Abdominal Fat Deposition Research Articles

Gut Microbiome-Host Genetics Co-Evolution Shapes Adiposity by Modulating Energy and Lipid Metabolism in Selectively Bred Broiler Chickens

Optimizing fat deposition is crucial for improving chicken production and meat quality. This study investigated the interactive roles of host genetics and gut microbiome in regulating abdominal fat deposition in selectively bred broiler chicken lines. We compared the gut microbiome composition and host whole-genome profiles between fat-line and lean-line broiler chickens that had been selectively bred for divergent abdominal fat levels over 15 generations. Despite identical dietary and environmental conditions, the two chicken lines exhibited significant differences in their gut microbiota. Lean-line broiler chickens exhibited an increased abundance of intestinal Lactobacillus and a decreased presence of potentially pathogenic species, such as Campylobacter coli, Corynebacterium casei, and Enterococcus faecalis. These microbial alterations were accompanied by shifts in the functional metagenome, with enrichment in pathways involved in energy metabolism and nutrient utilization in the lean-line chickens. Notably, the selective breeding process also led to genomic variations in the lean broilers, with single nucleotide polymorphisms predominantly observed in genes related to energy and lipid metabolism. Our findings suggest that the host–microbiome interactions play a key role in the divergent abdominal fat deposition phenotypes observed in these selectively bred chicken lines. The co-evolution of the gut microbiome and host genetics highlights the importance of considering both factors to optimize poultry production efficiency and meat quality. This study offers new insights into the intricate gut–genome interactions in chicken fat metabolism, paving the way for more effective breeding and microbiome-based strategies to manage adiposity in poultry.

Characterization of the regulatory network and pathways in duodenum affecting chicken abdominal fat deposition

The excessive accumulation of abdominal fat in chickens has resulted in a reduction in both the feed conversion efficiency and the slaughter yield. To elucidate the regulatory mechanisms and metabolic pathways affecting abdominal fat deposition in the context of broiler breeding, a cohort of 400 Qingyuan partridge chickens with varying abdominal fat deposition was established. Whole transcriptome sequencing analyses were conducted on the duodenum of 20 representative chickens to ascertain the regulatory networks at this vital digestive and absorptive organ. Consequently, 116 differentially expressed genes were identified, exhibiting a trend of increasing or decreasing expression in correlation with the accumulation of abdominal fat. A total of 36 DEmRNAs, 170 DElncRNAs, 92 DEcircRNAs and 88 DEmiRNAs were identified as differentially expressed between chickens with extremely high and low abdominal fat deposition. The functional enrichment analyses demonstrated that the differentially expressed RNA in the duodenum were involved in the regulation of chicken abdominal fat deposition by mediating a series of metabolic pathways, including the Wnt signaling pathway, the PPAR signaling pathway, the Hippo signaling pathway, the FoxO signaling pathway, the MAPK signaling pathway and other signaling pathways that are involved in fatty acid metabolism and degradation. The construction of putative interaction pairs led to the suggestion of two lncRNA-miRNA-mRNA ceRNA networks comprising two mRNAs, two miRNAs, and 29 lncRNAs, as well as two circRNA-lncRNA-miRNA-mRNA ceRNA networks comprising 26 mRNAs, 12 miRNAs, 17 lncRNAs, and nine circRNAs, as core regulatory networks in the duodenum affecting chicken abdominal fat deposition. The aforementioned genes including TMEM150C, REXO1, PIK3C2G, ppp1cb, PARP12, SERPINE2, LRAT, CYP1A1, INSR and APOA4, were proposed as candidate genes, while the miRNAs, including miR-107-y, miR-22-y, miR-25-y, miR-2404-x and miR-16-x, as well as lncRNAs such as ENSGALT00000100291, TCONS_00063508, TCONS_00061201 and TCONS_00079402 were the candidate regulators associated with chicken abdominal fat deposition. The findings of this study provide a theoretical foundation for the molecular mechanisms of mRNAs and non-coding RNAs in duodenal tissues on abdominal fat deposition in chickens.

Integrative 3D genomics with multi-omics analysis and functional validation of genetic regulatory mechanisms of abdominal fat deposition in chickens

Chickens are the most abundant agricultural animals globally, with controlling abdominal fat deposition being a key objective in poultry breeding. While GWAS can identify genetic variants associated with abdominal fat deposition, the precise roles and mechanisms of these variants remain largely unclear. Here, we use male chickens from two lines divergently selected for abdominal fat deposition as experimental models. Through the integration of genomic, epigenomic, 3D genomic, and transcriptomic data, we build a comprehensive chromatin 3D regulatory network map to identify the genetic regulatory mechanisms that influence abdominal fat deposition in chickens. Notably, we find that the rs734209466 variant functions as an allele-specific enhancer, remotely enhancing the transcription of IGFBP2 and IGFBP5 by the binding transcription factor IRF4. This interaction influences the differentiation and proliferation of preadipocytes, which ultimately affects phenotype. This work presents a detailed genetic regulatory map for chicken abdominal fat deposition, offering molecular targets for selective breeding.

Consensus gene co-expression analysis across multiple intestinal tissues to identify key genes and pathways associated with abdominal fat deposition in broilers

ABSTRACT 1. Abdominal fat deposition (AFD) is regulated by multiple intestinal tissues, and changes in the function of intestinal tissues are associated with AFD. Currently, integration of transcriptomic data across multiple intestinal tissues to explore excessive AFD has rarely been reported in broilers. 2. In this study, a consensus gene co-expression network across the duodenum, jejunum, ileum and caecum of high- and low-abdominal fat broiler lines (HL and LL) was constructed using a publicly available transcriptomic data set. Combining the results of functional enrichment analyses and differential gene expression analyses, this investigated the genes and biological pathways across the four intestinal tissues that might influence AFD. 3. In one expression module, NDUFA5, NDUFS6, NDUFA4, NDUFS4, ATP5H, ATP5J and ATP5C1 were significantly enriched in the oxidative phosphorylation pathway, with GPX2 and GSR significantly enriched in the glutathione metabolism pathway. These genes were significantly downregulated in the four intestinal tissues of the HL compared to LL chickens, which may be associated with AFD by increasing intestinal permeability. 4. Lipid metabolism relevant genes were identified in other modules (ALDH7A1, ACSBG1, THEM4 and DECR1), which may be linked to AFD through regulation of lipid metabolism. Interestingly, in the first module, 12 genes were significantly enriched in the proteasome pathway and significantly downregulated in the four intestinal tissues in HL birds compared to LL birds, indicating a link between the proteasome and AFD.

Unraveling the role of long non-coding RNAs in chronic heat stress-induced muscle injury in broilers

BackgroundChronic heat stress (CHS) is a detrimental environmental stressor with a negative impact on the meat quality of broilers. However, the underlying mechanisms are not fully understood. This study investigates the effects of CHS on long non-coding RNA (lncRNA) expression and muscle injury in broilers, with a focus on its implications for meat quality.ResultsThe results showed that CHS diminished breast muscle yield, elevated abdominal fat deposition, induced cellular apoptosis (P < 0.05), and caused myofibrosis. Transcriptomic analysis revealed 151 differentially expressed (DE) lncRNAs when comparing the normal control (NC) and HS groups, 214 DE lncRNAs when comparing the HS and PF groups, and 79 DE lncRNAs when comparing the NC and pair-fed (PF) groups. After eliminating the confounding effect of feed intake, 68 lncRNAs were identified, primarily associated with cellular growth and death, signal transduction, and metabolic regulation. Notably, the apoptosis-related pathway P53, lysosomes, and the fibrosis-related gene TGF-β2 were significantly upregulated by lncRNAs.ConclusionsThese findings indicate that chronic heat stress induces cellular apoptosis and muscle injury through lncRNA, leading to connective tissue accumulation, which likely contributes to reduced breast muscle yield and meat quality in broilers.

Association between abdominal obesity indices and falls among older community-dwellers in Guangzhou, China: a prospective cohort study

BackgroundCentral obesity was considered as a risk factor for falls among the older population. Waist circumference (WC), lipid accumulation product (LAP), visceral adiposity index (VAI), and the Chinese visceral adiposity index (CVAI) are considered as surrogate markers for abdominal fat deposition in increasing studies. Nevertheless, the longitudinal relationship between these indices and falls among the older population remains indistinct. This study aimed to explore the association between abdominal obesity indices and falls among older community-dwellers.MethodsOur study included 3501 individuals aged ≥ 65 years from the Guangzhou Falls and Health Status Tracking Cohort at baseline in 2021 and then prospectively followed up in 2022. The outcome of interest was the occurrence of falls. The Kaplan-Meier curves and multivariable Cox regression analysis were used to explore the associations between abdominal obesity indices and falls. Moreover, the restricted cubic spline analysis (RCS) was conducted to test the non-linear relationships between abdominal obesity indices and hazards of falls incident.ResultsAfter a median follow-up period of 551 days, a total of 1022 participants experienced falls. The cumulative incidence rate of falls was observed to be higher among individuals with central obesity and those falling within the fourth quartile (Q4) of LAP, VAI, and CVAI. Participants with central obesity and those in Q4 of LAP, VAI, and CVAI were associated with higher risk of falls, with hazard ratios (HRs) of 1.422 (HR 95%CI: 1.255–1.611), 1.346 (1.176–1.541), 1.270 (1.108–1.457), 1.322 (1.154–1.514), respectively. Each 1-SD increment in WC, LAP, VAI, and CVAI was a significant increased risk of falls among participants. Subgroup analysis further revealed these results were basically stable and appeared to be significantly stronger among those females, aged 65–69 years, and with body mass index (BMI) ≥ 28 kg/m2. Additionally, RCS curves showed an overall upward trend in the risk of falls as the abdominal indices increased.ConclusionsAbdominal obesity indices, as WC, LAP, VAI, and CVAI were significantly associated with falls among older community-dwellers. Reduction of abdominal obesity indices might be suggested as the strategy of falls prevention.

Evaluating Candidate Gene Expressions, pH Levels, and Growth Hormone Gene Polymorphisms in different Chicken Breeds: Investigations for Meat Color Regulation and Abdominal Fat Deposition

Evaluating Candidate Gene Expressions, pH Levels, and Growth Hormone Gene Polymorphisms in different Chicken Breeds: Investigations for Meat Color Regulation and Abdominal Fat Deposition

Embryonic thermal manipulation and post-hatch dietary guanidinoacetic acid supplementation alleviated chronic heat stress impact on broiler chickens

The study investigated the effects of embryonic thermal manipulation (TM) and post-hatch guanidinoacetic acid (GAA) supplementation on male broiler chickens exposed to chronic heat stress (HS). Ross 308 eggs (n = 710) were randomly assigned to control (37.8 °C, 56% RH) or TM (39.5 °C, 65% RH for 12 h/day from embryonic day 7–16) treatments. After hatching, chicks were further assigned to four dietary treatments (n = 12 birds/pen, 5 replicates/treatment): control, control with 1.2 g/kg GAA supplementation (CS), TM, and TM with 1.2 g/kg GAA supplementation (TMS). All birds were subjected to chronic HS (32–36 °C and 55% RH for 6 h/day) from day 28–42. Embryonic TM treatment decreased hatchability, hatching weight (HW), and facial temperature (FT). During the pre-HS period (days 1–28), no significant differences in feed conversion ratio (FCR) and mortality were observed, although the TM group exhibited the lowest body weight gain (BWG). Following HS exposure (days 29–42), the TMS group displayed significantly higher BWG than the control and CS groups. The TM and TMS groups also demonstrated significantly lower FCR and mortality rates during this period. Across the entire period (days 1–42), BWG was significantly higher in the TMS group compared to other groups. Furthermore, TM and TMS treatments were associated with lower mortality rates, improved FCR, better European Performance Efficiency Index (EPEI), and reduced abdominal fat deposition. The experimental treatments did not significantly affect intestinal morphology or most blood parameters, except triiodothyronine (T3), thyroxine (T4), and uric acid. Plasma concentrations of T3, T4, and uric acid were significantly lower in the TM and TMS groups compared to the control and CS treatments. The findings suggest that a combined strategy of embryonic TM and post-hatch dietary GAA supplementation may not only alleviate the detrimental effects of HS but also promote beneficial physiological responses in broiler chickens.

Association between body condition score and abdominal fat assessed by ultrasound in Jersey cows.

Body condition score (BCS) is a subjective tool and the deposition of subcutaneous fat differs from the deposition of abdominal fat. The aim of this study was to evaluate by multivariate regression models and ultrasonography the amount of fat accumulated in different areas of the abdominal cavity in Jersey non-pregnant non-lactating cows and its association with their BCS. From a commercial farm, 21 non-pregnant non-lactating Jersey cows were selected at random. Cows were placed in a headlock line, and BCS was evaluated (scale 1-5 with a 0.25 unit increment) by the same assessor. Ultrasonographic evaluation was performed using a Sonosite machine in duplicate, considering key anatomical points of the body to predict total abdominal fat (AT), retroperitoneal fat (RT), omental fat (OT) and mesenteric fat (MT). A regression analysis for each abdominal fat depot and the BCS was run using SAS. Models from the lowest to the largest r2 are reported. The r2 for the models were MT r2=0.023; RT r2=0.1047; OT r2=0.323 and AT r2=0.369. Correlation between BCS and abdominal fat depots was positive, lower for mesenteric and retroperitoneal fat, but higher for omental and total abdominal fat. Cows were divided on the basis of the median of BCS distribution to high (≥3.5) and low (≤3.25). Those with high BCS had significantly larger amounts of fat in different anatomical areas of abdominal cavity than cows with low BCS. BCS has a low-to-moderate association with abdominal fat depots, but a high variability exists within each BCS punctuation, which supports the notion that fat accumulation patterns and metabolic turnover between abdominal and subcutaneous fat differ from each other.

The impact of NUMB on chicken abdominal adipogenesis: A comprehensive analysis

Excessive abdominal fat deposition negatively impacts poultry meat production and carcass yield. Identification of novel adipogenesis regulators may help improve production performance declines caused by excessive fat deposition. NUMB Endocytic Adaptor Protein (NUMB) typically functions as a cell fate determinant and plays a significant role in cell development and various diseases. Here, we found that NUMB is abundantly expressed in chicken abdominal fat depots and is induced in cultured adipocytes following adipogenic treatment. The gain- and loss-of-function experiments demonstrated that NUMB promotes the proliferation and G1/S transition of chicken adipocytes, enhances adipocyte differentiation, and increases the expression of PPARγ1 transcript. Through mRNA-seq analysis and molecular experiments, we further confirmed that NUMB inhibits the transcriptional activation of the NOTCH1 pathway and the expression of the downstream transcription factor HES1 by inducing NOTCH1 degradation. Nevertheless, the inhibition of the NOTCH1/HES1 axis alone cannot fully explain NUMB's role in adipogenesis, as NUMB also regulates the expression of multiple adipogenic transcription factors such as E2F1, EGR2, and NR4A3. Our data suggest that NUMB is a potent activator of adipogenesis and enhances our understanding of its regulatory mechanisms in chicken abdominal fat deposition.

Low Testosterone and High Leptin Activate PPAR Signaling to Induce Adipogenesis and Promote Fat Deposition in Caponized Ganders.

Low or insufficient testosterone levels caused by caponization promote fat deposition in animals. However, the molecular mechanism of fat deposition in caponized animals remains unclear. This study aimed to investigate the metabolomics and transcriptomic profiles of adipose tissues and study the effect of testosterone and leptin on the proliferation of adipocytes. We observed a significant enlargement in the areas of adipocytes in the abdominal fat tissues in capon, as well as increased luciferase activity of the serum leptin and a sharp decrease in the serum testosterone in caponized gander. Metabolomics and transcriptomic results revealed differentially expressed genes and differentially expressed metabolites with enhanced PARR signal pathway. The mRNA levels of peroxisome proliferators-activated receptor γ, fatty acid synthase, and suppressor of cytokine signaling 3 in goose primary pre-adipocytes were significantly upregulated with high leptin treatment and decreased significantly with increasing testosterone dose. Hence, reduced testosterone and increased leptin levels after caponization possibly promoted adipocytes proliferation and abdominal fat deposition by altering the expression of PPAR pathway related genes in caponized ganders. This study provides a new direction for the mechanism through which testosterone regulates the biological function of leptin and fat deposition in male animals.

Tanycytic transcytosis inhibition disrupts energy balance, glucose homeostasis and cognitive function in male mice

ObjectivesIn Western society, high-caloric diets rich in fats and sugars have fueled the obesity epidemic and its related disorders. Disruption of the body-brain communication, crucial for maintaining glucose and energy homeostasis, arises from both obesogenic and genetic factors, leading to metabolic disorders. Here, we investigate the role of hypothalamic tanycyte shuttles between the pituitary portal blood and the third ventricle cerebrospinal fluid in regulating energy balance. MethodsWe inhibited vesicle-associated membrane proteins (VAMP1-3)-mediated release in tanycytes by expressing the botulinum neurotoxin type B light chain (BoNT/B) in a Cre-dependent manner in tanycytes. This was achieved by injecting either TAT-Cre in the third ventricle or an AAV1/2 expressing Cre under the control of the tanycyte-specific promoter iodothyronine deiodinase 2 into the lateral ventricle of adult male mice. ResultsIn male mice fed a standard diet, targeted expression of BoNT/B in adult tanycytes blocks leptin transport into the mediobasal hypothalamus and results in normal-weight central obesity, including increased food intake, abdominal fat deposition, and elevated leptin levels but no marked change in body weight. Furthermore, BoNT/B expression in adult tanycytes promotes fatty acid storage, leading to glucose intolerance and insulin resistance. Notably, these metabolic disturbances occur despite a compensatory increase in insulin secretion, observed both in response to exogenous glucose boluses in vivo and in isolated pancreatic islets. Intriguingly, these metabolic alterations are associated with impaired spatial memory in BoNT/B-expressing mice. ConclusionsThese findings underscore the central role of tanycytes in brain-periphery communication and highlight their potential implication in the age-related development of type 2 diabetes and cognitive decline. Our tanycytic BoNT/B mouse model provides a robust platform for studying how these conditions progress over time, from prediabetic states to full-blown metabolic and cognitive disorders, and the mechanistic contribution of tanycytes to their development. The recognition of the impact of tanycytic transcytosis on hormone transport opens new avenues for developing targeted therapies that could address both metabolic disorders and their associated cognitive comorbidities, which often emerge or worsen with advancing age.

Diacerein mitigates endocrine and cardio-metabolic disruptions in experimental PCOS mice model by modulating AdipoR1/ PON 1

BackgroundThis study aimed to explore the impact of Diacerein (DIC) on endocrine and cardio-metabolic changes in polycystic ovarian syndrome (PCOS) mouse model.MethodsA total of 18 adult female mice (Parkes strain), aged 4–5 weeks, were randomly assigned to three groups, each comprising 6 animals, as follows: Group I (control), received normal diet and normal saline as vehicle for 51 days; Group II received Letrozole (LET; 6 mg/kg bw) for 21 days to induce PCOS; Group III received LET, followed by daily oral gavage administration of DIC (35 mg/kg bw) for 30 days.ResultsThis study indicates that treatment with LET resulted in PCOS with characteristics such as polycystic ovaries, elevated testosterone, weight gain, visceral adiposity, high levels of insulin as well as fasting blood glucose in addition to insulin resistance, improper handling of ovarian lipids, atherogenic dyslipidemia, impaired Na + /K + -ATPase activity and serum, cardiac, and ovarian oxidative stress. Serum/ovarian adiponectin levels were lowered in LET-treated mice. In mice treated with LET, we also discovered a reduction in cardiac and serum paraoxonase 1 (PON1). Interestingly, DIC restored ovarian andcardio-metabolic abnormalities in LET-induced PCOS mice. DIC prevented the endocrine and cardio-metabolic changes brought on by letrozole-induced PCOS in mice.ConclusionThe ameliorative effects of DIC on letrozole-induced PCOS with concurrent oxidative stress, abdominal fat deposition, cardiac and ovarian substrate mishandling, glucometabolic dysfunction, and adiponectin/PON1 activation support the idea that DIC perhaps, restore compromised endocrine and cardio-metabolic regulators in PCOS.

Assessment of dietary supplementation of green iron oxide nanoparticles: impact on growth performance, ammonia emissions, carcass criteria, tissue iron content, and meat quality in broiler chickens under hot climate conditions.

The potential significance and importance of green iron nanoparticles (Nano-Fe) in poultry production lie in their capability to effectively tackle iron deficiency in poultry. Iron, an indispensable mineral for numerous physiological functions in birds, such as oxygen transport, energy metabolism, and immune response, underscores the critical need for adequate iron levels. Nevertheless, conventional iron supplementation methods frequently face hurdles like limited bioavailability rates in poultry. To enhance performance, and promote sustainable broiler productivity, Nano-Fe showed promise as an efficient feed supplement for broiler chickens. The objective of this study was to assess the impact of green Nano-Fe inclusions in diets on growth, ammonia excretion, carcass criteria, and meat quality in broiler chickens. A total of 192 one-day-old male Ross 308 broiler chicks, were assigned to three treatment diets including Nano-Fe oxide at 0, 20, or 40 mg/kg, respectively, for 42 days. Each treatment comprised eight replicates, each with eight broiler chicks. Two phases comprised the 42-day study (0 to 21 days for the starter and 21 to 42 days for the finisher). In comparison to the control group, the Nano-Fe oxide groups 20 mg/kg and 40 mg/kg linearly improved (p < 0.05) body weight (R 2 = 0.574) and body weight gain (R 2 = 0.367) under hot climatic conditions at 42 days of age. Furthermore, Nano-Fe oxide to broiler diets, improved (linear, p < 0.05) feed conversion ratio (R 2 = 0.424) throughout whole periods. The feed intake did not show any significant difference (p > 0.05) among groups during the experimental periods under hot climatic conditions. The ammonia content of excreta (R 2 = 0.454) was linearly decreased (p < 0.05) with increasing Nano-Fe oxide levels in broiler diets compared to control at 21 and 42 days of age under hot climatic conditions. Nano-Fe oxide positively influences cook loss, water-holding capacity, and iron content in various tissues. Moreover, it contributes to a healthier carcass yield and reduced abdominal fat. In conclusion, broiler chickens fed diets containing Nano-Fe oxide at 20 mg/kg and 40 mg/kg demonstrated enhanced growth performance, improved meat quality, increased iron content in tissues, higher dressing percentage, and reduced abdominal fat deposition. Future research should explore the impact of green Nano-Fe oxide on additional factors such as the microbiome and gene expression related to immunity and heat stress.

Comprehensive analysis of changes in expression of lncRNA, microRNA and mRNA in liver tissues of chickens with high or low abdominal fat deposition

ABSTRACT 1. The liver of chickens is a dominant lipid biosynthetic tissue and plays a vital role in fat deposition, particularly in the abdomen. To determine the molecular mechanisms involved in its lipid metabolism, the livers of chickens with high (H) or low (L) abdominal fat content were sampled and sequencing on long non-coding RNA (lncRNA), messenger RNA (mRNA) and small RNA (microRNA) was performed. 2. In total, 351 expressed protein-coding genes for long non-coding RNA (DEL; 201 upregulated and 150 downregulated), 400 differentially expressed genes (DEG; 223 upregulated and 177 downregulated) and 10 differentially expressed miRNA (DEM; four upregulated and six downregulated) were identified between the two groups. Multiple potential signalling pathways related to lipogenesis and lipid metabolism were identified via pathway enrichment analysis. In addition, 173 lncRNA – miRNA – mRNA interaction regulatory networks were identified, including 30 lncRNA, 27 mRNA and seven miRNA. 3. These networks may help regulate lipid metabolism and fat deposition. Five promising candidate genes and two lncRNA may play important roles in the regulation of adipogenesis and lipid metabolism in chickens.

Liraglutide induced browning of visceral white adipose through regulation of miRNAs in high-fat-diet-induced obese mice.

Obesity is characterized by excessive accumulation of white adipose tissue (WAT). Conversely, brown adipose tissue is protective against obesity. We recently reported liraglutide, a glucagon-like peptide-1 receptor agonist (GLP-1RA), could inhibit high-fat-diet-induced obesity by browning of WAT. However, the molecular mechanism involved is not well defined. Hence, we aimed to explore whether GLP-1RA could promote brown remodeling in WAT by regulating miRNAs. After the obesity model was successfully constructed, C57BL/6J mice were treated with liraglutide (200 μg/kg/d) or equivoluminal saline subcutaneously for 12 weeks. Then, the deposition of abdominal fat was measured by CT scanning. At the end of the treatments, glucose and insulin tolerance in mice were assessed. Serum lipid levels were monitored and epididymal WAT (eWAT) were collected for analysis. Quantitative real-time PCR and western blot analyses were conducted to evaluate the expression of genes and miRNAs associated with white fat browning. Liraglutide significantly reduced body weight and visceral fat mass. Levels of lipid profile were also improved. Liraglutide upregulated the expression of browning-related genes in eWAT. Meanwhile, the expression level of miRNAs (miR-196a and miR-378a) positively associated with the browning of WAT were increased, while the expression of miR-155, miR-199a, and miR-382 negatively related with browning of WAT were decreased. Our findings suggest that liraglutide could promote brown remodeling of visceral WAT by bi-regulating miRNAs; this might be one of the mechanisms underlying its effect on weight loss.

Fecal microbiota transplantation ameliorates abdominal obesity through inhibiting microbiota-mediated intestinal barrier damage and inflammation in mice

Abdominal obesity (AO), characterized by the excessive abdominal fat accumulation, has emerged as a significant public health concern due to its metabolic complications and escalating prevalence worldwide, posing a more pronounced threat to human health than general obesity. While certain studies have indicated that intestinal flora contributed to diet-induced general obesity, the precise involvement of gut microbiota in the development of AO, specifically the accumulation of abdominal fat, remains inadequately explored. In this study, the 16 S rDNA sequencing was employed to analyze gut flora alterations, and the intestinal microbiota dysbiosis characterized by a vanishing decline of Akkermansia was found in the AO group. Along with notable gut microbiota changes, the intestinal mucosal barrier damage and metabolic inflammation were detected, which collectively promoted metabolic dysregulation in AO. Furthermore, the metabolic inflammation and AO were ameliorated after the intestinal microbiota depletion with antibiotics (ABX) drinking, underscoring a significant involvement of gut microbiota dysbiosis in the progression of AO. More importantly, our findings demonstrated that the transplantation of healthy intestinal flora successfully reversed the gut microbiota dysbiosis, particularly the decline of Akkermansia in the AO group. The gut flora reshaping has led to the repair of gut barrier damage and mitigation of metabolic inflammation, which ultimately ameliorated abdominal fat deposition. Our study established the role of interactions between gut flora, mucus barrier, and metabolic inflammation in the development of AO, thereby offering a theoretical foundation for the clinical application of fecal microbiota transplantation (FMT) as a treatment for AO.

RNA-Seq Analysis Revealed circRNAs and Genes Associated with Abdominal Fat Deposition in Ducks.

Fat deposition is an important factor affecting meat quality and feed conversion efficiency in meat ducks. This study aims to identify key circRNAs and genes affecting abdominal fat deposition. The correlations between abdominal fat and other growth performances were analyzed in 304 F2 generation of Cherry Valley duck Runzhou Crested White ducks, and an RNA-seq analysis of abdominal fat tissues from ducks with high and low rates of abdominal fat was performed. Growth performance results showed that Abdominal fat ratio and Intramuscular fat were significantly higher in the high rates of abdominal fat (HF)group than in the low rates of abdominal fat (LF) group for ducks. RNA-seq analysis of abdominal fat tissue unveiled 85 upregulated and 72 downregulated circRNAs among the differentially expressed ones. Notably, 74 circRNAs displayed more than four-fold differential expression, constituting 47.13% of the differentially expressed genes. Functional enrichment analysis of the differentially expressed circRNA source and target genes indicated that 17 circRNAs might partake in regulating duck abdominal fat production by influencing pathways like PPAR signaling, lipid droplets, and triglyceride metabolism. Lastly, multiple circRNA-microRNA-messenger RNA interaction networks were constructed. The results of this study establish the groundwork for understanding the molecular mechanisms that regulate abdominal fat deposition in ducks, offering a theoretical reference for the selective breeding of high-quality meat-producing ducks.

Early fecal microbiota transplantation from high abdominal fat chickens affects recipient cecal microbiome and metabolism.

Abdominal fat deposition (AFD) in chickens is closely related to the gut microecological balance. In this study, the gut microbiota from high-AFD chickens was transplanted into the same strain of 0-day-old chicks via fecal microbiota transplantation (FMT). The FTM from chickens with high AFD had no obvious effects on growth traits, adult body weight, carcass weight, abdominal fat weight, and abdominal fat percentage, but did reduce the coefficient of variation of AFD traits. FMT significantly decreased cecal microbiome richness, changed the microbiota structure, and regulated the biological functions associated with energy metabolism and fat synthesis. Additionally, the cecal metabolite composition and metabolic function of FMT recipient chickens were also significantly altered from those of the controls. Transplantation of high-AFD chicken gut microbiota promoted fatty acid elongation and biosynthesis and reduced the metabolism of vitamins, steroids, and carbohydrates in the cecum. These findings provide insights into the mechanisms by which chicken gut microbiota affect host metabolic profiles and fat deposition.

Identification of central regulators related to abdominal fat deposition in chickens based on weighted gene co-expression network analysis

Abdominal fat (AF) is one of the most important economic traits in chickens. Excessive AF in chickens will reduce feed utilization efficiency and negatively affect reproductive performance and disease resistance. However, the regulatory network of AF deposition needs to be further elucidated. In the present study, 300 one-day-old female Wannan chickens were reared to 17 wk of age, and 200 Wannan hens were selected to determine the abdominal fat percentage (AFP). Twenty AF tissue samples with the lowest AFP were selected as the low abdominal fat group (L-AFG), and 20 AF tissue samples with the highest AFP were selected as the high abdominal fat group (H-AFG). Eleven samples from L-AFG and 14 samples from H-AFG were selected for RNA-seq and used for weighted gene co-expression network analysis (WGCNA). Among the 25 RNA-seq samples, 5 samples with the lowest and highest AFP values were selected for differential expression gene analysis. Compared with the L-AFG, 225 and 101 genes were upregulated and downregulated in the H-AFG, respectively. A total of 20,503 genes were used to construct the WGCNA, and 44 co-expression gene modules were identified. Among these modules, 3 modules including turquoise, darkorange2, and floralwhite were identified as significantly associated with AFP traits. Furthermore, several genes including acyl-CoA oxidase 1 (ACOX1), stearoyl-CoA desaturase (SCD), aldehyde dehydrogenase 6 family member A1 (ALDH6A1), jun proto-oncogene, AP-1 transcription factor subunit (JUN), and fos proto-oncogene, AP-1 transcription factor subunit (FOS) involved in the "PPAR signaling pathway," "fatty acid metabolism," and "MAPK signaling pathway" were identified as central regulators that contribute to AF deposition. These results provide valuable information for further understanding of the gene expression and regulation of AF traits and contribute to future molecular breeding for AF in chickens.