Exploring Bile-Acid Changes and Microflora Profiles in Chicken Fatty Liver Disease Model.

Excessive liver fat causes non-alcoholic fatty liver disease (NAFLD) in laying hens, reducing egg production. Addressing NAFLD via bile-acid metabolism is gaining attention. We induced NAFLD in 7-week-old ISA female chickens with a high-cholesterol, low-choline diet (CLC) for 6 weeks. LC/MS was used to analyze serum and cecal bile acids, while cecal digesta DNA underwent 16S rRNA sequencing. The distribution of bile acid varied in healthy (CON) and CLC-fed chickens. CLC increased secondary bile acids (TLCA, TUDCA, THDCA, TDCA) in serum and primary bile acids (CDCA, TCDCA, isoDCA) in serum, as well as glycochenodeoxycholic acid (GCDCA) in cecal contents. CLC upregulated bile-acid synthesis enzymes (CYP7A1, CYP8B1) in the liver. Bile-acid receptor gene expression (HNF4A, FXR, LXR) was similar between groups. Microbiota abundance was richer in CON (alpha-diversity), with distinct separation (beta-diversity) between CON and CLC. The Firmicutes/Bacteroidetes ratio slightly decreased in CLC. Taxonomic analysis revealed higher Bacteroides, Alistipes, Megamonas in CLC but lower Barnesiella. CLC had more Mucispirillum, Eubacterium_coprostanoligenes_group, Shuttleworthia, and Olsenella, while CON had more Enterococcus, Ruminococcaceae_UCG_014, and Faecalibacterium. This study unveils bile-acid and microflora changes in a chicken NAFLD model, enhancing our understanding of fatty liver disease metabolism and aiding targeted interventions.

Mesobiliverdin IXα-enriched microalgae feed additive eliminates reliance on antibiotic tylosin to promote intestinal health of weaning piglets.

Weaning is a critical period in raising pigs. Novel animal feed additives that promote gut health and regulate immune function of piglets without antibiotics are needed. In this study, we aimed to test the ability of mesobiliverdin IXα-enriched microalgae (MBV IXα-enriched microalgae) to eliminate reliance on antibiotics to promote intestinal health in piglets. Eighty 28-day-old weaned piglets were randomly allocated to four groups each with four replicate pens and five piglets per pen. The dietary treatments were a basal diet as control (NC), basal diet plus 0.05% tylosin (PC), basal diet plus 0.1% or 0.5% MBV IXα-enriched microalgae as low (MBV-SP1) or high (MBV-SP2) dose respectively. All treated animals showed no significant differences in live weight, average daily gain and feed efficiency compared to control animals. Histological examination showed that MBV-SP1 and particularly MBV-SP2 increased the ratio of villus height to crypt depth in the jejunum and ileum compared to NC (p < 0.05). Similarly, tylosin treatment also increased villi lengths and the ratio of villus height to crypt depth in the jejunum and ileum compared to the NC (p < 0.05). MBV-SP1 and particularly MBV-SP2 reduced the levels of inflammatory cytokines interleukin-6 and tumour necrosis factor-alpha in the small intestine. MBV-SP2 and tylosin similarly reduced the lipid peroxidation marker (TBARS value) in the duodenum and ileum. In conclusion, feed supplementation with MBV IXα-enriched microalgae improved gut health by villus height and production of immunomodulators that correlated with down-regulated secretion of inflammatory cytokines.

Effects of indoor and outdoor rearing system on geese biochemical parameters and cecal microbial composition.

The present study aimed to investigate the impact of indoor and outdoor rearing systems on the biochemistry and microbial composition of White Roman geese, with a particular focus on the gut microbiome. Our results showed that geese reared in an outdoor system had significantly lower serum aspartate aminotransferase (AST) compared to those reared indoors, but lower levels of high-density lipoprotein (HDL) and higher levels of low-density lipoprotein (LDL). Moreover, the cecal microbiota of geese reared outdoors exhibited higher species evenness and increased alpha diversity, with a significant alteration in the F/B ratios. The bacterial taxonomy composition also differed between the 2 rearing systems, with higher relative abundances of the Firmicutes and Actinobacteria and lower relative abundances of the Bacteroidetes and Proteobacteria in the outdoor system. These findings suggest that rearing systems may play a critical role in shaping the gut microbiome and overall health of geese. Notably, our data demonstrated that indoor rearing was associated with a higher abundance of pathogenic genera and a lower abundance of commensal genera compared to outdoor rearing. Our study supports the hypothesis that rearing systems may alter the physiological functions and microbial composition of geese, and highlights the need for further research to confirm and expand upon these findings. In summary, our study underscores the importance of considering the impact of rearing systems on the gut microbiome and health of geese.

Determination of mitochondrial functions and damage in kidney in female LeeSung minipigs with a high-fat diet-induced obesity.

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.

Software-Based Process Simulation and Feasibility Assessment of Black Soldier Fly Larvae Fatty Acid Extraction and Fractionation.

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.

Mesobiliverdin IXα ameliorates osteoporosis via promoting osteogenic differentiation of mesenchymal stem cells.

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.

Effects of essential oil mixtures on nitrogen metabolism and odor emission via in vitro simulated digestion and in vivo growing pig experiments.

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 < 0.05). EO supplementation decreased the emission of ammonia (130-140 vs. 223 mg g-1 ) and total fecal nitrogen (8.0-9.9 vs. 12.4 g d-1 ) (P < 0.05). Microbial protease and urease activities were inhibited by EO treatments (P < 0.01). Both 2EO and 3EO reduced the content of indole and 3-methylindole (P < 0.01), whereas only 2EO caused a decrease in p-cresol (P < 0.1). CONCLUSION: 2EO was suitable for reducing waste emission and odorous compounds in growing pigs, whereas 3EO was optimal for increasing nitrogen utilization and partially reducing waste odorous compounds. © 2021 Society of Chemical Industry.

The Effect of Feeding Restriction on the Microbiota and Metabolome Response in Late-Phase Laying Hens.

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.

Effects of Dietary Inclusion of Dry Hydrastis canadensis on Laying Performance, Egg Quality, Serum Biochemical Parameters and Cecal Microbiota in Laying Hens.

Alternative growth promoters are able to not only effectively replace the traditional use of antibiotics but also provide additional health benefits for livestock and reduce food safety concerns. This study investigated the effects of dry Hydrastis canadensis on the laying performance and fecal microbial community of laying hens. Twenty-four Lohmann (LSL, white layer strain) hens were reared from 40 to 48 weeks of age and randomly allotted to four dietary treatments (six birds/treatment). The dietary treatments comprised a basal diet with no treatment as control, a basal diet plus 0.6% powder of dry Hydrastis canadensis roots (R) or leaves (L), and a basal diet plus 0.6% powder of a mixture of dry Hydrastis canadensis roots and leaves (1:1, LR). No mortality was observed in the whole experimental period. The results indicated that albumen height in the LR group was significantly greater than that in the control group. The diet supplemented with Hydrastis canadensis had no significant effects on egg production rate, egg weight, eggshell strength, eggshell thickness, Haugh unit, or yolk height during the whole experimental phase. However, principal coordinate analysis, comparative heat map analysis, and cluster dendrogram analysis of cecal microbiota showed distinct clusters among the groups treated with Hydrastis canadensis and the control group. Regarding blood biochemical parameters, serum cholesterol levels were significantly lower in all Hydrastis canadensis-treated groups compared with those in the control group. Moreover, serum low-density lipoprotein levels were lower in hens supplemented with the leaf of Hydrastis canadensis. The abundances of the phyla Fusobacteria and Kiritimatiellaeota were increased (p < 0.05) in laying hens fed with 0.6% Hydrastis canadensis leaves, whereas the abundance of the phylum Firmicutes in cecum digesta decreased in response to treatment with Hydrastis canadensis roots and leaves. The relative abundance of the Fusobacterium genus was higher in the LR group compared with that in the control. On the contrary, we found a different trend in the Synergistes genus. The potential influences of these microbiota on the performance of laying hens were discussed. The results demonstrate that Hydrastis canadensis can improve the egg albumen height and modulate the cecum digesta microbiota composition of laying hens.

Representative Diatom and Coccolithophore Species Exhibit Divergent Responses throughout Simulated Upwelling Cycles.

Wind-driven upwelling followed by relaxation results in cycles of cold nutrient-rich water fueling intense phytoplankton blooms followed by nutrient depletion, bloom decline, and sinking of cells. Surviving cells at depth can then be vertically transported back to the surface with upwelled waters to seed another bloom. As a result of these cycles, phytoplankton communities in upwelling regions are transported through a wide range of light and nutrient conditions. Diatoms appear to be well suited for these cycles, but their responses to them remain understudied. To investigate the bases for diatoms' ecological success in upwelling environments, we employed laboratory simulations of a complete upwelling cycle with a common diatom, Chaetoceros decipiens, and coccolithophore, Emiliania huxleyi We show that while both organisms exhibited physiological and transcriptomic plasticity, the diatom displayed a distinct response enabling it to rapidly shift-up growth rates and nitrate assimilation when returned to light and available nutrients following dark nutrient-deplete conditions. As observed in natural diatom communities, C. decipiens highly expresses before upwelling, or frontloads, key transcriptional and nitrate assimilation genes, coordinating its rapid response to upwelling conditions. Low-iron simulations showed that C. decipiens is capable of maintaining this response when iron is limiting to growth, whereas E. huxleyi is not. Differential expression between iron treatments further revealed specific genes used by each organism under low iron availability. Overall, these results highlight the responses of two dominant phytoplankton groups to upwelling cycles, providing insight into the mechanisms fueling diatom blooms during upwelling events.IMPORTANCE Coastal upwelling regions are among the most biologically productive ecosystems. During upwelling events, nutrient-rich water is delivered from depth resulting in intense phytoplankton blooms typically dominated by diatoms. Along with nutrients, phytoplankton may also be transported from depth to seed these blooms then return to depth as upwelling subsides creating a cycle with varied conditions. To investigate diatoms' success in upwelling regions, we compare the responses of a common diatom and coccolithophore throughout simulated upwelling cycles under iron-replete and iron-limiting conditions. The diatom exhibited a distinct rapid response to upwelling irrespective of iron status, whereas the coccolithophore's response was either delayed or suppressed depending on iron availability. Concurrently, the diatom highly expresses, or frontloads, nitrate assimilation genes prior to upwelling, potentially enabling this rapid response. These results provide insight into the molecular mechanisms underlying diatom blooms and ecological success in upwelling regions.

Overexpression of Adiponectin Receptor 1 Inhibits Brown and Beige Adipose Tissue Activity in Mice.

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 "healthy obese" 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.

A novel chicken model of fatty liver disease induced by high cholesterol and low choline diets.

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.

APPL1 negatively regulates bone mass, possibly by controlling the fate of bone marrow mesenchymal progenitor cells.

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.

LRRK2 Regulates CPT1A to Promote ß-Oxidation in HepG2 Cells.

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 ß-oxidation in HepG2 cells was promoted by LRRK2 overexpression, whereas LRRK2 knockdown inhibited ß-oxidation. The critical enzyme of ß-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 α (PPARα). The overexpression of LRRK2 reduced the concentration of a pro-inflammatory cytokine, tumor necrosis factor α (TNFα), induced by PA. The increase in ß-oxidation may promote lipid catabolism to suppress inflammation induced by PA. These results indicated that LRRK2 participated in the regulation of ß-oxidation and suggested that the decreased LRRK2 may promote inflammation by suppressing ß-oxidation in the liver.

Effects of Mesobiliverdin IXα-Enriched Microalgae Feed on Gut Health and Microbiota of Broilers.

Gut inflammatory bowel diseases (IBDs) links to animal medicinal feed and antibiotic-resistance are fueling major economic impacts in the agricultural livestock industry. New animal feeds that promote livestock gut health and control of IBDs without antibiotics are needed. This study investigates the effects of mesobiliverdin IXα (MBV)-enriched microalgae spirulina extracts on the growth performance, blood parameters, intestinal morphology, and gut microbiota of broilers. A total of 288 1-day-old broiler chicks (Arbor Acres) were randomly allotted to six dietary treatments (4 pens/treatment and 12 birds/pen). The dietary treatments comprised a basal diet as control (CON), basal diet plus 0.05 and 0.1% microalgae extract as low and high dose, respectively (SP1 and SP2), basal diet plus 0.05 and 0.1% MBV-enriched microalgae extract as low and high dose, respectively (MBV-SP1 and MBV-SP2), and basal diet plus 0.1% amoxicillin (AMX). All treated animals showed no significant differences in live weight, average daily gain, and feed efficiency compared to control animals. Histological examination showed that AMX treatment decreased the villi lengths of the duodenum and ileum below control villi length (P < 0.05) while MBV-SP1 and particularly MBV-SP2 increased villi lengths in the duodenum, jejunum, and ileum above AMX -treatment lengths (P < 0.05). The Firmicutes/Bacteroidetes ratio increased in the cecum of broilers fed AMX (P < 0.05) while SP2, MBV-SP1, and MBV-SP2-fed animals showed (in order) increasing ratios up to the AMX level. The abundance of bacterial species of the genus Lactobacillus increased in MBV-SP1 and MBV-SP2-fed groups including a striking increase in Lactobacillus salivarius abundance with MBV-SP2 (P < 0.05). Feeding MBV-SP1 and MBV-SP2 decreased the level of pro-inflammatory cytokine IL-6 in plasma of broilers to a greater extent than SP1 and SP2. These results reveal that MBV-enriched microalgae extracts improve the intestinal health and beneficial microflora composition of broilers.

Expression profile of adiponectin and adiponectin receptors in high-fat diet feeding chickens.

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.

Adiponectin receptor 1 resists the decline of serum osteocalcin and GPRC6A expression in ovariectomized mice.

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.

Embryonic cholesterol esterification is regulated by a cyclic AMP-dependent pathway in yolk sac membrane-derived endodermal epithelial cells.

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.

Chitosan-assisted differentiation of porcine adipose tissue-derived stem cells into glucose-responsive insulin-secreting clusters.

The unique advantage of easy access and abundance make the adipose-derived stem cells (ADSCs) a promising system of multipotent cells for transplantation and regenerative medicine. Among the available sources, porcine ADSCs (pADSCs) deserve especial attention due to the close resemblance of human and porcine physiology, as well as for the upcoming availability of humanized porcine models. Here, we report on the isolation and conversion of pADSCs into glucose-responsive insulin-secreting cells. We used the stromal-vascular fraction of the dorsal subcutaneous adipose from 9-day-old male piglets to isolate pADSCs, and subjected the cells to an induction scheme for differentiation on chitosan-coated plates. This one-step procedure promoted differentiation of pADSCs into pancreatic islet-like clusters (PILC) that are characterized by the expression of a repertoire of pancreatic proteins, including pancreatic and duodenal homeobox (Pdx-1), insulin gene enhancer protein (ISL-1) and insulin. Upon glucose challenge, these PILC secreted high amounts of insulin in a dose-dependent manner. Our data also suggest that chitosan plays roles not only to enhance the differentiation potential of pADSCs, but also to increase the glucose responsiveness of PILCs. Our novel approach is, therefore, of great potential for transplantation-based amelioration of type 1 diabetes.

MafB deficiency accelerates the development of obesity in mice.

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.