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Black soldier flies have been studied as an alternative animal feed. On the other hand, they could be used to yield an abundance of fatty acids. Their omnivorous diet and low space requirements allow for the mass breeding of black soldier flies, using widely available food wastes as feedstock. This study simulates the industrial upscaling of an extraction process for black soldier fly larvae using SuperPro™ 9.5 simulation software. This software contains an extensive material library that regulated physical data for the chemical composition of the larvae and the products. It also bundled several types of bioreactors utilized in bioprocessing. The scheduling of the plant was aided by SchedulePro, which allows for the generation of batch durations and Gantt charts. Four fatty acids were chosen as the main revenue source, with simulated proteins assigned as by-products of the plant. Ash and cellulose were the wastes of the plant, and were separated through multiple filters. The plants were later assessed for their economic feasibility. The kitchen waste plant was the most profitable, and the control variable was the only unprofitable plant. These results may have been impacted by the waste content found in the control variable and the abundance of revenue products in the kitchen-waste-fed larvae.

Heme oxygenase-1 (HO-1) expression promotes osteogenesis, but the mechanisms remain unclear and therapeutic strategies using it to target bone disorders such as osteoporosis have not progressed. Mesobiliverdin IXα is a naturally occurring bilin analog of HO-1 catalytic product biliverdin IXα. Inclusion of mesobiliverdin IXα in the feed diet of ovariectomized osteoporotic mice was observed to increase femur bone volume, trabecular thickness and osteogenesis serum markers osteoprotegrin and osteocalcin and to decrease bone resorption serum markers cross-linked N-teleopeptide and tartrate-resistant acid phosphatase 5b. Moreover, in vitro exposure of human bone marrow mesenchymal stem cells to mesobiliverdin IXα enhanced osteogenic differentiation efficiency by two-fold over non-exposed controls. Our results imply that mesobiliverdin IXα promotes osteogenesis in ways that reflect the potential therapeutic effects of induced HO-1 expression in alleviating osteoporosis.

Simple Summary Feeding restriction (FR) is essential to reduce excessive fat deposits caused by overfeeding in hens and to ensure their reasonable nutritional requirements for egg production. Effective FR is particularly crucial for raising hens in the late phase of laying; because hens require lower energy at this stage, overfeeding reduces their feed efficiency and increase feed costs. The gut microbiota is involved in various metabolic pathways of laying hens, including in late-phase age. Thus, changes in feeding interventions can alter the presence of gut microorganisms and the structure of the microbial community, resulting in altered metabolic regulation. In this study, we investigate the microbiota and metabolome responses of late-phase laying hens under FR. Our results provide data to access the profile of the cecal bacteria community, their relevance to cecal and serum metabolites, and their FR biosynthetic pathways related to host nutritional requirements and intestinal nutrient availability. Moreover, understanding the principles of host-microbial interaction is essential for developing cost-effective strategies to improve laying hens’ production. Abstract This study investigated cecal bacterial community profile, cecal and serum metabolites, and its biosynthesis pathway in late-phase laying hens during 6 weeks feeding restriction (FR), using 16S rDNA as gene sequencing and non-targeted LC-MS/MS as metabolomics approach. We used three groups (ad libitum, FR20, and FR40). FR can reduce excessive fat in late-phase laying hens, while egg production rate is not affected, except for the FR40 group. In phylum level, FR20 had more population of Bacteriodetes and Firmicutes amongst groups. The same result is at genus level, FR20 were higher of the predominant genus (Bacteroides and Rikenellaceae_RC9_gut_group). Both of FR20 and FR40 reduced Proteobacteria as potential pathogenic bacteria. Non-targeted metabolomic analysis revealed that FR20 modified 20 metabolites in cecal and 10 metabolites in serum of laying hens, whereas 48 cecal metabolites and 31 serum metabolites has revealed in FR40. KEGG assay showed FR20 and FR40 upregulated lipid, carbohydrate, amino acid, nucleic acid pathway, and FR40 modified steroid metabolism in cecal analysis. In serum, only FR40 modified lipid, amino acid pathway, and carbohydrate biosynthesis were shown. This study showed that FR during late-phase laying hens altered the microbiome composition, modified metabolites profile and biosynthesis of the cecal as well as serum.

Adiponectin is an adipokine that can exert a regulatory function on bone metabolism. However, there are many contradictions between clinical and pre-clinical studies on adiponectin. APPL1 is an adaptor protein that can interact with adiponectin receptors. In the current study, we found that knockout of the Appl1 gene in male mice was associated with higher bone volume and numbers of trabeculae than in females or controls. The trabecular thickness, cortical thickness, ratio of bone volume/trabecular volume, cross-sectional bone area, and mean polar moment of inertia increased in Appl1 KO mice compared with wild-type mice. The number of osteoblasts increased but the number of adipocytes decreased in Appl1 KO mice. Knockdown of Appl1 impaired adipogenesis in bone marrow-derived mesenchymal stem cells. Mineralization was increased by knockdown of Appl1 during osteoblast differentiation. Data from differentiation-related genes showed results consistent with the in vivo effects. In summary, this study provides further clarification of the effect of the adiponectin signaling pathway on bone metabolism.

BACKGROUND Essential oils (EOs) are extensively used in swine production because of their bioactive action in gut health. In addition, some EOs have the potential to reduce waste emission. The present study aimed to find an optimal combination of carvacrol, thymol and cinnamaldehyde to promote nitrogen utilization and reduce waste emission by a model in vitro and an animal study. RESULTS In the study in vitro, various dosages of essential oils (EOs) were used to evaluate the effect on nitrogen metabolism through a three-step model. Compared with other EO combinations, 2EO (10 ppm cinnamaldehyde and 20 ppm thymol), and 3EO (10 ppm cinnamaldehyde, 20 ppm thymol and 200 ppm carvacrol) displayed greater nitrogen digestibility, lesser ammonia production and lower activity of microbial enzymes. In the animal study, growing male Landrace × Yorkshire pigs (initial body weight: 31.8 ± 3.3 kg, n = 18) were randomly divided into three groups and fed the control, 2EO or 3EO diet for 4 weeks. Pigs fed 3EO exhibited the greatest nitrogen digestibility (85.4%, P

The purpose of this study was to investigate the nexus between mitochondrial function and kidney injury by using a dietary-induced obese minipig model. Female Lee-Sung minipigs feeding a high-fat diet (HFD) for 6 months exhibited obesity, hyperglycaemia and dyslipidemia. HFD elevated the levels of plasma biomarkers related to renal injury, including symmetric dimethylarginine, creatinine and urea nitrogen. An extensive structural change in tubules and glomeruli was observed in HFD-fed pigs. A great amount of triacylglycerol was accumulated in HFD kidney compared to control kidney, whereas a reduction of ATP level and antioxidant capacity were exhibited in HFD kidney. Moreover, HFD altered the expressions of mitochondrial-related protein in renal cortex. To conclude, long-term HFD feeding to Lee-Sung minipigs induced obesity and kidney injury accompanied by abnormal mitochondrial functions in the renal cortex, suggesting an interrelationship with renal disease progression.

Leucine-rich repeat kinase 2 (LRRK2) is involved in lipid metabolism, however, the role of LRRK2 in lipid metabolism to affect non-alcoholic fatty liver disease (NAFLD) is still unclear. In the mouse model of NAFLD induced by a high-fat diet, we observed that LRRK2 was decreased in livers. In HepG2 cells, exposure to palmitic acid (PA) down-regulated LRRK2. Overexpression and knockdown of LRRK2 in HepG2 cells were performed to further investigate the roles of LRRK2 in lipid metabolism. Our results showed that &beta, oxidation in HepG2 cells was promoted by LRRK2 overexpression, whereas LRRK2 knockdown inhibited &beta, oxidation. The critical enzyme of &beta, oxidation, carnitine palmitoyltransferase 1A (CPT1A), was positively regulated by LRRK2. Our data suggested that the regulation of CPT1A by LRRK2 may be via the activation of AMP-activated protein kinase (AMPK) and peroxisome proliferator-activated receptor &alpha, (PPAR&alpha, ). The overexpression of LRRK2 reduced the concentration of a pro-inflammatory cytokine, tumor necrosis factor &alpha, (TNF&alpha, ), induced by PA. The increase in &beta, oxidation may promote lipid catabolism to suppress inflammation induced by PA. These results indicated that LRRK2 participated in the regulation of &beta, oxidation and suggested that the decreased LRRK2 may promote inflammation by suppressing &beta, oxidation in the liver.

Fatty liver diseases, common metabolic diseases in chickens, can lead to a decrease in egg production and sudden death of chickens. To solve problems caused by the diseases, reliable chicken models of fatty liver disease are required. To generate chicken models of fatty liver, 7-week-old ISA female chickens were fed with a control diet (17% protein, 5.3% fat, and 1,300 mg/kg choline), a low protein and high fat diet (LPHF, 13% protein, 9.1% fat, and 1,300 mg/kg choline), a high cholesterol with low choline diet (CLC, 17% protein, 7.6% fat with additional 2% cholesterol, and 800 mg/kg choline), a low protein, high fat, high cholesterol, and low choline diet (LPHFCLC, 13% protein, 12.6% fat with additional 2% cholesterol, and 800 mg/kg choline) for 4 wk. Our data showed that the CLC and LPHFCLC diets induced hyperlipidemia. Histological examination and the content of hepatic lipids indicated that the CLC and LPHFCLC diets induced hepatic steatosis. Plasma dipeptidyl peptidase 4, a biomarker of fatty liver diseases in laying hens, increased in chickens fed with the CLC or LPHFCLC diets. Hepatic ballooning and immune infiltration were observed in these livers accompanied by elevated interleukin 1 beta and lipopolysaccharide induced tumor necrosis factor mRNAs suggesting that the CLC and LPHFCLC diets also caused steatohepatitis in these livers. These diets also induced hepatic steatosis in Plymouth Rock chickens. Thus, the CLC and LPHFCLC diets can be used to generate models for fatty liver diseases in different strains of chickens. In ISA chickens fed with the CLC diet, peroxisome proliferator-activated receptor γ, sterol regulatory element binding transcription factor 1, and fatty acid synthase mRNAs increased in the livers, suggesting that lipogenesis was enhanced by the CLC treatment. Our data show that treatment with CLC or LPHFCLC for 4 wk induces fatty liver disease in chickens. These diets can be utilized to rapidly generate chicken models for fatty liver research.

The classification of nominal measure words is a long-standing problem in Chinese syntactics circle. This paper tries to solve it based on dictionary definition. Through analyzing the definition mode, we find there are some rules hidden in the meaning of nominal measure words, which can be used to reclassify these words into the following categories. When the definition mode is “yongyu(used before)…xing (shape)…”, they belong to the subcategory of highlighting shape of things, such as “tiao (strip)”; when the definition mode is “yongyu (used before) fen (divide)…”, they fall into the subcategory of highlighting constitutive aspect of things, such as “ban (piece)”; when the definition mode is “yongyu (used before)… cheng (become)…”, they fit into the subcategory of highlighting agentive aspect of things, such as “dui (pair)”, etc.…. Compared with the previous classifications, this paper unifies the classification criteria, and enhances the universality and exclusiveness of classification.

Oxytocin (OT) is a hypothalamic neuropeptide synthesized and secreted by OT neurons. In addition to its conventional role in reproductive physiology, central OT also regulates various social behaviors, such as care, trust, and emotions. Central and subcutaneous OT infusions stimulate lipid metabolism in mice and rats when fed standard or high fat diets. Mice lacking the OT receptor (OTR) or OT peptide develop late-onset obesity with greater fat pad weights, larger adipocyte size and elevated plasma levels of leptin. To study the effects of OT on lipid metabolism, we examined the effects of serial OT doses (0, 10, 30, 100, 150, 300 nM) on 3T3L1 adipocytes, together with long (144 hours, 6 days) and short (24 hours, 1 day) term treatments. The short-term treatment with 150 nM OT increased triacylglycerol (TAG) accumulation and decreased mRNA expressions of carnitine palmitoyltransferase 1α (CPT-1α) and fatty acid binding protein 4 (FABP4). After long-term incubation with 150 nM OT, only the CPT-1α mRNA was decreased. In differentiated adipocytes derived from pig adipose tissue stem cells, only hormone sensitive lipase mRNA was decreased after short- or long-term treatment with OT. To obtain further insight into the underlying mechanism of OT induction, we tested the involvement of the AKT/PKB pathway; however, AKT phosphorylation was decreased after treatment with 150 nM OT, suggesting that OT effects may be independent from the AKT/PKB pathway. Taken together, OT effects on adipocyte glucose and lipid metabolism are probably through mechanisms other than the AKT/PKB pathway.

MafB, a transcription factor expressed selectively in macrophages, has important roles in some macrophage-related diseases, especially in atherosclerosis. In this study, we investigated the mechanism by which hematopoietic-specific MafB deficiency induces the development of obesity. Wild-type and hematopoietic cell-specific Mafb-deficient mice were fed a high-fat diet for 10 weeks. The Mafb-deficient mice exhibited higher body weights and faster rates of body weight increase than control mice. The Mafb-deficient mice also had a higher percentage of body fat than the wild-type mice, due to increased adipocyte size and serum cholesterol levels. Reverse transcription-PCR analysis showed a reduction in apoptosis inhibitor of macrophage (AIM) in Mafb-deficient adipose tissue. AIM is known as an inhibitor of lipogenesis in adipocytes and is expressed in adipose tissue macrophages. Collectively, our data suggest that Mafb deficiency in hematopoietic cells accelerates the development of obesity.

Adult humans and mice possess significant classical brown adipose tissues (BAT) and, upon cold-induction, acquire brown-like adipocytes in certain depots of white adipose tissues (WAT), known as beige adipose tissues or WAT browning/beiging. Activating thermogenic classical BAT or WAT beiging to generate heat limits diet-induced obesity or type-2 diabetes in mice. Adiponectin is a beneficial adipokine resisting diabetes, and causing &ldquo, healthy obese&rdquo, by increasing WAT expansion to limit lipotoxicity in other metabolic tissues during high-fat feeding. However, the role of its receptors, especially adiponectin receptor 1 (AdipoR1), on cold-induced thermogenesis in vivo in BAT and in WAT beiging is still elusive. Here, we established a cold-induction procedure in transgenic mice over-expressing AdipoR1 and applied a live 3-D [18F] fluorodeoxyglucose-PET/CT (18F-FDG PET/CT) scanning to measure BAT activity by determining glucose uptake in cold-acclimated transgenic mice. Results showed that cold-acclimated mice over-expressing AdipoR1 had diminished cold-induced glucose uptake, enlarged adipocyte size in BAT and in browned WAT, and reduced surface BAT/body temperature in vivo. Furthermore, decreased gene expression, related to thermogenic Ucp1, BAT-specific markers, BAT-enriched mitochondrial markers, lipolysis and fatty acid oxidation, and increased expression of whitening genes in BAT or in browned subcutaneous inguinal WAT of AdipoR1 mice are congruent with results of PET/CT scanning and surface body temperature in vivo. Moreover, differentiated brown-like beige adipocytes isolated from pre-adipocytes in subcutaneous WAT of transgenic AdipoR1 mice also had similar effects of lowered expression of thermogenic Ucp1, BAT selective markers, and BAT mitochondrial markers. Therefore, this study combines in vitro and in vivo results with live 3-D scanning and reveals one of the many facets of the adiponectin receptors in regulating energy homeostasis, especially in the involvement of cold-induced thermogenesis.

Passivation is a challenging issue for the oxide thin-film transistor (TFT) technologies because it requires prolonged high-temperature annealing treatments to remedy defects produced in the process, which greatly limits its manufacturability as well as its compatibility with temperature-sensitive materials such as flexible plastic substrates. This study investigates the defect-formation mechanisms incurred by atomic layer deposition (ALD) passivation processes on ZnO TFTs, based on which we demonstrate for the first time degradation-free passivation of ZnO TFTs by a TiO2/Al2O3 nanolaminated (TAO) film deposited by a low-temperature (110 °C) ALD process. By combining the TAO passivation film with ALD dielectric and channel layers into an integrated low-temperature ALD process, we successfully fabricate flexible ZnO TFTs on plastics. Thanks to the exceptional gas-barrier property of the TAO film (water vapor transmission rate (WVTR)10(-6) g m(-2) day(-1)) as well as the defect-free nature of the ALD dielectric and ZnO channel layers, the TFTs exhibit excellent device performance with high stability and flexibility: field-effect mobility20 cm2 V(-1) s(-1), subthreshold swing0.4 V decade(-1) after extended bias-stressing (10,000 s), air-storage (1200 h), and bending (1.3 cm radius for 1000 times).

This study investigated the effects of online collaborative note-taking strategies on English as a Foreign Language (EFL) beginners' literacy development. Fifty-two EFL beginners enrolled in literacy instruction to learn how to read texts (up to 350 words) and write the main ideas by using collaborative note-taking strategies. They were separated into a control group (N = 26), which received paper-based instruction, and an experimental group (N = 26), which received online instruction. The results indicate that the EFL beginners in the experimental group made greater progress than those in the control group as they actively utilized the online collaborative note-taking strategies available to comprehend the texts, and more particularly, in clarifying and reflecting on their own and their peers' reading and writing difficulties. In contrast, the beginners in the control group had few or no opportunities to collaborate with peers in sharing notes, nor did they explicitly observe their peers' learning process by checking log files, or save peers' important words, leading to little literacy improvement. Online collaborative note-taking strategies facilitate EFL beginners' literacy development to construct new language knowledge through text decoding (note-taking), text encoding (writing main ideas), and text discussion (collaborative interaction).

Adiponectin is a circulatory cytokine secreted from adipose tissues and exerts critical metabolic functions in mammals. However, expression profiles of adiponectin and adiponectin receptors in the avian species that may be very different from mammals, especially under affluent nutrition conditions, remain unexplored to examine the effects of adiponectin and adiponectin receptors in chicken adipose tissues under high-fat diet (HFD) feeding. Twenty Taiwan country chickens (L2 bred) of 12 weeks old were challenged with a 10% high-fat diet for 6 weeks. Results showed that body weights and plasma triglycerides, cholesterol and dipeptidyl peptidase-4 (DPP4) were all increased in the HFD treatments. Interestingly, we first demonstrated that chicken circulating macromolecule adiponectin and fat disulphide-bond A oxidoreductase-like protein (DsbA-L), a regulator involved in adiponectin secretion, were elevated upon HFD feeding. Moreover, the mRNA expression of adiponectin and adiponectin receptors as well as additional adipose-related genes such as fatty acid synthase (FAS), adipose triglyceride lipase (ATGL), lipoprotein lipase (LPL), and peroxisome proliferator-activated receptor γ (PPARγ) were also increased in the chicken abdominal fats under HFD conditions. These results suggest that HFD treatment alters adiponectin and metabolic genes in chicken adipose tissues. In conclusion, in the present study, we examine expression profiles of adiponectin, adiponectin receptors, adiponectin secretion regulator DsbA-L, and metabolic genes in chicken fats upon HFD supplementation and provide new insights for how adiponectin entail the pathophysiologically obesogenic conditions in the avian species.

Hormonal changes that cause metabolic complications are a common problem in postmenopausal women. Adiponectin and osteocalcin are cytokines associated with glucose regulatory and insulin sensitized function in postmenopausal stages. The current study investigated the role of adiponectin signaling and osteocalcin mediated function in glucose metabolism in ovariectomized mice. In a mouse menopausal-related metabolic disorder model, overexpression of adiponectin receptor 1 improved glucose tolerance and caused resistance to body weight increase and decline of serum osteocalcin. Furthermore, adiponectin receptor 1 transgenic ovariectomized mice had higher GPRC6A (the putative osteocalcin receptor) expression in muscle tissue. Immunofluorescence indicated that GPRC6A and adiponectin receptor 1 were co-localized in mouse muscle tissues. The present finding suggested adiponectin receptor 1 can mediate the improvement of glucose metabolism by osteocalcin in ovariectomized mice. Our findings imply the possibility to ameliorate menopause-induced metabolic disorder by GPRC6A and adiponectin signaling.

During avian embryonic development, endodermal epithelial cells (EECs) absorb yolk through the yolk sac membrane. Sterol O-acyltransferase (SOAT) is important for esterification and yolk lipid utilization during development. Because the major enzyme for yolk sac membrane cholesteryl ester synthesis is SOAT1, we cloned the avian SOAT1 promoter and elucidated the cellular functions of SOAT1. Treatments with either glucagon, isobutylmethylxanthine (IBMX), an adenylate cyclase activator (forskolin), a cAMP analog (dibutyryl-cAMP), or a low glucose concentration all increased SOAT1 mRNA accumulation in EECs from Japanese quail, suggesting that SOAT1 is regulated by nutrients and hormones through a cAMP-dependent pathway. Activity of protein kinase A (PKA) was increased by IBMX, whereas co-treatment with the PKA inhibitor, H89 negated the increase in PKA activity. Cyclic AMP-induced EECs had greater cholesterol esterification than untreated EECs. By promoter deletion and point-mutation, the cAMP-response element (-349 to -341 bp) was identified as critical in mediating transcription of SOAT1. In conclusion, expression of SOAT1 was regulated by a cAMP-dependent pathway and factors that increase PKA will increase SOAT1 to improve the utilization of lipids in the EECs and potentially modify embryonic growth.

Fatty liver disease is the most common pathological condition in the liver. Here, we generated high-fat diet-(HFD-) induced nonalcoholic fatty liver disease (NAFLD) in mice and tested the effects of docosahexaenoic acid (DHA) and lysine during a four-week regular chow (RC)feeding. Our results showed that 1% lysine and the combination of 1% lysine + 1% DHA reduced body weight. Moreover, serum triglyceride levels were reduced by 1% DHA and 1% lysine, whereas serum alanine transaminase activity was reduced by 1% DHA and 1% DHA + 0.5% lysine. Switching to RC reduced hepatic lipid droplet accumulation, which was further reduced by the addition of DHA or lysine. Furthermore, the mRNA expressions of hepatic proinflammatory cytokines were suppressed by DHA and combinations of DHA + lysine, whereas the mRNA for the lipogenic gene, acetyl-CoA carboxylase 1 (ACC1), was suppressed by DHA. In the gonadal adipose tissues, combinations of DHA and lysine inhibited mRNA expression of lipid metabolism-associated genes, including ACC1, fatty acid synthase, lipoprotein lipase, and perilipin. In conclusion, the present study demonstrated that, in conjunction with RC-induced benefits, supplementation with DHA or lysine further ameliorated the high-fat diet-induced NAFLD and provided an alternative strategy to treat, and potentially prevent, NAFLD.

Osteoporosis and its related bone fractures are growing medical problems, especially in industrial countries, and thus the knowledge of regulation of bone metabolism is critical to develop therapeutic approaches. Bone adipocytes share common mesenchymal precursors with osteoblasts and chondrocytes and their numbers in bone marrow are altered in various pathophysiological conditions. Several findings suggest that accelerated adipogenesis in bone marrow, known as fatty marrow, is associated with the progression of osteoporosis. Apart from its demonstrated anti-atherosclerogenic and insulin-sensitizing actions, the adipokine adiponectin and its receptors have been shown to be expressed in bone tissues and participate in bone metabolism. Here we review recent findings regarding the regulation of bone metabolism by adiponectin and its receptors and the underlying mechanisms. We also provide future perspectives for research.