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Energy status and nutrients regulate photosynthetic protein expression. The unicellular green alga Chromochloris zofingiensis switches off photosynthesis in the presence of exogenous glucose (+Glc) in a process that depends on hexokinase (HXK1). Here, we show that this response requires that cells lack sufficient iron (-Fe). Cells grown in -Fe+Glc accumulate triacylglycerol (TAG) while losing photosynthesis and thylakoid membranes. However, cells with an iron supplement (+Fe+Glc) maintain photosynthesis and thylakoids while still accumulating TAG. Proteomic analysis shows that known photosynthetic proteins are most depleted in heterotrophy, alongside hundreds of uncharacterized, conserved proteins. Photosynthesis repression is associated with enzyme and transporter regulation that redirects iron resources to (a) respiratory instead of photosynthetic complexes and (b) a ferredoxin-dependent desaturase pathway supporting TAG accumulation rather than thylakoid lipid synthesis. Combining insights from diverse organisms from green algae to vascular plants, we show how iron and trophic constraints on metabolism aid gene discovery for photosynthesis and biofuel production.

Statin drugs lower blood cholesterol levels for cardiovascular disease prevention. Women are more likely than men to experience adverse statin effects, particularly new-onset diabetes (NOD) and muscle weakness. Here we find that impaired glucose homeostasis and muscle weakness in statin-treated female mice are associated with reduced levels of the omega-3 fatty acid, docosahexaenoic acid (DHA), impaired redox tone, and reduced mitochondrial respiration. Statin adverse effects are prevented in females by administering fish oil as a source of DHA, by reducing dosage of the X chromosome or the Kdm5c gene, which escapes X chromosome inactivation and is normally expressed at higher levels in females than males. As seen in female mice, we find that women experience more severe reductions than men in DHA levels after statin administration, and that DHA levels are inversely correlated with glucose levels. Furthermore, induced pluripotent stem cells from women who developed NOD exhibit impaired mitochondrial function when treated with statin, whereas cells from men do not. These studies identify X chromosome dosage as a genetic risk factor for statin adverse effects and suggest DHA supplementation as a preventive co-therapy.

Background: Women with abnormal glucose tolerance during pregnancy are at risk for cardiovascular disease (CVD), with higher rates among Hispanics. However, studies on the impact of lifestyle interventions on postpartum CVD profiles are sparse. Methods: This is a secondary analysis of a controlled trial among a subsample of Hispanic women with abnormal glucose tolerance participating in Estudió PARTO (Project Aiming to Reduce Type twO diabetes; mean age = 28.2 y, SD: 5.8) who were randomized to a culturally modified Lifestyle intervention (n = 45) or a comparison Health and Wellness intervention (n = 55). Primary endpoints were biomarkers of cardiovascular risk (lipids, C-reactive protein, fetuin-A, and albumin-to-creatinine ratio) and insulin resistance (fasting insulin, glucose, HbA1c, homeostasis model assessment, leptin, tumor necrosis factor-alpha, and adiponectin) measured at baseline (6-wk postpartum) and 6 and 12 months. Results: In intent-to-treat analyses, there were no significant differences in changes in biomarkers of CVD risk or insulin resistance over the postpartum year. In prespecified sensitivity analyses, women adherent with the Lifestyle Intervention had more favorable improvements in insulin (intervention effect = −4.87, SE: 1.93, P =.01) and HOMA-IR (intervention effect = −1.15, SE: 0.53, P =.03) compared with the Health and Wellness arm. In pooled analyses, regardless of intervention arm, women with higher postpartum sports/exercise had greater increase in HDL-cholesterol (intervention effect = 6.99, SE: 1.72, P =.0001). Conclusions: In this randomized controlled trial among Hispanic women with abnormal glucose tolerance, we did not observe a significant effect on postpartum biomarkers of CVD risk or insulin resistance. Women adherent to the intervention had more favorable changes in insulin and HOMA-IR. [ABSTRACT FROM AUTHOR]

Rapid and precise detection of hydrogen peroxide (H2O2) holds great significance since it is linked to numerous physiological and inorganic catalytic processes. We herein developed a label-free and washing-free strategy to detect H2O2 by employing a hand-held personal glucose meter (PGM) as a signal readout device. By focusing on the fact that the reduced redox mediator ([Fe(CN)6]4-) itself is responsible for the final PGM signal, we developed a new PGM-based strategy to detect H2O2 by utilizing the target H2O2-mediated oxidation of [Fe(CN)6]4- to [Fe(CN)6]3- in the presence of horseradish peroxidase (HRP) and monitoring the reduced PGM signal in response to the target amount. Based on this straightforward and facile design principle, H2O2 was successfully determined down to 3.63 μM with high specificity against various non-target molecules. We further demonstrated that this strategy could be expanded to identify another model target choline by detecting H2O2 produced through its oxidation promoted by choline oxidase. Moreover, we verified its practical applicability by reliably determining extracellular H2O2 released from the breast cancer cell line, MDA-MB-231. This work could evolve into versatile PGM-based platform technology to identify various non-glucose target molecules by employing their corresponding oxidase enzymes, greatly advancing the portable biosensing technologies.

Food insecurity is highly prevalent and linked to poorer diet and worse metabolic outcomes. Food insecurity can be stressful, and could elicit chronic psychological and physiological stress. In this study, we tested whether stress could be used to identify those at highest risk for worse diet and metabolic measures from food insecurity. Specifically, we hypothesized that cortisol (a physiological marker of stress) and perceived psychological stress would amplify the link between food insecurity and hyperpalatable food intake as well as metabolic measures. In a sample of 624 Black and White women aged 36-43 who participated in the NHLBI Growth and Health Study's midlife assessment, we assessed associations between food insecurity with hyperpalatable food intake (high fat + high sodium foods; high fat + high sugar foods; and high carbohydrate + high sodium foods), and metabolic measures (fasting glucose, insulin resistance, and waist circumference). We found that food insecurity was associated with higher levels of perceived stress (R2 = 0.09), and greater intake of high fat + high sugar (hyperpalatable) foods (R2 = 0.03). In those with higher cumulative cortisol (as indexed by hair cortisol), food insecurity was associated with higher levels of fasting glucose. Neither cortisol nor perceived stress moderated any other relationships, and neither variable functioned as a mediator in sensitivity analyses. Given these largely null findings, further research is needed to understand the role stress plays in the chronic health burdens of food insecurity.

Adaptive laboratory evolution experiments provide a controlled context in which the dynamics of selection and adaptation can be followed in real-time at the single-nucleotide level. And yet this precision introduces hundreds of degrees-of-freedom as genetic changes accrue in parallel lineages over generations. On short timescales, physiological constraints have been leveraged to provide a coarse-grained view of bacterial gene expression characterized by a small set of phenomenological parameters. Here, we ask whether this same framework, operating at a level between genotype and fitness, informs physiological changes that occur on evolutionary timescales. Using a strain adapted to growth in glucose minimal medium, we find that the proteome is substantially remodeled over 40 000 generations. The most striking change is an apparent increase in enzyme efficiency, particularly in the enzymes of lower-glycolysis. We propose that deletion of metabolic flux-sensing regulation early in the adaptation results in increased enzyme saturation and can account for the observed proteome remodeling.

Dietary glucose in excess is stored in the liver in the form of glycogen. As opposed to direct conversion of glucose into glycogen, the hypothesis of the postprandial lactate shuttle (PLS) proposes that dietary glucose uptake is metabolized to lactate in the gut, thereby being transferred to the liver for glycogen storage. In the present study, we provide evidence of a PLS in young healthy men and women. Overnight fasted participants underwent an oral glucose tolerance test, and arterialized lactate concentration and rate of appearance were determined. The concentration of lactate in the blood rose before the concentration of glucose, thus providing evidence of an enteric PLS. Secondary increments in the concentration of lactate in the blood and its rate of appearance coincided with those of glucose, which indicates the presence of a larger, secondary, systemic PLS phase driven by hepatic glucose release. The present study challenges the notion that lactate production is the result of hypoxia in skeletal muscles, because our work indicates that glycolysis proceeds to lactate in fully aerobic tissues and dietary carbohydrate is processed via lactate shuttling. Our study proposes that, in humans, lactate is a major vehicle for carbohydrate carbon distribution and metabolism.

Maternal hyperglycemia contributes to abnormal fetal development; yet, how it affects fetal metabolism is poorly understood. Perez-Ramirez and colleagues recently provided a comprehensive metabolic atlas of fetal organs isolated from normal and diabetic pregnant mice, identifying novel metabolites and alterations in tissue glucose utilization throughout mid-to-late gestation by maternal hyperglycemia.

PURPOSE: Data are limited on sodium glucose co-transport 2 inhibitors (SGLT2-is) and glucagon-like peptide-1 receptor agonists (GLP-1 RAs) among real-world cohorts of underrepresented patients. We examined these therapies and glycemic control in US adults with diabetes mellitus (DM) by atherosclerotic cardiovascular disease (ASCVD) risk and sociodemographic factors. METHODS: In the NIH Precision Medicine Initiative All of Us Research Program, we categorized DM as (1) moderate risk, (2) high risk, and (3) with ASCVD. We examined proportions on DM therapies, including SGLT2-i or GLP-1 RA, and at glycemic control by sociodemographic factors and CVD risk groups. RESULTS: Our 81,332 adults aged ≥ 18 years with DM across 340 US sites included 22.3% non-Hispanic Black, 17.2% Hispanic, and 1.8% Asian participants; 31.1%, 30.3%, and 38.6% were at moderate risk, high risk, or with ASCVD, respectively. Those with DM and ASCVD were most likely on SGLT2-i (8.6%) or GLP-1 RA (11.9%). SGLT2-i use was

Insulin is an essential regulator of blood glucose homeostasis that is produced exclusively byβcells within the pancreatic islets of healthy individuals. In those affected by diabetes, immune inflammation, damage, and destruction of isletβcells leads to insulin deficiency and hyperglycemia. Current efforts to understand the mechanisms underlyingβcell damage in diabetes rely onin vitro-cultured cadaveric islets. However, isolation of these islets involves removal of crucial matrix and vasculature that supports islets in the intact pancreas. Unsurprisingly, these islets demonstrate reduced functionality over time in standard culture conditions, thereby limiting their value for understanding native islet biology. Leveraging a novel, vascularized micro-organ (VMO) approach, we have recapitulated elements of the native pancreas by incorporating isolated human islets within a three-dimensional matrix nourished by living, perfusable blood vessels. Importantly, these islets show long-term viability and maintain robust glucose-stimulated insulin responses. Furthermore, vessel-mediated delivery of immune cells to these tissues provides a model to assess islet-immune cell interactions and subsequent islet killing-key steps in type 1 diabetes pathogenesis. Together, these results establish the islet-VMO as a novel,ex vivoplatform for studying human islet biology in both health and disease.

We assessed the causal relation of four glycemic traits and type 2 diabetes liability with 167 metabolites using Mendelian randomization with various sensitivity analyses and a reverse Mendelian randomization analysis. We extracted instruments for fasting glucose, 2-h glucose, fasting insulin, and glycated hemoglobin from the Meta-Analyses of Glucose and Insulin-related traits Consortium (n = 200,622), and those for type 2 diabetes liability from a meta-analysis of multiple cohorts (148,726 cases, 965,732 controls) in Europeans. Outcome data were from summary statistics of 167 metabolites from the UK Biobank (n = 115,078). Fasting glucose and 2-h glucose were not associated with any metabolite. Higher glycated hemoglobin was associated with higher free cholesterol in small low-density lipoprotein. Type 2 diabetes liability and fasting insulin were inversely associated with apolipoprotein A1, total cholines, lipoprotein subfractions in high-density-lipoprotein and intermediate-density lipoproteins, and positively associated with aromatic amino acids. These findings indicate hyperglycemia-independent patterns and highlight the role of insulin in type 2 diabetes development. Further studies should evaluate these glycemic traits in type 2 diabetes diagnosis and clinical management.

OBJECTIVE: Modeling the effect of meal composition on glucose excursion would help in designing decision support systems (DSS) for type 1 diabetes (T1D) management. In fact, macronutrients differently affect post-prandial gastric retention (GR), rate of appearance (R[Formula: see text]), and insulin sensitivity (S[Formula: see text]). Such variables can be estimated, in inpatient settings, from plasma glucose (G) and insulin (I) data using the Oral glucose Minimal Model (OMM) coupled with a physiological model of glucose transit through the gastrointestinal tract (reference OMM, R-OMM). Here, we present a model able to estimate those quantities in daily-life conditions, using minimally-invasive (MI) technologies, and validate it against the R-OMM. METHODS: Forty-seven individuals with T1D (weight =78±13 kg, age =42±10 yr) underwent three 23-hour visits, during which G and I were frequently sampled while wearing continuous glucose monitoring (CGM) and insulin pump (IP). Using a Bayesian Maximum A Posteriori estimator, R-OMM was identified from plasma G and I measurements, and MI-OMM was identified from CGM and IP data. RESULTS: The MI-OMM fitted the CGM data well and provided precise parameter estimates. GR and R[Formula: see text] model parameters were not significantly different using the MI-OMM and R-OMM (p 0.05) and the correlation between the two S[Formula: see text] was satisfactory ( ρ =0.77). CONCLUSION: The MI-OMM is usable to estimate GR, R[Formula: see text], and S[Formula: see text] from data collected in real-life conditions with minimally-invasive technologies. SIGNIFICANCE: Applying MI-OMM to datasets where meal compositions are available will allow modeling the effect of each macronutrient on GR, R[Formula: see text], and S[Formula: see text]. DSS could finally exploit this information to improve diabetes management.

OBJECTIVE: To study the impact of vigorous vs. moderate exercise on metabolic parameters in polycystic ovary syndrome (PCOS). DESIGN: Randomized controlled trial. SETTING: Unsupervised home-based exercise program. PATIENTS: Patients with PCOS on the basis of the Rotterdam criteria with insulin resistance. INTERVENTIONS: Participants were block randomized to a home-based exercise program of 75 minutes of vigorous exercise or 150 minutes of moderate exercise per week, for 8 weeks total. MAIN OUTCOME MEASURES: Changes in glucose, insulin, and insulin resistance. RESULTS: In total, 36 participants were randomized, of whom 20 completed the study. The percentage changes from baseline at 4 and 8 weeks for fasting glucose, insulin, and homeostatic model assessment for insulin resistance did not significantly differ between the groups, except for the change in the 8-week glucose level, which was more favorable in the moderate arm (8.06% [standard deviation, 6.44%] in the vigorous group compared with -0.32% [standard deviation, 4.91%] in the moderate group). The absolute values of the main outcomes (fasting glucose, insulin, and homeostatic model assessment for insulin resistance) at baseline and 4 and 8 weeks did not significantly differ between trial arms. When assessing the change from baseline at 4 and 8 weeks, overall and within each trial arm, only the 8-week fasting glucose level was significantly greater than the baseline value in the vigorous arm (93.5 [95% confidence interval, 88.7-98.3] vs. 86.8 [95% confidence interval, 81.1-92.4]). CONCLUSIONS: Unsupervised short-term exercise programs may not achieve significant metabolic improvements in patients with PCOS, regardless of vigorous vs. moderate intensity. Future studies should investigate this question in larger sample sizes and longer or structured exercise programs. CLINICAL TRIAL REGISTRATION NUMBER: ClinicalTrials.gov identifier, NCT02303470.

Actin mediates insulin secretion in pancreatic β-cells through remodeling. Hampered by limited resolution, previous studies have offered an ambiguous depiction as depolymerization and repolymerization. We report the in situ structure of actin remodeling in INS-1E β-cells during glucose-stimulated insulin secretion at nanoscale resolution. After remodeling, the actin filament network at the cell periphery exhibits three marked differences: 12% of actin filaments reorient quasi-orthogonally to the ventral membrane; the filament network mainly remains as cell-stabilizing bundles but partially reconfigures into a less compact arrangement; actin filaments anchored to the ventral membrane reorganize from a netlike to a blooming architecture. Furthermore, the density of actin filaments and microtubules around insulin secretory granules decreases, while actin filaments and microtubules become more densely packed. The actin filament network after remodeling potentially precedes the transport and release of insulin secretory granules. These findings advance our understanding of actin remodeling and its role in glucose-stimulated insulin secretion.

BACKGROUND: To investigate the individual profile of each SGLT2 (sodium-glucose cotransoporter-2) inhibitor in patients with different backgrounds. METHODS AND RESULTS: This study included 21 placebo-controlled randomized controlled trials with a total of 96 196 participants, investigating empagliflozin, ertugliflozin, dapagliflozin, canagliflozin, and sotagliflozin. The primary efficacy end point was the composite of cardiovascular death and hospitalizations for heart failure. The secondary efficacy end points were all-cause death, cardiovascular death, hospitalizations for heart failure, kidney disease progression, and acute kidney injury. We conducted subgroup analyses based on the underlying comorbidities, including diabetes and chronic kidney disease. Safety end points were also assessed among SGLT2 inhibitors in the overall cohort. In the overall cohort, there were no significant differences in the primary efficacy outcome among the SGLT2 inhibitors, while empagliflozin (hazard ratio [HR], 0.70 [95% CI, 0.53-0.92]) and dapagliflozin (HR, 0.73 [95% CI, 0.56-0.96]) were associated with lower risk of acute kidney injury than sotagliflozin. The presence or absence of diabetes did not alter the results. In patients with chronic kidney disease, there were no differences in the efficacy outcomes among SGLT2 inhibitors, while in patients without chronic kidney disease, empagliflozin was associated with lower risk of the primary outcome compared with ertugliflozin (HR, 0.77 [95% CI, 0.60-0.98]). For safety outcomes, no significant differences were observed in amputation, urinary tract infection, genital infection, hypoglycemia, and diabetic ketoacidosis. CONCLUSIONS: The differences in reducing cardiovascular and kidney outcomes as well as safety profiles across SGLT2 inhibitors were not consistently significant, although empagliflozin might be preferred in patients without chronic kidney disease. Further investigations are needed to better understand the mechanism and clinical effectiveness of each SGLT2 inhibitor in certain populations.

Hepatocellular carcinoma (HCC) is the fifth leading cause of cancer-related mortality worldwide. Programmed cell death ligand-1 (PD-L1) is an immune checkpoint protein that binds to programmed cell death-1 (PD-1), which is expressed in activated T cells and other immune cells and has been employed in cancer therapy, including HCC. Recently, PD-L1 overexpression has been documented in treatment-resistant cancer cells. Sorafenib is a multikinase inhibitor and the only FDA-approved treatment for advanced HCC. However, several patients exhibit resistance to sorafenib during treatment. This study aimed to assess the effect of glucose deprivation on PD-L1 expression in HCC cells. We used PD-L1-overexpressing HepG2 cells and IFN-γ-treated SK-Hep1 cells to explore the impact of glycolysis on PD-L1 expression. To validate the correlation between PD-L1 expression and glycolysis, we analyzed data from The Cancer Genome Atlas (TCGA) and used immunostaining for HCC tissue analysis. Furthermore, to modulate PD-L1 expression, we treated HepG2, SK-Hep1, and sorafenib-resistant SK-Hep1R cells with rapamycin. Here, we found that glucose deprivation reduced PD-L1 expression in HCC cells. Additionally, TCGA data and immunostaining analyses confirmed a positive correlation between the expression of hexokinase II (HK2), which plays a key role in glucose metabolism, and PD-L1. Notably, rapamycin treatment  decreased the expression of PD-L1 and HK2 in both high PD-L1-expressing HCC cells and sorafenib-resistant cells. Our results suggest that the modulation of PD-L1 expression by glucose deprivation may represent a strategy to overcome PD-L1 upregulation in patients with sorafenib-resistant HCC.

UNLABELLED: The industrial amino acid production workhorse, Corynebacterium glutamicum naturally produces low levels of 2,3,5,6-tetramethylpyrazine (TMP), a valuable flavor, fragrance, and commodity chemical. Here, we demonstrate TMP production (∼0.8 g L-1) in C. glutamicum type strain ATCC13032 via overexpression of acetolactate synthase and/or α-acetolactate decarboxylase from Lactococcus lactis in CGXII minimal medium supplemented with 40 g L-1 glucose. This engineered strain also demonstrated growth and TMP production when the minimal medium was supplemented with up to 40% (v v-1) hydrolysates derived from ionic liquid-pretreated sorghum biomass. A key objective was to take the fully engineered strain developed in this study and interrogate medium parameters that influence the production of TMP, a critical post-strain engineering optimization. Design of experiments in a high-throughput plate format identified glucose, urea, and their ratio as significant components affecting TMP production. These two components were further optimized using response surface methodology. In the optimized CGXII medium, the engineered strain could produce up to 3.56 g L-1 TMP (4-fold enhancement in titers and 2-fold enhancement in yield, mol mol-1) from 80 g L-1 glucose and 11.9 g L-1 urea in shake flask batch cultivation. ONE-SENTENCE SUMMARY: Corynebacterium glutamicum was metabolically engineered to produce 2,3,5,6-tetramethylpyrazine followed by a design of experiments approach to optimize medium components for high-titer production.

Glucose is the primary energy source for most mammalian cells and its transport is affected by a family of facilitative glucose transporters (GLUTs) encoded by the SLC2 gene. GLUT1 and GLUT3, highly expressed isoforms in the blood-brain barrier and neuronal membranes, respectively, are associated with multiple neurodevelopmental disorders including epilepsy, dyslexia, ADHD, and autism spectrum disorder (ASD). Dietary therapies, such as the ketogenic diet, are widely accepted treatments for patients with the GLUT1 deficiency syndrome, while ameliorating certain symptoms associated with GLUT3 deficiency in animal models. A ketogenic diet, high-fat diet, and calorie/energy restriction during prenatal and postnatal stages can also alter the placental and brain GLUTs expression with long-term consequences on neurobehavior. This review focuses primarily on the role of diet/energy perturbations upon GLUT isoform-mediated emergence of neurodevelopmental and neurodegenerative disorders.

While pancreatic β and α cells are considered the main drivers of blood glucose homeostasis through insulin and glucagon secretion, the contribution of δ cells and somatostatin (SST) secretion to glucose homeostasis remains unresolved. Here we provide a quantitative assessment of the physiological contribution of δ cells to the glycaemic set point in mice. Employing three orthogonal mouse models to remove SST signalling within the pancreas or transplanted islets, we demonstrate that ablating δ cells or SST leads to a sustained decrease in the glycaemic set point. This reduction coincides with a decreased glucose threshold for insulin response from β cells, leading to increased insulin secretion to the same glucose challenge. Our data demonstrate that β cells are sufficient to maintain stable glycaemia and reveal that the physiological role of δ cells is to provide tonic feedback inhibition that reduces the β cell glucose threshold and consequently lowers the glycaemic set point in vivo.

There is a bidirectional pathophysiological interaction between the heart and the kidneys, and prolonged physiological stress to the heart and/or the kidneys can cause adverse cardiorenal complications, including but not limited to subclinical cardiomyopathy, heart failure and chronic kidney disease. Whilst more common in individuals with Type 2 diabetes, cardiorenal complications also occur in the absence of diabetes. Sodium-glucose cotransporter 2 inhibitors (SGLT2i) were initially approved to reduce hyperglycaemia in patients with Type 2 diabetes. Recently, these agents have been shown to significantly improve cardiovascular and renal outcomes in patients with and without Type 2 diabetes, demonstrating a robust reduction in hospitalisation for heart failure and reduced risk of progression of chronic kidney disease, thus gaining approval for use in treatment of heart failure and chronic kidney disease. Numerous potential mechanisms have been proposed to explain the cardiorenal effects of SGLT2i. This review provides a simplified summary of key potential cardiac and renal mechanisms underlying the cardiorenal benefits of SGT2i and explains these mechanisms in the clinical context. Key mechanisms related to the clinical effects of SGLT2i on the heart and kidneys explained in this publication include their impact on (1) tissue oxygen delivery, hypoxia and resultant ischaemic injury, (2) vascular health and function, (3) substrate utilisation and metabolic health and (4) cardiac remodelling. Knowing the mechanisms responsible for SGLT2i-imparted cardiorenal benefits in the clinical outcomes will help healthcare practitioners to identify more patients that can benefit from the use of SGLT2i.

Among exclusively breastfed infants, human milk (HM) provides complete nutrition in the first mo of life and remains an important energy source as long as breastfeeding continues. Consisting of digestible carbohydrates, proteins, and amino acids, as well as fats and fatty acids, macronutrients in human milk have been well studied; however, many aspects related to their relationship to growth in early life are still not well understood. We systematically searched Medline, EMBASE, the Cochrane Library, Scopus, and Web of Science to synthesize evidence published between 1980 and 2022 on HM components and anthropometry through 2 y of age among term-born healthy infants. From 9992 abstracts screened, 57 articles reporting observations from 5979 dyads were included and categorized based on their reporting of HM macronutrients and infant growth. There was substantial heterogeneity in anthropometric outcome measurement, milk collection timelines, and HM sampling strategies; thus, meta-analysis was not possible. In general, digestible carbohydrates were positively associated with infant weight outcomes. Protein was positively associated with infant length, but no associations were reported for infant weight. Finally, HM fat was not consistently associated with any infant growth metrics, though various associations were reported in single studies. Fatty acid intakes were generally positively associated with head circumference, except for docosahexaenoic acid. Our synthesis of the literature was limited by differences in milk collection strategies, heterogeneity in anthropometric outcomes and analytical methodologies, and by insufficient reporting of results. Moving forward, HM researchers should accurately record and account for breastfeeding exclusivity, use consistent sampling protocols that account for the temporal variation in HM macronutrients, and use reliable, sensitive, and accurate techniques for HM macronutrient analysis.

(1) Background: Clinical results on the effects of excess sugar consumption on insulin sensitivity are conflicting, possibly due to differences in sugar type and the insulin sensitivity index (ISI) assessed. Therefore, we compared the effects of consuming four different sugars on insulin sensitivity indices derived from oral glucose tolerance tests (OGTT). (2) Methods: Young adults consumed fructose-, glucose-, high-fructose corn syrup (HFCS)-, sucrose-, or aspartame-sweetened beverages (SB) for 2 weeks. Participants underwent OGTT before and at the end of the intervention. Fasting glucose and insulin, Homeostatic Model Assessment-Insulin Resistance (HOMA-IR), glucose and insulin area under the curve, Surrogate Hepatic Insulin Resistance Index, Matsuda ISI, Predicted M ISI, and Stumvoll Index were assessed. Outcomes were analyzed to determine: (1) effects of the five SB; (2) effects of the proportions of fructose and glucose in all SB. (3) Results: Fructose-SB and the fructose component in mixed sugars negatively affected outcomes that assess hepatic insulin sensitivity, while glucose did not. The effects of glucose-SB and the glucose component in mixed sugar on muscle insulin sensitivity were more negative than those of fructose. (4) Conclusion: the effects of consuming sugar-SB on insulin sensitivity varied depending on type of sugar and ISI index because outcomes assessing hepatic insulin sensitivity were negatively affected by fructose, and outcomes assessing muscle insulin sensitivity were more negatively affected by glucose.

Summary The quality of processed products can be adversely affected by uncontrollable batches of mangoes, which exhibit heterogeneous characteristics. This study aimed to establish predictive models for sugar and organic acid contents (dependent variables) in processed products using the initial compositions of fresh mangoes. Three mango cultivars (cv. ‘Kent’, cv. ‘Keo Romeat’, and cv. ‘Keo Chen’) were classified as low‐density and high‐density groups. Each group of mangoes at the green‐mature, mid‐ripe, and ripe stages was processed into pasteurised purees, dried slices, and mango chips. Prediction models were established using a mix of simple linear regression (SLR) based on the initial content and Analysis of Variance (ANOVA) to identify the impact of qualitative variables (ripening stage, cultivar‐density, and processing technique). In processed mangoes, 13% sucrose content was estimated to accumulate with the three qualitative variables, whereas glucose and fructose contents decreased from their initial levels by 10% and 7%, respectively. Processing techniques can predict the ratio of sugars/acids (S/A) in processed products, regardless of the ripening stage or cultivar‐density. Similar to S/A, citric acid and malic acid contents in mango products were significantly increased by processing techniques. The initial content and processes were insufficient to predict the final contents of the same parameters in processed mangoes; therefore, some models need to include the effects of ripening stage and cultivar‐density to improve the prediction. These relevant explanatory variables contributed significantly to the development of the models, resulting the accuracy of predictive models with normalised root mean square errors (NRMSEs) lower than 10%, except for malic acid (14.04%). In conclusion, it is feasible to estimate the sugar and acidity levels in processed mangoes, offering promising possibilities for ensuring consistent quality of mango‐based products. [ABSTRACT FROM AUTHOR]

Background: Posterior reversible encephalopathy syndrome (PRES) is an uncommon neurological disorder which is characterised by variable symptoms. The transient clinical condition may be underestimated and misdiagnosed as other conditions, especially, among pregnant women with severe preeclampsia, eclampsia, and HELLP (hemolysis, elevated liver enzymes, and low platelets) syndrome in the puerperium. We hereby contribute to the literature this rare complication and hightlight the appropriate management of PRES. Presentation case: A pregnant woman (gravida 3, parity 2) had a normal antenatal course. However, she was diagnosed with severe preeclampsia and HELLP syndrome at 29 weeks and 5 days of gestation. Therefore, she was indicated for a medical termination of pregnancy following a patient's consent at our tertiary referral hospital. Severely, the patient developed rapidly with altered mental health in early puerperium. In result, PRES was diagnosed based on a brain magnetic resonance imaging (MRI) evidence with typical findings. After a strict multidisciplinary management, the clinical condition improved after 5 days of onset and recovered completely after a 4-month follow-up without any sequelae. Conclusion: In summary, despite its rarity, clinicians ought to be knowledgeable and raise an aware of PRES during pregnancy. Importantly, a brain imaging modalities should be taken into account among pregnant women with neurological symptoms subsequent to severe preeclampsia. In addition to early diagnosis, a timely appropriate treatment with multidisciplinary team is strongly indicated. Further studies with a large case series are required for this uncommon entity. [ABSTRACT FROM AUTHOR]

By pre-milling in glucose aqueous solution, γ-Al 2 O 3 particles were uniformly mixed with carbon via hydrothermal treatment technique. Then, directly heating the γ-Al 2 O 3 /C precursor at 50 °C/min to 1775 °C for 15–30 min in N 2 , single phase AlON powder was fast obtained through one-step carbothermal reduction and nitridation (CRN). By approaching the evolution of phase assemblages and morphology during heating and dwelling, the one-step fast CRN mechanism for preparing fine AlON powder was revealed. The carbon around γ-Al 2 O 3 particles delayed the phase transformation of Al 2 O 3 from γ phase to α one. The undesired particle aggregation and growth before formation of AlON was also auxiliarily inhibited by swiftly achieving AlON formation temperature via high heating speed. Further elevating synthesis temperature enabled high reaction kinetics to boost the speed of AlON formation. By these ways, CRN reactions were quickly completed to fast obtain pure AlON powder with small primary particles due to limited particle aggregation and growth. The as-prepared fine AlON powder was easy to be ball-milled to prepare highly transparent AlON ceramics by pressureless sintering. [ABSTRACT FROM AUTHOR]

Glucokinase (GCK), a key enzyme in glucose metabolism, plays a central role in glucose sensing and insulin secretion in pancreatic β-cells, as well as glycogen synthesis in the liver. Mutations in the GCK gene have been associated with various monogenic diabetes (MD) disorders, including permanent neonatal diabetes mellitus (PNDM) and maturity-onset diabetes of the young (MODY), highlighting its importance in maintaining glucose homeostasis. Additionally, GCK gain-of-function mutations lead to a rare congenital form of hyperinsulinism known as hyperinsulinemic hypoglycemia (HH), characterized by increased enzymatic activity and increased glucose sensitivity in pancreatic β-cells. This review offers a comprehensive exploration of the critical role played by the GCK gene in diabetes development, shedding light on its expression patterns, regulatory mechanisms, and diverse forms of associated monogenic disorders. Structural and mechanistic insights into GCK's involvement in glucose metabolism are discussed, emphasizing its significance in insulin secretion and glycogen synthesis. Animal models have provided valuable insights into the physiological consequences of GCK mutations, although challenges remain in accurately recapitulating human disease phenotypes. In addition, the potential of human pluripotent stem cell (hPSC) technology in overcoming current model limitations is discussed, offering a promising avenue for studying GCK-related diseases at the molecular level. Ultimately, a deeper understanding of GCK's multifaceted role in glucose metabolism and its dysregulation in disease states holds implications for developing targeted therapeutic interventions for diabetes and related disorders. [ABSTRACT FROM AUTHOR]

Tumor reliance on glycolysis is a hallmark of cancer. Immunotherapy is more effective in controlling glycolysis-low tumors lacking lactate dehydrogenase (LDH) due to reduced tumor lactate efflux and enhanced glucose availability within the tumor microenvironment (TME). LDH inhibitors (LDHi) reduce glucose uptake and tumor growth in preclinical models, but their impact on tumor-infiltrating T cells is not fully elucidated. Tumor cells have higher basal LDH expression and glycolysis levels compared with infiltrating T cells, creating a therapeutic opportunity for tumor-specific targeting of glycolysis. We demonstrate that LDHi treatment (a) decreases tumor cell glucose uptake, expression of the glucose transporter GLUT1, and tumor cell proliferation while (b) increasing glucose uptake, GLUT1 expression, and proliferation of tumor-infiltrating T cells. Accordingly, increasing glucose availability in the microenvironment via LDH inhibition leads to improved tumor-killing T cell function and impaired Treg immunosuppressive activity in vitro. Moreover, combining LDH inhibition with immune checkpoint blockade therapy effectively controls murine melanoma and colon cancer progression by promoting effector T cell infiltration and activation while destabilizing Tregs. Our results establish LDH inhibition as an effective strategy for rebalancing glucose availability for T cells within the TME, which can enhance T cell function and antitumor immunity [ABSTRACT FROM AUTHOR]

Development of elegant, selective, and efficient strategies for the production of value‐added platform chemicals from renewable feedstocks are in high demand to achieve the future needs and sustainable goals. In this context, an efficient acid‐promoted synthesis of highly valuable hydroxymethylfurfural (HMF) has been demonstrated from glucose, a major constituent of lignocellulosic biomass. The major challenge in the conversion of glucose to HMF is the selective isomerization of glucose to ketose, which in the present work has been successfully addressed through the amine‐mediated rearrangement of glucose to aminofructose under Amadori rearrangement. Importantly, subsequent dehydration step affords HMF and regenerates the amine employed in the first step, which could be readily recovered. In addition, scale‐up and successful integration into one‐pot synthesis of HMF proves the efficiency and applicability of the present transformation in large scale application. In addition, the method was also successfully extended to other monosaccharides and disaccharides to produce HMF. [ABSTRACT FROM AUTHOR]

The use of glucose sensors to triage post‐discharge follow‐up was investigated among hospital inpatients with type 2 diabetes. Feasibility, utility and patient satisfaction with this model of care were studied. Feasibility was 36.5%, with 90/198 (45.5%) inpatients discharged with glucose sensors but 9.0% unable to use glucose sensors effectively. Follow‐up plans were altered in 76.3% of the patients able to use the sensor technology. Patient satisfaction was high and was improved on follow‐up after 6 months. [ABSTRACT FROM AUTHOR]

The present study was conducted to determine certain haemolymph parameters of natural populations of two freshwater snails Pila globosa and Filopaludina bengalensis, and four unionid mussels Lamellidens jenkinsianus, L. phenchooganjensis, L. marginalis, and L. corrianus collected from Darikanthal Beel, Trishal, Mymensingh. Twenty apparently healthy live snails and mussels from each population collected at the same date were selected for haemolymph analysis. A non-lethal sampling technique was adopted for collecting haemolymph from the snails and mussels. The haemolymph parameters Na+, K+, Cl−, glucose concentrations and pH levels were determined for each specimen. Significant differences (P < 0.05) were found in almost all the haemolymph parameters among the sampled snail and mussel populations. This study provided reference ranges for some vital haemolymph parameters of the two freshwater snail species and four unionid mussel species. These ranges are measurable non-lethally and could be applied to biological monitoring of environmental stressors using the molluscs as indicator species. [ABSTRACT FROM AUTHOR]

Local inflammatory microenvironment in the early stage of myocardial infarction (MI) severely impaired cardiac recovery post-MI. Macrophages play a pivotal role in this process. A classical glycolytic inhibitor, 2-Deoxy-Glucose (2-DG), has been found to regulate the excessive pro-inflammatory macrophage polarization in the infarcted myocardium. This study investigated the effect of 2-DG-loaded chitosan/gelatin composite patch on the infarct microenvironment post-MI and its impact on cardiac repair. The results showed that the 2-DG patch significantly inhibited the expression of inflammatory cytokines, alleviated reactive oxygen species (ROS) accumulation, repressed the proinflammatory polarization of macrophages, attenuated local inflammatory microenvironment in the ischemic hearts, as well as improved cardiac function, reduced scar size, and promoted angiogenesis post-MI. In terms of mechanism, 2-DG exerts anti-inflammatory effects through inhibiting the NF-κB signaling pathway and reducing the assembly and activation of the NLRP3 inflammasome. These findings suggest that 2-DG composite patch may represent a promising therapeutic strategy for cardiac repair after MI. [ABSTRACT FROM AUTHOR]

Aim Patients and Methods Results Conclusion To evaluate the efficacy and safety of dapagliflozin versus placebo as an add‐on in patients with type 2 diabetes who did not achieve adequate glycaemic control with evogliptin and metformin combination.In this multicentre, randomized, double‐blind, placebo‐controlled Phase 3 trial, patients with glycated haemoglobin (HbA1c) levels ≥7.0% (≥53 mmol/mol) and ≤10.5% (≤91 mmol/mol) who had received stable‐dose metformin (≥1000 mg) and evogliptin (5 mg) for at least 8 weeks were randomized to receive dapagliflozin 10 mg or placebo once daily for 24 weeks. Participants continued treatment with metformin and evogliptin. The primary endpoint was change in HbA1c level after 24 weeks of treatment from baseline level.In total, 198 patients were randomized, and 195 patients were included in the efficacy analyses (dapagliflozin: 96, placebo: 99). At Week 24, dapagliflozin significantly reduced HbA1c levels. The least squares mean difference in HbA1c level change from baseline after 24 weeks of treatment was −0.70% (−7.7 mmol/mol) (p < 0.0001). The proportion of participants achieving HbA1c <7.0% (≥53 mmol/mol) was higher in the dapagliflozin group than in the placebo group. Compared to placebo, dapagliflozin significantly reduced fasting plasma glucose, mean daily glucose, 2‐h postprandial plasma glucose, fasting insulin, uric acid and gamma‐glutamyl transferase levels, homeostatic model assessment for insulin resistance index, body weight, hepatic steatosis index, and albuminuria. Adiponectin level significantly increased from baseline level after 24 weeks of dapagliflozin treatment. Adverse event rates were similar in the two groups.Dapagliflozin add‐on to evogliptin plus metformin improved glycaemic control and was well tolerated by the target patients. [ABSTRACT FROM AUTHOR]

Ferroptosis is a novel form of programmed cell death caused by damage to lipid membranes due to the accumulation of lipid peroxides in response to various stimuli, such as high levels of iron, oxidative stress, metabolic disturbance, etc. Sugar, lipid, amino acid, and iron metabolism are crucial in regulating ferroptosis. The solute carrier transporters (SLCs) family, known as the "metabolic gating" of cells, is responsible for transporting intracellular nutrients and metabolites. Recent studies have highlighted the significant role of SLCs family members in ferroptosis by controlling the transport of various nutrients. Here, we summarized the function and mechanism of SLCs in ferroptosis regulated by ion, metabolic control of nutrients, and multiple signaling pathways, with a focus on SLC–related transporters that primarily transport five significant components: glucose, amino acid, lipid, trace metal ion, and other ion. Furthermore, the potential clinical applications of targeting SLCs with ferroptosis inducers for various diseases, including tumors, are discussed. Overall, this paper delves into the novel roles of the SLCs family in ferroptosis, aiming to enhance our understanding of the regulatory mechanisms of ferroptosis and identify new therapeutic targets for clinical applications. [ABSTRACT FROM AUTHOR]

Objective: Expanding on previous investigations, this study aims to elucidate the role of lipid metabolism disorders in the development of intracranial atherosclerotic stenosis (ICAS) and the determination of stroke risk. The primary objective is to explore the connections between lipid parameters and acute ischemic stroke (AIS), while also examining the potential mediating influence of fasting glucose levels. Methods: Retrospectively, we collected data from symptomatic ICAS patients at the First Affiliated Hospital of Soochow University, including their baseline information such as medical histories and admission blood biochemical parameters. Stenotic conditions were evaluated using magnetic resonance imaging, computed tomography angiography, or digital subtraction angiography. The associations between lipid parameters and AIS risks were investigated via multivariate logistic regression analysis. Results: A total of 1103 patients with symptomatic ICAS were recruited, among whom 441 (40.0%) suffered new ischemic events during hospitalization. After adjusting for confounding factors, the RCS curves exhibited a dose-response relationship between the atherogenic index of plasma (AIP), total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), and AIS. Further multivariate analysis revealed significant associations between these parameters and AIS. Furthermore, mediation analysis indicated that fasting blood glucose (FBG) acted as a mediator in the association between lipid parameters (AIP, TC, and TG) and AIS. Conclusion: Higher lipid parameters in ICAS patients, particularly AIP, TC, and TG, were associated with an increased AIS risk. Additionally, FBG may mediate stroke risk in ICAS patients, highlighting the need for further exploration of underlying mechanisms. [ABSTRACT FROM AUTHOR]

The study was conducted on 70 blood samples, which were divided into two parts: • Patient group: 35 samples were from patients with polycystic ovary syndrome. • Control group (healthy women): 35 samples were from healthy women (as a control group). The ages of both groups ranged between (18-45) years for the period from 4/1/2024 - 6/1/2024. From Samarra General Hospital in Salah al-Din Governorate, blood was then collected from patients and healthy people and separated using a centrifuge. Then biochemical variables were measured, which included (glucose, LH, FSH, iron, magnesium, and vitamin D). The results of the current research showed a significant increase in each of the levels (glucose, LH, iron, and magnesium). In the blood serum of patients with polycystic ovary syndrome compared with the control group, there was a significant decrease in the level of (Vit D, FSH) in both groups at its level, probability P ≤ 0.001. [ABSTRACT FROM AUTHOR]

Glucose has been extensively studied as a targeting ligand on nanoparticles for biomedical nanoparticles. A promising nanocarrier platform are single-chain polymer nanoparticles (SCNPs). SCNPs are well-defined 5–20 nm semi-flexible nano-objects, formed by intramolecularly crosslinked linear polymers. Functionality can be incorporated by introducing labile pentafluorophenyl (PFP) esters in the polymer backbone, which can be readily substituted by functional amine-ligands. However, not all ligands are compatible with PFP-chemistry, requiring different ligation strategies for increasing versatility of surface functionalization. Here, we combine active PFP-ester chemistry with copper(I)-catalyzed azide alkyne cycloaddition (CuAAC) click chemistry to yield dual-reactive SCNPs. First, the SCNPs are functionalized with increasing amounts of 1-amino-3-butyne groups through PFP-chemistry, leading to a range of butyne-SCNPs with increasing terminal alkyne-density. Subsequently, 3-azido-propylglucose is conjugated through the glucose C1- or C6-position by CuAAC click chemistry, yielding two sets of glyco-SCNPs. Cellular uptake is evaluated in HeLa cancer cells, revealing increased uptake upon higher glucose-surface density, with no apparent positional dependance. The general conjugation strategy proposed here can be readily extended to incorporate a wide variety of functional molecules to create vast libraries of multifunctional SCNPs. [Display omitted] [ABSTRACT FROM AUTHOR]

OBJECTIVE To determine the accuracy of a continuous glucose monitoring system (CGMS) device by comparing glucose concentrations measured over time as determined by the CGMS to those of the chemistry analyzer (reference method). ANIMALS 7 healthy goats and 7 dairy calves. METHODS A randomized, crossover design with 3 treatments: control, hypoglycemia, and hyperglycemia. The CGMS device was applied to the neck. Hypoglycemia and hyperglycemia were induced by insulin and xylazine, respectively. Glucose concentrations were measured by the chemistry analyzer CGMS, point-of-care glucometer, and intensive care unit machine at 0 (before treatment), 2, 4, 6, 8, 10, and 12 hours. Agreement between the CGMS and the chemistry analyzer was determined by Bland-Altman plots. The analytical and clinical accuracy of the CGMS was determined using the International Organization for Standardization (ISO) 15197:2013 criteria and the Parkes error grid analysis. RESULTS In goats, the CGMS overestimated glucose concentrations during the hypoglycemic, normoglycemia, and hyperglycemia treatments. In calves, the CGMS underestimated glucose concentrations during the hypoglycemic treatment but overestimated glucose concentrations in normoglycemia and hyperglycemic treatments. The CGMS met the ISO clinical accuracy criteria for goats and calves, with > 99% of the glucose measurements in zones A and B of the Parkes grid. However, the CGMS did not meet the ISO 15197:2013 criteria for analytical accuracy. CLINICAL RELEVANCE The CGMS evaluated in our study only met the ISO 15197:2013 clinical accuracy criteria, not the analytical accuracy. Therefore, the device might be considered for clinical use. [ABSTRACT FROM AUTHOR]

The overconsumption of added sugars makes people vulnerable to a myriad of diseases. Several biochemical and developmental assays were performed in the current study to assess the effect of fructose on Drosophila melanogaster and to find substitutes for fructose by comparing it to well-known sweeteners. Drosophila was exposed separately to the same ratio of sugar 9.21% (w/v) of several types of sweeteners (sucrose, fructose, glucose syrup, high-fructose corn syrup and stevia). Results revealed that fructose might induce recombination, whereas stevia lacks genotoxic potential. No developmental delay, growth defects, or neurotoxic effects were recorded for any of the sweeteners. We also observed no striking differences in reactive oxygen species levels. Thus, stevia seems to be an alternative sweetener to fructose that can be consumed to reduce fructose-induced anomalies. [ABSTRACT FROM AUTHOR]

Mammalian cells utilize glucose as a primary carbon source to produce energy for most cellular functions. However, the bioenergetic homeostasis of cells can be perturbed by environmental alterations, such as changes in oxygen levels which can be associated with bacterial infection. Reduction in oxygen availability leads to a state of hypoxia, inducing numerous cellular responses that aim to combat this stress. Importantly, hypoxia strongly augments cellular glycolysis in most cell types to compensate for the loss of aerobic respiration. Understanding how this host cell metabolic adaptation to hypoxia impacts the course of bacterial infection will identify new anti-microbial targets. This review will highlight developments in our understanding of glycolytic substrate channeling and spatiotemporal enzymatic organization in response to hypoxia, shedding light on the integral role of the hypoxia-inducible factor (HIF) during host–pathogen interactions. Furthermore, the ability of intracellular and extracellular bacteria (pathogens and commensals alike) to modulate host cellular glucose metabolism will be discussed. [ABSTRACT FROM AUTHOR]

Objective: The aim of the study is to evaluate whether the application of an interfascial injection with dextrose water could result in reduced pain and improved shoulder function and range of motion. Design: This is a double-blind randomized controlled trial. Thirty-five patients with chronic shoulder pain were randomly assigned to receive either an interfascial injection of 10 mL of 10% dextrose water guided by ultrasound or a sham injection of 0.5 mL of 10% dextrose water into the subcutaneous layer. All patients received education on a home program of self-massage and self-stretching. Shoulder pain, shoulder range of motion, and neck and shoulder function were measured before injection and at 4 and 12 wks after injection. Results: Both groups showed significant improvements in visual analog scale scores at 12-wk follow-up. The interfascial injection group exhibited a significant pain reduction compared with the sham group at the 12-wks follow-up. No between-group differences were observed in shoulder range of motion, pain threshold, and neck and shoulder function. Conclusions: Interfascial injection is effective in decreasing pain in patients with myofascial pain syndrome. [ABSTRACT FROM AUTHOR]

Alternative mRNA splicing promotes the diversity of protein isoforms. Metabolic regulation of mRNA splicing enables cells to adapt their proteome to external stimuli. The interplay between metabolites and alternative mRNA splicing can take place through biochemical and biophysical changes of cellular compartments in which splicing takes place and/or through interactions between metabolites and splicing factors. Central cell signaling pathways that are regulated by metabolites crosstalk with alternative splicing regulators. Alternative mRNA splicing enables the diversification of the proteome from a static genome and confers plasticity and adaptiveness on cells. Although this is often explored in development, where hard-wired programs drive the differentiation and specialization, alternative mRNA splicing also offers a way for cells to react to sudden changes in outside stimuli such as small-molecule metabolites. Fluctuations in metabolite levels and availability in particular convey crucial information to which cells react and adapt. We summarize and highlight findings surrounding the metabolic regulation of mRNA splicing. We discuss the principles underlying the biochemistry and biophysical properties of mRNA splicing, and propose how these could intersect with metabolite levels. Further, we present examples in which metabolites directly influence RNA-binding proteins and splicing factors. We also discuss the interplay between alternative mRNA splicing and metabolite-responsive signaling pathways. We hope to inspire future research to obtain a holistic picture of alternative mRNA splicing in response to metabolic cues. [ABSTRACT FROM AUTHOR]

The first cell differentiation event that occurs in the embryo determines the inner cell mass (ICM) and the trophectoderm (TE). In the mouse, glucose (GLC) is essential for this process, while oxygen tension (O 2) also interferes with TE formation. The roles of GLC and O 2 in this event in bovine embryos are not completely elucidated. We hypothesized that the absence of glucose and a higher O 2 tension negatively impact ICM and TE cell allocation in the bovine embryo. The objective of this study was to evaluate the effect of GLC within different O 2 levels on the formation of the TE. In vitro-produced embryos were cultured in serum-free KSOM medium and randomly submitted to treatments on the day of IVC, according to a 2x2 factorial model, in which GLC (present [+GLC] or absent [-GLC]) and O 2 (low [5%O 2 ] or high [20%O 2 ]) were the independent variables. Cleavage and blastocyst rates were obtained at D4 and D8, respectively. Embryos at D8 were subjected to autofluorescence analysis to quantitate NADH and FAD + or fixed for GATA3 and YAP1 immunostaining using a laser scanning confocal microscope. Total, TE, and ICM cell counts were obtained. Embryos were also harvested for gene expression quantification of GATA3, YAP1, SOX2, CDX2, TFAP2C and OCT4. Results indicate that there was an effect of O 2 (p = 0.018) on cleavage rates, although no differences were observed in blastocyst rates. NADH was higher in -GLC compared to + GLC (p = 0.014) and no differences in FAD+ were observed. Total cell count data were not different between variables. There was an increase in the ICM cell count in the +GLC 5%O 2 condition compared to the other three conditions. No effects of GLC, O 2 , or their interactions were observed on TE cell count or the TE/total cell ratio. CDX2 (p = 0.007) and TFAP2C (p = 0.038) were increased in -GLC 20%O 2 compared to + GLC 20%O 2. SOX2 was decreased in +GLC 20%O 2 compared to + GLC 5%O 2 (p = 0.027) or compared to -GLC 20%O 2 (p = 0.005). GATA3, YAP1, and OCT4 genes did not present differences among conditions. In conclusion, both GLC and high oxygen tension did not impair TE formation and TE cell number, although a +GLC-low oxygen environment led to a higher number of ICM cells. Interestingly, the expression of TE-related gene CDX2 was increased in the absence of glucose within higher O 2 tension. Our results implicate that according to the oxygen tension used in IVC, glucose can exert different effects on blastocyst cell allocation or gene expression. • Differentiation of the TE occurred in the absence of glucose. • Glucose plus 5 % oxygen tension increased the number of ICM cells. • Gene expression was influenced by glucose within a 20 % oxygen tension. [ABSTRACT FROM AUTHOR]

Paper sludge (PS) from paper mills has a significant potential for bioethanol production. In this study, waste-paper-containing PS is used as the raw material for bioethanol production because the annual waste paper utilization rate has increased globally. Although PS does not require delignification, the antiseptics and deinking agents in waste paper-containing PS inhibit enzymatic reactions such as saccharification and fermentation. Their removal is important, but it has not yet been reported. Using subcritical water pretreatment, the selective decomposition of enzyme inhibitors in PS is examined without the generation of other enzyme inhibitors. The optimum pretreatment conditions are identified as 240 °C, 3.3 MPa, 3 min, and pH 4.5. Glucose was obtained in 71% yield from pretreated 5 wt% PS using cellulase, which is 5.5 times higher than that from unpretreated PS. This is because the reactivity of the pretreated PS increases with increasing surface area of the cellulose fibers, and the cellulase inhibitors are decomposed by subcritical water. Next, semi-simultaneous saccharification and fermentation treatments are performed to produce bioethanol from waste-paper-containing PS. The bioethanol yield based on cellulose after 96 h is 68% for PS pretreated with subcritical water, whereas the bioethanol yield is 6% for unpretreated PS. Therefore, subcritical water pretreatment increases the bioethanol yield by 11 times. The proposed method may enable the use of large amounts of PS as ethanol feedstock in future. [ABSTRACT FROM AUTHOR]

To enhance cellulose hydrolysis under high solid loadings, increasing the mixing intensity is often necessary, but this can lead to heightened product inhibition. In this work, the effect of mixing on high-solid cellulose hydrolysis was investigated. Through response surface optimization experiments, the optimal mixing intensities for 15%, 25%, and 35% (w/v) cellulose hydrolysis were obtained under different levels of product inhibition. A combined mixing optimization strategy was developed for different solid concentrations, aiming to enhance both the glucose yield and the conversion rate of microcrystalline cellulose and corn cobs. After optimization, the hydrolysis of microcrystalline cellulose resulted in glucose concentrations of 85 g/L, 130 g/L, and 167 g/L, corresponding to maximal conversion enhancements of 23%, 13%, and 8.6%, respectively. Similarly, the hydrolysis of corn cobs achieved glucose concentrations of 81 g/L, 124.6 g/L, and 140 g/L, with maximal conversion improvements of 4%, 5%, and 13%. These results indicate that the optimized strategy can effectively improve the conversion rate of high-solid enzymatic hydrolysis of cellulose. [ABSTRACT FROM AUTHOR]

This work presents the preparation of a gold-polypyrrole (Au-PPy) composite film on a silicon (Si) semiconductor supported by electrodeposition, and the study of its electrocatalytic activity as an anode catalyst for the glucose oxidation reaction in alkaline media. The microstructure of the as-prepared Au-PPy film is characterized by scanning electron microscopy (SEM) and atomic force microscopy (AFM). The results show that the presence of the polymer film on the Si support improves the conductivity of the latter and enables better distribution of the Au microparticles on the electrode surface, thus helping to increase their catalytic activity for glucose oxidation. [ABSTRACT FROM AUTHOR]

This study reports a micromachined parylene-C-coated integrated electrode (IDE) sensor fabricated on a polyimide film. Glucose and uric acid within the human sweat concentration range were tested using hydrothermally grown ZnO nanoparticles (NPs) immobilized on the IDE regions of sensors and modified with urate oxidase and glucose oxidase enzymes. Four important sensing parameters, including capacitance, impedance, resistance, and phase, were simultaneously investigated during the dynamic test. The sensor fabrication and characterization of ZnO NPs and ZnO NP formed sensing film were described in detail. The experimental results show that the amount of capacitance change and phase change vs. the concentration variation of glucose and uric acid exhibits an excellent linear regression relationship. On the other hand, the amount of impedance change vs. concentration variation of glucose and uric acid exhibits a power regression relationship. Sensitivities of uric acid and glucose detection based on capacitance changes were 0.1131 pF/µM and 0.7875 pF/µM, respectively. Limits of detection of uric acid and glucose were 1.23 µM and 0.311 µM, respectively. Thus, the developed sensor can be applied to wearable devices for the quantitative analysis of sweat composition in the future. [ABSTRACT FROM AUTHOR]

Gluconic acid and sorbitol are among the value-added chemicals that can be derived from biomass. Nowadays, these compounds are typically produced through biotechnological processes, but electrochemical methods offer numerous advantages over alternative approaches. While studies have extensively explored metals like copper, palladium, gold, and platinum, nickel has received relatively limited attention in this context. Notably, nickel exhibits electrochemical activity suitable for organic electrosynthesis. This work has been achieved with 5-h long-term electrolysis, glucose as a reactant, utilizing modified nickel electrodes in a KOH solution. While these studies achieved substantial conversion rates, the selectivities and Faraday efficiencies toward gluconic acid and sorbitol remained comparatively low. The long-term electrolysis of glucose using modified nickel electrodes resulted in the identification of various side products. These include formic acid, oxalic acid, glycolic acid, tartronic acid, glyceric acid, and arabinose. [ABSTRACT FROM AUTHOR]

Objective: The aim of the study is to analyze microstate patterns in GLUT1-DS, both before and after the ketogenic diet (KD). Methods: We conducted microstate analysis of a patient with GLUT-1 DS and 27 healthy controls. A systematic literature review and meta-analysis was done. We compared the parameters of the patients with those of healthy controls and the incorporating findings in literature. Results: The durations of the patient were notably shorter, and the occurrence rates were longer than those of healthy controls and incorporating findings from the review. After 10 months of KD, the patient's microstate durations exhibited an increase from 53.05 ms, 57.17 ms, 61.80 ms, and 49.49 ms to 60.53 ms, 63.27 ms, 71.11 ms, and 66.55 ms. The occurrence rates changed from 4.0774 Hz, 4.9462 Hz, 4.8006 Hz, and 4.0579 Hz to 3.3354 Hz, 3.7893 Hz, 3.5956 Hz, and 4.1672 Hz. In healthy controls, the durations of microstate class A, B, C, and D were 61.86 ms, 63.58 ms, 70.57 ms, and 72.00 ms, respectively. Conclusions: Our findings suggest EEG microstates may be a promising biomarker for monitoring the effect of KD. Administration of KD may normalize the dysfunctional patterns of temporal parameters. [ABSTRACT FROM AUTHOR]

Cancer is a global health concern influenced by genetics, environment and lifestyle choices. Recent research shows that a ketogenic diet (KD) might ease cancer symptoms and reduce tumour size. We hypothesised that the KD could result in improvements in cancer‐related variables. Therefore, this study aims to perform a systematic review and meta‐analysis to assess the KD's efficacy for patients with cancer. The databases PubMed (MEDLINE), Web of Science, CINAHL and Open Grey were utilised for conducting a systematic review and meta‐analysis. The analysis was limited to randomised controlled trials with adult participants aged 18 years and above. Levels of glucose, cholesterol, insulin‐like growth factor 1, weight and quality of life were evaluated following the KD. After identifying 596 articles in the initial search, eight studies, lasting between 4 and 16 weeks, were included in the systematic review and seven in the meta‐analysis. The KD led to decreased glucose levels in patients with cancer but did not show significant improvements in cholesterol, insulin‐like growth factor 1, weight or quality of life. Based on the results of this systematic review and meta‐analysis, there is insufficient evidence to establish a definitive link between the KD and cancer‐related parameters. While some studies suggest potential benefits in terms of some outcomes and tumour size reduction, further research is required to fully comprehend the effects of this diet. [ABSTRACT FROM AUTHOR]