeutic based approaches for BV treatment are being evaluated. Here, we summarize current knowledge regarding vaginal microbiota in BV, explore geographical differences in vaginal microbiota, and argue that novel BV therapeutics should be tailored specifically to meet the needs of African women. Recent findings: Cervicovaginal microbiota dominated by Lactobacillus crispatus are optimal, although these are uncommon in African women. Besides socio-behavioural and environmental influences on the vaginal microbiota, host and microbial genetic traits should be considered, particularly those relating to glycogen metabolism. Novel microbiome-directed approaches being developed to treat BV should employ transfers of multiple microbial strains to ensure sustained colonization and BV cure. Summary: Improving the efficacy and durability of BV treatment with microbiome-directed therapies by appropriately accounting for host and microbial genetic factors, could potentially reduce the risk of HIV infection in African women. [ABSTRACT FROM AUTHOR]

This study aimed to study the histo-architectural and histochemical changes in the liver and intestine of Labeo rohita fingerlings due to the integrative effect of short-term exposure to higher temperature and dietary protein levels. Six hundred Labeo rohita fingerlings (average weight 6.78 ± 0.05 g) were distributed into 24 tanks, with 25 fingerlings in each tank. The tanks were divided into eight experimental groups, with three replicates for each tank. Half of the experimental groups were maintained at an ambient water temperature of 260C, while the other half were kept at 320C for one week and then shifted back to 260C for four weeks. The fingerlings were fed with either of four diets, each containing different protein levels of 20%, 30%, 40% or 45% protein. At the end of the experiment, the hepatosomatic index (HSI) and visceral index (VI) of the juveniles were increased with the increase in dietary protein level, however significantly lower HSI was recorded at 320C compared to 260C. Juveniles exposed to elevated temperature (320C) for one week registered significantly higher (p < 0.05) liver glycogen content compared to 260C. Amylase, protease, and alkaline phosphatase activity in the intestine of juveniles were significantly (p < 0.05) higher at elevated temperature (320C) and decreased after 4 weeks of decrease in temperature from elevated temperature (320C) to ambient temperature (260C). The 45% CP fed group at 260C showed mildly desquamated mucosa in the liver whereas mucosa was found absent at 320C. Marked loss of mucosa was found in the intestine of L. rohita fed with 45% dietary protein after five weeks either at 260C or 320C. Overall it concludes that the dietary protein level and water temperature interactions are more effective in maintaining the histo-architectural structure of the liver and intestine, which responds to increased digestive enzyme activity. [ABSTRACT FROM AUTHOR]

A systematic review with meta-analysis was conducted to analyze the effect of carbohydrate (CHO) intake during exercise and some variables that could moderate this effect on endurance performance. We included 136 studies examining the effect of CHO ingestion during endurance exercise in the meta-analysis. The overall effect on performance showed a significant increase after CHO intake compared to the placebo/control groups. A larger effect of CHO consumption is observed in time to exhaustion than in time trials performance test. Moreover, the effectiveness of CHO supplementation was greater the longer the duration of the events. Also, there seems to be a higher effect of CHO intake in lower trained than in higher trained participants. In contrast, the magnitude of performance change of CHO intake is not affected by the dosage, ergometer used, the type of intake of the CHO ingestion and the type of CHO. In addition, a lower rate of perceived exertion and higher power and heart rate are significantly associated with the ingestion of CHO during endurance exercise. These results reinforce that acute CHO feeding is an effective strategy for improving endurance performance, especially, in less trained subjects participating in time to exhaustion tests of longer durations. [ABSTRACT FROM AUTHOR]

Background: Chicken embryos emerge from their shell by the piercing movement of the hatching muscle. Although considered a key player during hatching, with activity that imposes a substantial metabolic demand, data are still limited. The study provides a bioenergetic and transcriptomic analyses during the pre-post-hatching period. Methods: Weight and morphology alongside content determination of creatine and glycogen were analysed. Transcriptome identified differentially expressed genes and enriched biological processes associated with hatching muscle development, catabolism, and energy provision. Using gene set enrichment, we followed the dynamics of gene-sets involved in energy pathways of oxidative phosphorylation, protein catabolism, glycolysis/gluconeogenesis, and glycogen metabolism. Results: Results show several significant findings: (A) Creatine plays a crucial role in the energy metabolism of the hatching muscle, with its concentration remaining stable while glycogen concentration is depleted at hatch and placement. (B) The hatching muscle has the capacity for de-novo creatine synthesis, as indicated by the expression of related genes (AGAT, GAMT). (C) Transcriptome provided insights into genes related to energy pathways under conditions of pre-hatch oxygen and post-hatch glucose limitations (oxidative phosphorylation: NDUF, MT-ND, SDH, UQCR, COX, MT-CO, ATP5, MT-ATP; glycolysis/gluconeogenesis: FBP,G6PC, PFKM; glycogen metabolism: PPP1, PYGL, GYG1). (D) The post-hatch upregulation of protein catabolic processes genes (PSMA, RNF, UBE, FBX), which align with the muscle's weight dynamics, indicates a functional shift from movement during hatching to lifting the head during feeding. Conclusions: There is a dynamic metabolic switch in the hatching muscle during embryo-to-hatchling transition. When glycogen concentration depletes, energy supply is maintained by creatine and its de-novo synthesis. Understanding the hatching muscle's energy dynamics is crucial, for reducing hatching failures in endangered avian species, and in domesticated chickens. [ABSTRACT FROM AUTHOR]

Red microalgae from the Cyanidiophyceae, particularly Galdieria sulphuraria and Cyanidioschyzon merolae, are primitive photosynthetic thermoacidophiles that thrive in acidic hot springs and geysers. Unlike most Cyanidiophyceae, Galdieria strains are metabolically flexible as they can switch from photoautotrophic growth in the light to heterotrophic growth in complete darkness. Galdieria sulphuraria is especially noteworthy for its accumulation of various commercially valuable, functional compounds such as glycogen and phycocyanin. Glycogen, a branched fractal-like polysaccharide composed of several thousands of anhydroglucopyranose units, can be added to cosmetic products and sports drinks as a moisturizer or slow-digestible carbohydrate. While the production and structural characteristics of the glycogen of G. sulphuraria 108.79, isolated from Yellowstone National Park, have been previously described, our investigation aimed to explore glycogen production and properties across various Galdieria strains from different locations. Our findings reveal that all examined strains produce substantial amounts of highly branched glycogen when grown heterotrophically on glycerol in the dark. Notably, the structural characteristics of Galdieria glycogen distinguish it from both eukaryotic and prokaryotic glycogen, exhibiting a significantly higher degree of branching, substantially shorter side chains, and a considerable extent of indigestibility. These findings support the hypothesis that this highly branched, small glycogen is a long-term energy store, enabling survival during extended periods of complete darkness. [ABSTRACT FROM AUTHOR]

Zinc and iron as two important essential minerals for testis functions are controlled by Zinc transporters. It has been reported that zinc and its transporters are affected by nutrition and training. The main goals of the current experimentation were to the influences of training in combination with extraction of Ajwain seeds on rat testicular zinc and zinc transporters. Forty male rats were randomly assigned into four groups. Rats were orally received an aqueous Ajwain seed extraction (200 mg kg-1) and the saline groups were treated in the same manner. Results showed that gene expression of Znt5 had meaningfully changed in the ST group in comparison with SC (p = 0.004) and AT (p = 0.001) groups. Expression of this gene had meaningfully alteration in the AT group in comparison with ST (p = 0.036) and AC (p = 0.001) groups. Gene expression of Znt8 was also significantly increased in AT group compared to AC group (P = 0.010). Expression of Znt9 was also significantly increased in AT group in comparison with AC (P = 0.008) and ST (P = 0.026) groups. Expression of the other genes (Znt6, Zip7, Zip8, and Zip14) and also the content of Zn, Fe and glycogen did not show significant differences. The concurrent implementation of training and supplementation with the extract of Ajwain seed significantly modulated the expression levels of certain zinc transporters. These discoveries can offer new understandings into the underlying mechanisms of the effects of exercise and nutrition on testicular tissue. [ABSTRACT FROM AUTHOR]

Although physiology ensures homeostasis and fitness in a particular environment, and ecological shifts cannot be realized without physiological changes, metabolic transformations during animal adaptive radiations still remain unexplored. We present a study of energy reserve storage in the salmonid assemblage inhabiting a cold-water Lake Kronotskoe. This assemblage diversified from Salvelinus malma and includes eight distinct ecomorphs with contrasting lifestyles and trophic specializations. We hypothesized that ecomorphs differ in energy storage and expenditure, and that their metabolic phenotypes should be among the primary targets of natural selection. To test this hypothesis, we compared the stored amount and ratio of carbohydrates, lipids, circulating peptides that supply the citric acid cycle, as well as proxy indicators of metabolic rate, the blood levels of plasma proteins (including albumin) and hemoglobin. Among ecomorphs, numerous significant differences in physiological parameters were found, closely related to the composition of food, the depth of habitat, and determined by internal factors, probably genetics. Each ecomorph has a specific metabolic phenotype corresponding to its tropho-ecological specialization and lifestyle. Metabolically advanced predators accumulate lipids; littoral insectivorous morphs grow slower and accumulate glycogen; amphipod feeders do not accumulate spare substances; the deepwater consumer of silt benthos differs in the most divergent physiological characteristics. We assume a specific selection on endocrine regulators of energy metabolism during the adaptive radiation of the assemblage, among which the most plausible candidates are thyroid hormones and leptin. [ABSTRACT FROM AUTHOR]

Astrocyte glycogenolysis shapes ventromedial hypothalamic nucleus (VMN) regulation of glucostasis in vivo. Glucose transporter-2 (GLUT2), a plasma membrane glucose sensor, controls hypothalamic primary astrocyte culture glycogen metabolism in vitro. In vivo gene silencing tools and single-cell laser-catapult-microdissection/multiplex qPCR techniques were used here to examine whether GLUT2 governs dorsomedial (VMNdm) and/or ventrolateral (VMNvl) VMN astrocyte metabolic sensor and glycogen metabolic enzyme gene profiles. GLUT2 gene knockdown diminished astrocyte GLUT2 mRNA in both VMN divisions. Hypoglycemia caused GLUT2 siRNA-reversible up-regulation of this gene profile in the VMNdm, but down-regulated VMNvl astrocyte GLUT2 transcription. GLUT2 augmented baseline VMNdm and VMNvl astrocyte glucokinase (GCK) gene expression, but increased (VMNdm) or reduced (VMNvl) GCK transcription during hypoglycemia. GLUT2 imposed opposite control, namely stimulation versus inhibition of VMNdm or VMNvl astrocyte 5'-AMP-activated protein kinase-alpha 1 and -alpha 2 gene expression, respectively. GLUT2 stimulated astrocyte glycogen synthase (GS) gene expression in each VMN division. GLUT2 inhibited transcription of the AMP-sensitive glycogen phosphorylase (GP) isoform GP-brain type (GPbb) in each site, yet diminished (VMNdm) or augmented (VMNvl) astrocyte GP-muscle type (GPmm) mRNA. GLUT2 enhanced VMNdm and VMNvl glycogen accumulation during euglycemia, and curbed hypoglycemia-associated VMNdm glycogen depletion. Results show that VMN astrocytes exhibit opposite, division-specific GLUT2 transcriptional responsiveness to hypoglycemia. Data document divergent GLUT2 control of GCK, AMPK catalytic subunit, and GPmm gene profiles in VMNdm versus VMNvl astrocytes. Ongoing studies seek to determine how differential GLUT2 regulation of glucose and energy sensor function and glycogenolysis in each VMN location may affect local neuron responses to hypoglycemia. [ABSTRACT FROM AUTHOR]

This work aims to develop and implement a pulse‐acquire sequence for three‐dimensional (3D) single‐voxel localized 13C MRS in humans at 7 T, in conjunction with bilevel broadband 1H decoupling, and to test its feasibility in vitro and in vivo in human calf muscle with emphasis on the detection of glycogen C1‐C6. A localization scheme suitable for measuring fast‐relaxing 13C signals in humans at 7 T was developed and implemented using the outer volume suppression (OVS) and one‐dimensional image selected in vivo spectroscopy (ISIS‐1D) schemes, similar to that which was previously reported in humans at 4 T. The 3D 13C localization scheme was followed by uniform 13C adiabatic excitation, all complemented with an option for bilevel broadband 1H decoupling to improve both 13C sensitivity and spectral resolution at 7 T. The performance of the pulse‐acquire sequence was investigated in vitro on phantoms and in vivo in the human calf muscle of three healthy volunteers, while measuring glycogen C1‐C6. In addition, T1 and T2 of glycogen C1‐C6 were measured in vitro at 7 T, as well as T1 of glycogen C1 in vivo. The glycerol C2 and C1,3 lipid resonances were efficiently suppressed in vitro at 7 T using the OVS and ISIS‐1D schemes, allowing distinct detection of glycogen C2‐C6. While some glycerol remained in calf muscle in vivo, the intense lipid at 130 ppm was efficiently suppressed. The 13C sensitivity and spectral resolution of glycogen C1‐C6 in vitro and glycogen C1 in vivo were improved at 7 T using bilevel broadband 1H decoupling. The T1 and T2 of glycogen C1‐C6 in vitro at 7 T were consistent compared with those at 8.5 T, while the T1 of glycogen C1 in vivo at 7 T resulted similar to that in vitro. Localized 13C MRS is feasible in human calf muscle in vivo at 7 T, and this will allow further extension of this method for 13C MRS measurements such as in the brain. [ABSTRACT FROM AUTHOR]

Copyright of Kufa Journal for Agricultural Science is the property of Republic of Iraq Ministry of Higher Education & Scientific Research (MOHESR) and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Pharmaceutical polymers based on glycogen as prodrugs were synthesized to enhance the physical and chemical properties, thereby increasing the solubility of the drugs compared to the original drugs. This improvement leads to better efficacy and bioavailability, enhancing their absorption and distribution within the body. The drug release process in prodrugs contributes to sustained pharmacological effects, extending the duration of therapeutic effects compared to immediate-release formulations. This research involves the preparation of pharmaceutical polymers [FA6-FA10] based on glycogen through the reaction of glycogen with maleic anhydride, followed by the addition of thionyl chloride and amino drugs to obtain new pharmaceutical polymers. These polymers were characterized spectrally using Fourier-transform infrared (FTIR) spectroscopy and proton nuclear magnetic resonance (¹H NMR) spectroscopy. The physical properties of the polymers, such as swelling, viscosity, and controlled drug release in acidic, basic, and neutral media, were studied. The antibacterial properties were also investigated against two types of bacteria, namely Gram-positive and Gram-negative bacteria, using the disk diffusion technique. The results were compared with corresponding antibacterial drugs, indicating an increase in the antibacterial activity of the pharmaceutical polymers. [ABSTRACT FROM AUTHOR]

Methionine sulfoximine (MSO) is a compound originally discovered as a byproduct of agene-based milled flour maturation. MSO irreversibly inhibits the astrocytic enzyme glutamine synthase (GS) but also interferes with the transport of glutamine (Gln) and of glutamate (Glu), and γ-aminobutyric acid (GABA) synthesized within the Glu/Gln-GABA cycle, in this way dysregulating neurotransmission balance in favor of excitation. No wonder that intraperitoneal administration of MSO has long been known to induce behavioral and/or electrographic seizures. Recently, a temporal lobe epilepsy (TLE) model based on local continuous infusion of MSO into the hippocampus has been developed reproducing the main features of human mesial TLE: induction of focal seizures, their spreading, increase in intensity over time, and development of spontaneous recurrent seizures. Fully developed TLE in this model is associated with hippocampal degeneration, hallmarked by reactive astrogliosis, and causally related to the concomitant loss of GS-containing astrocytes. By contrast, short-term pre-exposure of rats to relatively low MSO doses that only moderately inhibited GS, attenuated and delayed the initial seizures in the lithium-pilocarpine model of TLE and in other seizure-associated contexts: in the pentylenetetrazole kindling model in rat, and in spontaneously firing or electrically stimulated brain slices. The anti-initial seizure activity of MSO may partly bypass inhibition of GS: the postulated mechanisms include: (i) decreased release of excitatory neurotransmitter Glu, (ii) prevention or diminution of seizure-associated brain edema, (iii) stimulation of glycogenesis, an energy-sparing process; (iv) central or peripheral hypothermia. Further work is needed to verify either of the above mechanisms. [ABSTRACT FROM AUTHOR]

Copyright of Food & Fermentation Industries is the property of Food & Fermentation Industries and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Background: Fatigue is a prevalent issue that can lead individuals to a sub-health condition, impacting their work efficiency and quality of life. There are limited effective treatment options available for fatigue. Ren-Shen-Bu-Qi decoction (RSBQD) is a proprietary herbal remedy that is designed to address fatigue. However, the specific pharmacological mechanisms and basis of RSBQD are not yet fully understood. Purpose: This study aimed to investigate the pharmacological effects and mechanisms of RSBQD in a mouse model of exercise fatigue. Materials and methods: UPLC-Q-Orbitrap HRMS was used to analyze the chemical composition of RSBQD. The pharmacological basis and molecular mechanism of RSBQD on exercise fatigue were predicted using network pharmacology analysis. Subsequently, an exercise fatigue mouse model was established and used to analysis the effects of RSBQD. The potential mechanisms were verified by hematoxylin–eosin (HE) staining, real-time fluorescence quantitative PCR (RT-qPCR), Western blot (WB) and molecular docking. Results: The results showed that 88 main components of RSBQD were identified, which have mainly belonged to flavonoids and carboxylic acid compounds. The network pharmacology analysis indicated that RSBQD ameliorate fatigue through PI3K/AKT signaling pathway. Notably, RSBQD prolonged the swimming time and diminished body weight loss of exercise fatigue mice (P < 0.05). Meanwhile, RSBQD significantly alleviated the injury of liver and kidney induced by exhaustive exercise, and decreasing the serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), urea and BUN levels (P < 0.05). In addition, RSBQD was found could relieve exercise fatigue by decreasing the content of creatine kinase (CK), lactate dehydrogenase (LDH), and lactic acid (LA), but increasing the blood glucose (GLU) and liver glycogen (HG) levels (P < 0.05). RSBQD also significantly increased the hepatic superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) but decreased hepatic malondialdehyde (MDA) levels. Moreover, RSBQD was able to upregulate protein level of activated Nrf2 and PI3K/AKT signaling pathways. Conclusions: RSBQD mitigates exercise fatigue by reversing metabolic changes and reducing oxidative damage through the PI3K/AKT/Nrf2 signaling pathway. This study offers pharmacological support for the utilization of RSBQD in exercise fatigue treatment. [ABSTRACT FROM AUTHOR]

Glycogen, a branched polysaccharide organized into glycogen granules (GGs), is delivered from the cytoplasm to the lysosomes of hepatocytes by STBD1-driven selective autophagy (glycophagy). Recently, we developed Komagataella phaffii yeast as a simple model of GG autophagy and found that it proceeds non-selectively under nitrogen starvation conditions. However, another group, using Saccharomyces cerevisiae as a model, found that glycogen is a non-preferred cargo of nitrogen starvation-induced bulk autophagy. To clarify cargo characteristics of K. phaffii GGs, we used the same glycogen synthase-based reporter (Gsy1-GFP) of GG autophagy in K. phaffii as was used in S. cerevisiae. The K. phaffii Gsy1-GFP marked the GGs and reported on their autophagic degradation during nitrogen starvation, as expected. However, unlike in S. cerevisiae, glycogen synthase-marked GGs were delivered to the vacuole and degraded there with the same efficiency as a cytosolic glycogen synthase in glycogen-deficient cells, suggesting that glycogen is a neutral cargo of bulk autophagy in K. phaffii. We verified our findings with a new set of reporters based on the glycogen-binding CBM20 domain of human STBD1. The GFP-CBM20 and mCherry-CBM20 fusion proteins tagged GGs, reported about the autophagy of GGs, and confirmed that GGs in K. phaffii are neither preferred nor non-preferred substrates of bulk autophagy. They are its neutral substrates. [ABSTRACT FROM AUTHOR]

Glycogen-storing so-called clear cell kidney tubules (CCTs), precursor lesions of renal cell carcinoma, have been described in diabetic rats and in humans. The lesions show upregulation of the Akt/mTOR-pathway and the related transcription factor carbohydrate responsive element binding protein (ChREBP), which is supposedly pro-oncogenic. We investigated the effect of ChREBP-knockout on nephrocarcinogenesis in streptozotocin-induced diabetic and normoglycemic mice. Diabetic, but not non-diabetic mice, showed CCTs at 3, 6 and 12 months of age. Glycogenosis was confirmed by periodic acid schiff reaction and transmission electron microscopy. CCTs in ChREBP-knockout mice consisted of larger cells and occurred more frequently compared to wildtype mice. Progression towards kidney tumors was observed in both diabetic groups but occurred earlier in ChREBP-knockout mice. Proliferative activity assessed by BrdU-labeling was lower in 1-week-old but higher in 12-month-old diabetic ChREBP-knockout mice. Surprisingly, renal neoplasms occurred spontaneously in non-diabetic ChREBP-knockout, but not non-diabetic wildtype mice, indicating an unexpected tumor-suppressive function of ChREBP. Immunohistochemistry showed upregulated glycolysis and lipogenesis, along with activated Akt/mTOR-signaling in tumors of ChREBP-knockout groups. Immunohistochemistry of human clear cell renal cell carcinomas revealed reduced ChREBP expression compared to normal kidney tissue. However, the molecular mechanisms by which loss of ChREBP might facilitate tumorigenesis require further investigation. [ABSTRACT FROM AUTHOR]

It is unknown whether changes in lactate concentration produced by different situations (e.g., glycogen depletion or heat) modify fat oxidation. If confirmed, we could determine a dose–response relationship between lactate and fat. The aim of this study was to determine whether changes in lactate concentration (due to glycogen depletion or heat) alter fat oxidation during exercise. 11 males and eight females performed an incremental exercise test under three situations: control, glycogen depletion, and heat. At rest, in the last minute of each step and immediately post‐exhaustion, lactate was analyzed and fat oxidation was estimated by indirect calorimetry. Lactate concentration was inversely associated with fat oxidation in the three aforementioned situations (r > 0.88 and p < 0.05). The highest lactate concentration was found in the heat situation, followed by the control situation, and finally the glycogen depletion situation (all p < 0.05). The opposite was found for fat oxidation, with the highest fat oxidation found in the glycogen depletion situation, followed by the control situation, and finally the heat situation (all p < 0.05). There is no association between the changes in lactate concentration between situations at each intensity and the changes in fat oxidation between situations at each intensity in males or females (p > 0.05). In conclusion, lactatemia is strongly and inversely associated with fat oxidation under the three different situations. Furthermore, the lowest lactate concentrations were accompanied by the highest fat oxidations in the glycogen depletion situation, whereas the highest lactate concentrations were accompanied by the lowest fat oxidations in the heat situation. Highlights: It was found that a very strong inverse association between lactatemia and fat oxidation in females and males despite changes in both substrates between situations. Hence, assessing blood lactate alone could be an effective way to indirectly assess fat oxidation when the situation is the same. Importantly, lactate‐fat relationship is different between situations, indicating to extrapolate fat oxidation from lactate, or vice versa, this relationship needs to be previously determined in each specific situation.Since the same blood lactate concentration does not imply the same fat oxidation in different situations, a fixed blood lactate concentration may not reflect the same metabolic response, even in the same individual, if he/she is exposed to different situations.Changes in lactate kinetics, due to heat or glycogen depletion, are accompanied by opposite changes in the fat oxidation pattern. However, changes in blood lactate concentration between situations at each intensity are not associated with changes in the fat oxidation between situations at each intensity. Therefore, these results suggest an absence of a dose–response relationship between both variables indicating that lactate may not be a major regulatory factor of changes in fat oxidation across different situations during exercise. [ABSTRACT FROM AUTHOR]

Fanconi-Bickel syndrome (FBS) is a rare genetic disorder of carbohydrate metabolism due to pathogenic variants in SLC2A2, a gene encoding glucose transporter 2 (GLUT2), which leads to accumulation of glycogen in the kidney and liver. While consequential complex proximal tubular dysfunction is well acknowledged in the literature, long-term trajectories of kidney function in patients with FBS have not been well characterized, and kidney biopsy is performed infrequently. Here, we report on a patient with FBS followed from infancy through young adulthood who presented early on with hypercalciuria, phosphaturia, and hypophosphatemia, complicated by chronic kidney disease development during childhood. Kidney biopsy, in addition to a widespread glycogen accumulation in proximal tubular epithelial cells, demonstrated medullary nephrocalcinosis. Screening for nephrocalcinosis may be warranted in pediatric patients with FBS, along with close surveillance of their kidney function. [ABSTRACT FROM AUTHOR]

The second-meal phenomenon refers to the improvement in glucose tolerance seen following a second identical meal. We previously showed that 4 h of morning hyperinsulinemia, but not hyperglycemia, enhanced hepatic glucose uptake (HGU) and glycogen storage during an afternoon hyperinsulinemic-hyperglycemic (HIHG) clamp. Our current aim was to determine if the duration or pattern of morning hyperinsulinemia is important for the afternoon response to a HIHG clamp. To determine this, the same total amount of insulin was administered either over 2 h in the first (Ins2h-A) or second (Ins2h-B) half of the morning or over the entire 4 h (Ins4h) of the morning. In the 4-h afternoon period, all three groups had 4x-basal insulin, 2x-basal glycemia, and portal glucose infusion to expose the liver to the primary postprandial regulators of hepatic glucose metabolism. During the afternoon clamp, there was a marked increase in HGU and hepatic glycogen synthesis in the Ins4h group compared with the Ins2h-A and Ins2h-B groups, despite matched hepatic glucose loads and total insulin infusion rates. Thus, the longer duration (Ins4h) of lower hyperinsulinemia in the morning seems to be the key to much greater liver glucose uptake during the afternoon clamp. NEW & NOTEWORTHY: Morning insulin exposure primes the liver for increased hepatic glucose uptake and glycogen storage during a subsequent hyperinsulinemic-hyperglycemic clamp. This study addressed whether the pattern and/or duration of insulin delivery in the morning influences insulin's ensuing priming effect. We found that despite receiving equal total doses of insulin in the morning, a prolonged, lower rate of morning insulin delivery improved afternoon liver glucose metabolism more effectively than a shorter, higher rate of delivery. [ABSTRACT FROM AUTHOR]

Mitochondria and glycogen are co-distributed in skeletal muscles to regulate the metabolic status. Mitochondria are also redox centers that regulate the muscle function during exercise. However, the pathophysiological relationship between the mitochondrial redox status and glycogen metabolism in the muscle remains unclear. In the present study, we examined the pathological effects of mitochondrial dysfunction induced by mitochondrial superoxide dismutase (SOD2) depletion on glycogen metabolism. We found that muscle glycogen was significantly accumulated in association with motor dysfunction in mice with a muscle-specific SOD2 deficiency. Muscle glycogen phosphorylase (GP-M) activity, which is a key enzyme for glycogen degradation at times when energy is needed (e.g., during exercise), was significantly decreased in the mutant muscle. Moreover, the GP-M activity on normal muscle sections decreased after treatment with paraquat, a superoxide generator. In contrast, treatment with antioxidants reversed the GP-M activity and motor disturbance of the mutant mice, indicating that GP-M activity was reversibly regulated by the redox balance. These results demonstrate that the maintenance of the mitochondrial redox balance regulates glycogen metabolism via GP-M activity. [ABSTRACT FROM AUTHOR]

Background: Post-hepatectomy liver failure (PHLF) is a fatal complication of hepatectomy. However, the mechanism of hepatocyte injury in PHLF remains elusive. Methods: PHLF was induced by extended 86% hepatectomy (eHx) in mice. Lipidomics was performed to investigate the eHx-induced lipid alteration in the residual liver. Ferroptosis was assessed to screen the hepatocyte injury induced by eHx. The therapeutic effects of ferrostatin-1 (Fer-1) on PHLF were evaluated. Results: PHLF was induced by eHx with elevation in markers of hepatocyte injury and mortality in mice within 48 h after surgery. eHx-induced hepatocyte injury was manifested by hepatocyte enlargement and hepatocyte death with glycogen depletion and lipid accumulation. Lipidomics revealed that eHx induced the accumulation of ferroptosis-favored polyunsaturated lipids. Ferroptosis was found to mediate the eHx-induced hepatocyte death in the residual liver during the development of PHLF. Fer-1 could attenuate the eHx-induced ferroptotic hepatocyte death and PHLF in mice. Conclusions: Ferroptosis partly mediates the eHx-induced hepatocyte injury during the development of PHLF. Accumulation of polyunsaturated lipids in hepatocytes may promote eHx-induced ferroptosis, and targeting lipid peroxidation is a potential therapeutic strategy for PHLF. [ABSTRACT FROM AUTHOR]

The impact of caffeine and glucose supplementation in a hypoxic environment on endurance exercise performance remains inconclusive. The current study examined the effect of pre-exercise carbohydrate and caffeine supplementation on endurance exercise performance in an acute hypoxic environment. Eight healthy active young males participated in this double-blind, within-subjects crossover study. Participants ingested the test drink 60 min before exercising at 50% Wmax for 90 min on a cycle ergometer (fatiguing preload); there followed an endurance performance test at 85% Wmax until exhaustion in a hypoxic chamber (~15%O2). Participants completed four experimental trials in a randomized order: caffeine (6 mg·kg−1; Caff), glucose (1 g·kg−1; CHO), caffeine (6 mg·kg−1) + glucose (1 g·kg−1; Caff−CHO), and taste- and color-matched placebo with no caffeine or CHO (PLA). Blood samples were collected during fasting, pre-exercise, every 30 min throughout the exercise, and immediately after exhaustion. The caffeine and glucose trials significantly enhanced endurance capacity in hypoxic conditions by Caff, 44% (68.8–31.5%, 95% confidence interval), CHO, 31% (44.7–15.6%), and Caff−CHO, 46% (79.1–13.2%). Plasma-free fatty-acid and glycerol concentrations were higher in Caff and PLA than in CHO and Caff−CHO (p < 0.05). The estimated rate of fat oxidation was higher in Caff and PLA than in CHO and Caff−CHO (p < 0.05). There were no significant differences in ratings of perceived exertion between trials. In conclusion, the ingestion of caffeine, glucose, or caffeine + glucose one hour before exercising in hypoxic conditions significantly improved 85% Wmax endurance performance after prolonged exercise. [ABSTRACT FROM AUTHOR]

Alzheimer’s disease (AD) is a debilitating progressively neurodegenerative disease. The best-characterized hallmark of AD, which is marked by behavioral alterations and cognitive deficits, is the aggregation of deposition of amyloid-beta (Aβ) and hyper-phosphorylated microtubule-associated protein Tau. Despite decades of experimental progress, the control rate of AD remains poor, and more precise deciphering is needed for potential therapeutic targets and signaling pathways involved. In recent years, phosphoinositide 3-kinase (PI3K) and Akt have been recognized for their role in the neuroprotective effect of various agents, and glycogen synthase kinase 3 (GSK3), a downstream enzyme, is also crucial in the tau phosphorylation and Aβ deposition. An overview of the function of PI3K/Akt pathway in the pathophysiology of AD is provided in this review, along with a discussion of recent developments in the pharmaceuticals and herbal remedies that target the PI3K/Akt signaling pathway. In conclusion, despite the challenges and hurdles, cumulative findings of novel targets and agents in the PI3K/Akt signaling axis are expected to hold promise for advancing AD prevention and treatment. [ABSTRACT FROM AUTHOR]

Introduction: Metabolic adaptability, including glucose metabolism, enables cells to survive multiple stressful environments. Glycogen may serve as a critical storage depot to provide a source of glucose during times of metabolic demand during the metastatic cascade; therefore, understanding glycogen metabolism is critical. Our goal was to determine mechanisms driving glycogen accumulation and its role in metastatic (MCF10CA1a) compared to nonmetastatic (MCF10A-ras) human breast cancer cells. Methodology:13C6-glucose flux analysis in combination with inhibitors of the gluconeogenic pathway via phosphoenolpyruvate carboxykinase (PCK), the anaplerotic enzyme pyruvate carboxylase (PC), and the rate-limiting enzyme of the pentose phosphate pathway (PPP) glucose 6-phosphate dehydrogenase (G6PD). To determine the requirement of glycogenolysis for migration or survival in extracellular matrix (ECM) detached conditions, siRNA inhibition of glycogenolysis (liver glycogen phosphorylase, PYGL) or glycophagy (lysosomal enzyme α-acid glucosidase, GAA) enzymes was utilized. Results: Metastatic MCF10CA1a cells had 20-fold greater glycogen levels compared to non-metastatic MCF10A-ras cells. Most glucose incorporated into glycogen of the MCF10CA1a cells was in the five13C-containing glucose (M+5) instead of the expected M+6 glycogen-derived glucose moiety, which occurs through direct glucose conversion to glycogen. Furthermore,13C6-glucose in glycogen was quickly reduced (~50%) following removal of13C-glucose. Incorporation of 13C6-glucose into the M+5 glucose in the glycogen stores was reduced by inhibition of PCK, with additional contributions from flux through the PPP. Further, inhibition of PC reduced total glycogen content. However, PCK inhibition increased total unlabeled glucose accumulation into glycogen, suggesting an alternative pathway to glycogen accumulation. Inhibition of the rate-limiting steps in glycogenolysis (PYGL) or glycophagy (GAA) demonstrated that both enzymes are necessary to support MCF10CA1a, but not MCF10A-ras, cell migration. GAA inhibition, but not PYGL, reduced viability of MCF10CA1a cells, but not MCF10A-ras, in ECM detached conditions. Conclusion: Our results indicate that increased glycogen accumulation is primarily mediated through the gluconeogenesis pathway and that glycogen utilization is required for both migration and ECM detached survival of metastatic MCF10CA1a cells. These results suggest that glycogen metabolism may play an important role in the progression of breast cancer metastasis. [ABSTRACT FROM AUTHOR]

Background: Cardiovascular function and metabolic homeostasis are closely linked, but the underlying mechanisms are not fully understood. Corin is a protease that activates atrial natriuretic peptide (ANP), an essential hormone for normal blood pressure and cardiac function. The goal of this study is to investigate a potential corin and ANP function in regulating liver glycogen metabolism and glucose homeostasis. Methods: Liver glycogen and blood glucose levels were analyzed in Corin or Nppa (encoding ANP) knockout (KO) mice. ANP signaling was examined in livers from Corin and Nppa KO mice and in cultured human and mouse hepatocytes by western blotting. Results: We found that Corin and Nppa KO mice had reduced liver glycogen contents and increased blood glucose levels. By analyzing conditional KO mice lacking either cardiac or renal Corin, we showed that cardiac corin and ANP act in an endocrine manner to enhance cGMP-protein kinase G (PKG)-AKT-GSK3 signaling in hepatocytes. In cultured hepatocytes, ANP treatment stimulated PKG signaling, glucose uptake, and glycogen production, which could be blocked by small molecule PKG and AKT inhibitors. Conclusions: Our results indicate that corin and ANP are important regulators in liver glycogen metabolism and glucose homeostasis, suggesting that defects in the corin and ANP pathway may contribute to both cardiovascular and metabolic diseases. [ABSTRACT FROM AUTHOR]

Both the quality of chicken meat and the quality of chicks are influenced by the level of breast muscle glycogen reserves. In order to study the role of digestive metabolism in establishing this muscular phenotype, we compared two divergent chicken lines for the ultimate pH (pHu) of the breast meat, a proxy for glycogen reserves. Males aged 4 weeks had twice the breast muscle glycogen content in the pHu- line (low pHu) than in the pHu + line (high pHu). The increase in glycogen reserves (pHu-) was associated with a higher relative weight of the proventriculus and gizzard, as well as better apparent ileal digestibility of nitrogen and calcium. The diversity of the cecal microbiota was comparable, but three bacterial genera (Lachnospira, Lachnospiraceae UCG-010, Caproiciproducens) varied between the lines. The differences observed could lead to down-regulation of carbon fixation in prokaryotes and of the citrate cycle in the pHu + line. RNA-seq analysis of the jejunum, the major site of nutrient absorption, revealed 149 genes differentially expressed (DE) between the lines, including several genes linked to immunity, hormonal response and circadian rhythms that are less expressed in pHu + animals. Others involved in cell migration and proliferation, and more generally tissue morphogenesis, also differed between the lines. Among the DE genes, several co-localized with Quantitative Trait Loci (QTL) controlling pHu and selection signatures identified in the divergent lines, such as the gene coding for ghrelin, a hormone regulating appetite. [ABSTRACT FROM AUTHOR]

The overall objective was to determine how no extracellular glucose and/or low glycogen content affect fatigue kinetics in mouse flexor digitorum brevis (FDB) single muscle fibers. High glycogen content (Hi GLY), near normal in situ level, was obtained by incubating fibers in culture medium containing glucose and insulin while low glycogen content (Lo GLY), at about 19% of normal in situ level, was achieved by incubating fibers without glucose. Neither Lo GLY nor the absence of extracellular glucose (0GLU) affected tetanic [Ca2+]i prior to fatigue. The number of contracting unfatigued fibers versus stimulus strength relationship of Lo GLY‐0GLU fibers was shifted to higher voltages compared to Hi GLY fibers exposed to 5.5 mM glucose (5GLU). The relationship for Lo GLY‐0GLU fibers was shifted back toward that of Hi GLY‐5GLU fibers when glucose was reintroduced, whereas the removal of glucose from Hi GLY‐5GLU fibers had no effect. Fatigue was elicited with one 200 ms long tetanic contraction every s for 3 min. Both Lo GLY and 0GLU increased the rate at which intracellular tetanic concentration ([Ca2+]i) declined and unstimulated [Ca2+]i increased during fatigue in the order of the least fatigue resistant > mid fatigue resistant > the most fatigue resistant fibers. [ABSTRACT FROM AUTHOR]

This study investigates the carbohydrate content of Schwenkiella orientalis, a nematode parasite infecting Periplaneta americana (American cockroach), focusing on its total sugar and glycogen levels. The study conducted in Bulandshahr (U.P.) and it employs the Anthrone method to quantitatively analyze carbohydrate reserves within the parasite. The findings reveal that the total sugar content increases from 42 µg/mg in 5 mg parasites to 85 µg/mg in 20 mg parasites, while glycogen levels rise from 18 µg/mg to 62 µg/mg for the same weight range. This indicates that larger parasites possess greater energy reserves. The data suggest that Schwenkiella orientalis efficiently absorbs carbohydrates from its host for immediate metabolic needs while utilizing glycogen as a crucial energy reserve during nutrient-scarce periods. This research underscores the significance of carbohydrate metabolism in parasitic nematodes, highlighting the adaptive strategies that enable their survival within host environments. The use of the Anthrone method provides reliable measurements, contributing to a deeper understanding of nematode physiology and energy dynamics. These insights not only enhance knowledge of Schwenkiella orientalis but also have broader implications for parasitology, paving the way for future studies on the metabolic processes of insect-parasitizing nematodes and their interactions with hosts. [ABSTRACT FROM AUTHOR]

Purpose. To assess the liver parenchyma of Prussian carp based on the analysis of histological parameters of the organ, to establish the level of the effect of alylacetate on the physiological status of fish and the degree of their damage. To determine the prospects for using the obtained results in ichthyological and ecological practice. Methodology. The primary materials were obtained in the summer of 2024 in the Ingul River, city of Mykolaiv. The processing of histological samples was performed at the laboratory of histology, cytology and embryology of the Petro Mohyla Black Sea National University in accordance with generally recognized manuals and the author’s methodology for histological diagnosis of fish tissues. Findings. The study showed that uner the action of allyl acetate, significant changes occur in the marginal and medial zones of the organ in the form of a shift in a certain function, which leads to a change in intracellular metabolism and narrow cellular specialization. With the potential effect of allyl acetate, the reaction of hepatocytes was manifested in an increase in the lipid content in the cytoplasm. The general effect was visualized through the development of a picture of total lipostasis. Fatty degeneration was accompanied by vascular disorders and hemodynamic disorders, the presence of an inflammatory reaction. Under conditions of prolonged exposure to the toxicant, the number of hepatocytes with two nuclei and nucleoli increased significantly, which was recorded in healthy individuals and was not considered a sign of pathology. Under conditions of prolonged exposure to chemical stress, carcinogenesis was activated in the fish liver. This was evidenced by a characteristic picture of a failure of the moment of transition of the sequence and periodicity of morphogenetic processes, which manifested itself in the form of atypical cellular polymorphism. Originality. New data are presented on the reaction of the histological structure of the liver parenchyma of fish under conditions of technogenic load in the water body. For the first time, a detailed histological analysis of the structure of the organ under conditions of prolonged exposure to allyl acetate has been carried out. Information on changes in liver tissue, which demonstrate the destruction of its adaptive potential, has been supplemented. Practical Value. The information obtained is valuable in morphophysiological studies, as well as in ichthyological and ecological practice in connection with the problem of reducing the vital status of fish under conditions of technogenic loads on water bodies. The use of the obtained data allows for a qualitative assessment of the physiological state of fish and can be used in the process of developing corrective measures for the purpose of environmental protection. [ABSTRACT FROM AUTHOR]

Aim: To investigate how delayed post‐exercise carbohydrate intake affects muscle glycogen, metabolic‐ and mitochondrial‐related molecular responses, and subsequent high‐intensity interval exercise (HIIE) capacity. Methods: In a double‐blind cross‐over design, nine recreationally active men performed HIIE (10 × 2‐min cycling, ~94% W˙peak) in the fed state, on two occasions. During 0–3 h post‐HIIE, participants drank either carbohydrates ("Immediate Carbohydrate" [IC], providing 2.4 g/kg) or water ("Delayed Carbohydrate" [DC]); total carbohydrate intake over 24 h post‐HIIE was matched (~7 g/kg/d). Skeletal muscle (sampled pre‐HIIE, post‐HIIE, +3 h, +8 h, +24 h) was analyzed for whole‐muscle glycogen and mRNA content, plus signaling proteins in cytoplasmic‐ and nuclear‐enriched fractions. After 24 h, participants repeated the HIIE protocol until failure, to test subsequent HIIE capacity; blood lactate, heart rate, and ratings of perceived effort (RPE) were measured throughout. Results: Muscle glycogen concentrations, and relative changes, were similar between conditions throughout (p > 0.05). Muscle glycogen was reduced from baseline (mean ± SD mmol/kg dm; IC: 409 ± 166; DC: 352 ± 76) at post‐HIIE (IC: 253 ± 96; DC: 214 ± 82), +3 h (IC: 276 ± 62; DC: 269 ± 116) and + 8 h (IC: 321 ± 56; DC: 269 ± 116), returning to near‐baseline by +24 h. Several genes (PGC‐1ɑ, p53) and proteins (p‐ACCSer79, p‐P38 MAPKThr180/Tyr182) elicited typical exercise‐induced changes irrespective of condition. Delaying carbohydrate intake reduced next‐day HIIE capacity (5 ± 3 intervals) and increased RPE (~2 ratings), despite similar physiological responses between conditions. Conclusion: Molecular responses to HIIE (performed in the fed state) were not enhanced by delayed post‐exercise carbohydrate intake. Our findings support immediate post‐exercise refueling if the goal is to maximize next‐day HIIE capacity and recovery time is ≤24 h. [ABSTRACT FROM AUTHOR]

Aim: AMP‐activated protein kinase (AMPK) is activated during cellular energy perturbation. AMPK complexes are composed of three subunits and several variants of AMPK are expressed in skeletal muscle. The regulatory AMPKγ3 subunit is predominantly expressed in fast‐twitch muscle fibers. A human AMPKγ3 R225W mutation has been described. The mutation increases the total pool of AMPK activity in cells cultured from R225W carrier muscle and is associated with increased glycogen levels in mature skeletal muscle. This led to the idea of AMPKγ3 being involved in the regulation of skeletal muscle glycogen levels. Evidence for this causative link remains to be provided. Methods: We studied muscle biopsies from human carriers of the AMPKγ3 R225W mutation and we developed a novel AMPKγ3 R225W knock‐in mouse model (KI HOM). Through in vitro, in situ, and ex vivo techniques, we investigated AMPK activity, AMPK function, and glycogen levels in skeletal muscle of humans and mice. Results: In human carriers, the basal AMPKγ3‐associated activity was reduced when assayed in the absence of exogenous AMP. No difference was observed when assayed under AMP saturation, which was supported by findings in muscle of KI HOM mice. Furthermore, effects of AICAR/muscle contraction on AMPKγ3‐associated activity were absent in KI HOM muscle. Muscle glycogen levels were not affected by the mutation in human carriers or in KI HOM mice. Conclusions: The AMPKγ3 R225W mutation does not impact the AMPK‐associated activity in human skeletal muscle and the mutation is not linked to glycogen accumulation. The R225W mutation ablates the AMPKγ3‐associated activation by AICAR/muscle contractions, presumably due to loss of nucleotide binding in the CBS 1 domain of AMPKγ3. [ABSTRACT FROM AUTHOR]

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Neutrophils utilize a variety of metabolic sources to support their crucial functions as the first responders in innate immunity. Here, through in vivo and ex vivo isotopic tracing, we examined the contributions of different nutrients to neutrophil metabolism under specific conditions. Human peripheral blood neutrophils, in contrast to a neutrophil-like cell line, rely on glycogen storage as a major metabolic source under resting state but rapidly switch to primarily using extracellular glucose upon activation with various stimuli. This shift is driven by a substantial increase in glucose uptake, enabled by rapidly increased GLUT1 on cell membrane, that dominates the simultaneous increase in gross glycogen cycling capacity. Shifts in nutrient utilization impact neutrophil functions in a function-specific manner: oxidative burst depends on glucose utilization, whereas NETosis and phagocytosis can be flexibly supported by either glucose or glycogen, and neutrophil migration and fungal control are enhanced by the shift from glycogen utilization to glucose utilization. This work provides a quantitative and dynamic understanding of fundamental features in neutrophil metabolism and elucidates how metabolic remodeling shapes neutrophil functions, which has broad health relevance. [ABSTRACT FROM AUTHOR]

A new Ru-catalyzed C–H activation/cyclization reaction for the synthesis of 3-C-glycosyl isocoumarins and 2-glycosyl-4H-chromen-4-ones with carbonyl sulfoxonium ylide glycogen are reported. In this catalytic system, benzoic acid and its derivatives react with carbonyl sulfoxonium ylide glycogen to yield isocoumarin C-glycosides, while 2-hydroxybenzaldehyde substrates react to produce chromone C-glycosides. These reactions were characterized by mild reaction conditions, broad substrate scope, high functional-group compatibility, and high stereoselectivity to yield several high-value isocoumarins and chromone skeleton-containing C-glycosides. The methods were successfully implemented in the context of large-scale reactions and the late-stage modification of complex natural products. [ABSTRACT FROM AUTHOR]

To investigate the effect of Tetrasphaera's enrichment on phosphorus removal mechanism, three micro-pressure swirl reactor (MPSR) groups were used to experiment on sewage treatment under different SRT (17.2, 50.8, and 68.2 d). Results showed that Tetrasphaera enrichment in the MPSR system was promoted by extending the SRT. After extending the SRT from 17.2 to 68.2 d, the relative abundance of Tetrasphaera increased from 3.1% to 12.1%, and the TP removal efficiency maintained above 92%. The internal circulation results indicated that after extending the SRT, glycogen and polyhydroxybutyrate were co-synthesized during the anaerobic stage, which enhanced the driving force of nutrient removal. Analysis of the microbial composition and functional gene prediction indicated that efficient phosphorus removal can be attributed to the enrichment of Tetrasphaera at long SRT. Overall, the synergistic mechanisms of Tetrasphaera in the organic matter degradation and phosphorus removal processes were integrated into the MPSR. [ABSTRACT FROM AUTHOR]