Specific Microbial Taxa and Functional Capacity Contribute to Chicken Abdominal Fat Deposition

Xiang, Hai; Gan, Jiankang; Zeng, Daoshu; Li, Jing; Yu, Hui; Zhao, Huabin; Yang, Ying; Tan, Shuo; Li, Gen; Luo, Chaowei; Xie, Zhen; Zhao, Guiping; Li, Hua

doi:10.3389/fmicb.2021.643025

Cited by 32 publications

(46 citation statements)

References 59 publications

(74 reference statements)

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“…Clarifying the mechanisms of lipogenesis is essential for the improvement of the fat trait in chicken. Studies have revealed that gut microbiota participates in the regulation of lipogenesis and fat deposition in chicken [ 7 , 10 ]. However, the precise molecular mechanisms by which gut microbiota regulates lipogenesis and fat deposition remain largely unknown.…”

Section: Discussionmentioning

confidence: 99%

Antibiotic-Induced Dysbiosis of Microbiota Promotes Chicken Lipogenesis by Altering Metabolomics in the Cecum

et al. 2021

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Elucidation of the mechanism of lipogenesis and fat deposition is essential for controlling excessive fat deposition in chicken. Studies have shown that gut microbiota plays an important role in regulating host lipogenesis and lipid metabolism. However, the function of gut microbiota in the lipogenesis of chicken and their relevant mechanisms are poorly understood. In the present study, the gut microbiota of chicken was depleted by oral antibiotics. Changes in cecal microbiota and metabolomics were detected by 16S rRNA sequencing and ultra-high performance liquid chromatography coupled with MS/MS (UHPLC–MS/MS) analysis. The correlation between antibiotic-induced dysbiosis of gut microbiota and metabolites and lipogenesis were analysed. We found that oral antibiotics significantly promoted the lipogenesis of chicken. 16S rRNA sequencing indicated that oral antibiotics significantly reduced the diversity and richness and caused dysbiosis of gut microbiota. Specifically, the abundance of Proteobacteria was increased considerably while the abundances of Bacteroidetes and Firmicutes were significantly decreased. At the genus level, the abundances of genera Escherichia-Shigella and Klebsiella were significantly increased while the abundances of 12 genera were significantly decreased, including Bacteroides. UHPLC-MS/MS analysis showed that antibiotic-induced dysbiosis of gut microbiota significantly altered cecal metabolomics and caused declines in abundance of 799 metabolites and increases in abundance of 945 metabolites. Microbiota-metabolite network revealed significant correlations between 4 differential phyla and 244 differential metabolites as well as 15 differential genera and 304 differential metabolites. Three metabolites of l-glutamic acid, pantothenate acid and N-acetyl-l-aspartic acid were identified as potential metabolites that link gut microbiota and lipogenesis in chicken. In conclusion, our results showed that antibiotic-induced dysbiosis of gut microbiota promotes lipogenesis of chicken by altering relevant metabolomics. The efforts in this study laid a basis for further study of the mechanisms that gut microbiota regulates lipogenesis and fat deposition of chicken.

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Section: Discussionmentioning

confidence: 99%

Antibiotic-Induced Dysbiosis of Microbiota Promotes Chicken Lipogenesis by Altering Metabolomics in the Cecum

et al. 2021

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“…However, R. bacterium CPB6 mainly produces caproate, which had positive relations with BMI ( Zhu et al, 2017 ; Fan et al, 2018 ). Similarly, R. bacterium has also been identified to significantly increase in cecum of high AFD chicken ( Xiang et al, 2021 ). Increased abundances of Alistipes sp.…”

Section: Discussionmentioning

confidence: 99%

“…In regard to microbial relative abundance, genera including Megamonas ( Maya-Lucas et al, 2019 ), Oscillospira , Ruminococcus ( Jiao et al, 2018 ), Fusobacterium , Escherichia-Shigella , and Pseudomonas ( Gao et al, 2018 ) were significantly increased in obese humans and mice. Recently, studies on chicken cecal microbiome showed that Microbacterium , Sphingonomas , Olsenella , Methanobrevibacter , and Slackia were positively correlated with fat metabolism ( Xiang et al, 2021 ; Zhang et al, 2021 ). Functional analysis of microbiome indicated that pyruvate metabolism, butanoate metabolism, propanoate metabolism, pentose phosphate pathway, fatty acid biosynthesis, and glycerolipid metabolism pathways were enriched in obese mice ( Jiao et al, 2018 ), while glycolysis I (from glucose 6-phosphate) and glycolysis II (from fructose 6-phosphate) were significantly overrepresented in normal individuals ( Maya-Lucas et al, 2019 ).…”

Section: Introductionmentioning

confidence: 99%

“…Functional analysis of microbiome indicated that pyruvate metabolism, butanoate metabolism, propanoate metabolism, pentose phosphate pathway, fatty acid biosynthesis, and glycerolipid metabolism pathways were enriched in obese mice ( Jiao et al, 2018 ), while glycolysis I (from glucose 6-phosphate) and glycolysis II (from fructose 6-phosphate) were significantly overrepresented in normal individuals ( Maya-Lucas et al, 2019 ). In chicken, functional enrichments of cecal microbiome found that microbial pathways including lipid metabolism, carbohydrate metabolism, and energy metabolism pathways were upregulated in high AFD group, when compared to low-AFD group ( Xiang et al, 2021 ).…”

Section: Introductionmentioning

confidence: 99%

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Multi-Omics Association Reveals the Effects of Intestinal Microbiome–Host Interactions on Fat Deposition in Broilers

et al. 2022

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Growing evidence indicates that gut microbiota factors cannot be viewed as independent in the occurrence of obesity. Because the gut microbiome is highly dimensional and complex, studies on interactions between gut microbiome and host in obesity are still rare. To explore the relationship of gut microbiome–host interactions with obesity, we performed multi-omics associations of gut metagenome, intestinal transcriptome, and host obesity phenotypes in divergently selected obese–lean broiler lines. Metagenomic shotgun sequencing generated a total of 450 gigabases of clean data from 80 intestinal segment contents of 20 broilers (10 of each line). The microbiome comparison showed that microbial diversity and composition in the duodenum, jejunum, ileum, and ceca were altered variously between the lean- and fat-line broilers. We identified two jejunal microbes (Escherichia coli and Candidatus Acetothermia bacterium) and four cecal microbes (Alistipes sp. CHKCI003, Ruminococcaceae bacterium CPB6, Clostridiales bacterium, and Anaeromassilibacillus sp. An200), which were significantly different between the two lines (FDR < 0.05). When comparing functional metagenome, the fat-line broilers had an intensive microbial metabolism in the duodenum and jejunum but degenerative microbial activities in the ileum and ceca. mRNA-sequencing identified a total of 1,667 differentially expressed genes (DEG) in the four intestinal compartments between the two lines (| log2FC| > 1.5 and FDR < 0.05). Multi-omics associations showed that the 14 microbial species with abundances that were significantly related with abdominal fat relevant traits (AFRT) also have significant correlations with 155 AFRT-correlated DEG (p < 0.05). These DEG were mainly involved in lipid metabolism, immune system, transport and catabolism, and cell growth-related pathways. The present study constructed a gut microbial gene catalog of the obese–lean broiler lines. Intestinal transcriptome and metagenome comparison between the two lines identified candidate DEG and differential microbes for obesity, respectively. Multi-omics associations suggest that abdominal fat deposition may be influenced by the interactions of specific gut microbiota abundance and the expression of host genes in the intestinal compartments in which the microbes reside. Our study explored the interactions between gut microbiome and host intestinal gene expression in lean and obese broilers, which may expand knowledge on the relationships between obesity and gut microbiome.

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“…The balance of Firmicutes and Bacteroidetes is measured as a ratio, Firmicutes / Bacteroidetes (F/B), which is a predictive marker reflecting gut microbiota dysbiosis ( 72 , 73 ). Besides, the increment of the F/B ratio induced by the contraction of Bacteroidetes and/or expansion of Firmicutes is tightly associated with fat accumulation and potential for obesity both in humans and other animals ( 74 , 75 ). Recently, several reports have suggested that the gut microbiota of stressed birds presented a significantly increased trend of the F/B ratio ( 76 – 78 ).…”

Section: Discussionmentioning

confidence: 99%

Gut Microbiota and Serum Metabolite Potential Interactions in Growing Layer Hens Exposed to High-Ambient Temperature

et al. 2022

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Emerging evidence has revealed the dysbiosis of gut microbiota contributes to development of metabolic diseases in animals. However, the potential interaction between gut microbiota and host metabolism in growing hens under metabolic disorder induced by chronic heat exposure (CHE) remains inconclusive. The aim of our study was to examine the potential association among the cecal microbiota community, physiological indicators, and serum metabolite profiles in CHE hens. One hundred and eighty Hy-Line Brown hens were randomly allocated into three groups: thermoneutral control (TN), heat stress (HS), and pair-fed (PF). The experiment lasted for 5 weeks, with the first 2 weeks serving as the adaptation period. Results showed that the expression level of heat shock protein 70 (HSP70) in both serum and cecal tissues was significantly increased in the HS group. Serum parameters analysis also revealed that CHE caused physiological function damage and metabolic disorders. These results suggest the experiment was successful, inducing chronic heat stress. 16S rRNA sequencing analysis showed that the CHE can clearly induce dysbiosis of the gut microbial community reflected in the increment of the F/B ratio. Besides, serum untargeted metabolomics revealed the relative concentrations of 40 metabolites were significantly altered in the HS group compared with the TN group. Pathway analysis showed that these metabolites were mainly involving the increased proteolysis rather than lipolysis, and this tendency could be a specific metabolic adaptation of the poultry. The pair-feed experiment showed that the above changes induced by CHE were partly independent from the reduction of feed intake. Mantel correlation analysis between gut microorganisms and physiological indicators showed that the phylum Firmicutes and Euryarchaeota have a potential interaction with a serum lipid parameter. Random forest analysis showed that both genus Faecalibacterium and Methanobrevibacter were important predictors of the CHE-induced lipid metabolism disorder. Taken together, our findings may contribute to a better understanding of the metabolic mechanisms underlying the energy metabolism imbalance caused by the CHE and provide novel insights into the host-microbes interactions and its effects on the metabolic adaptation of hens under chronic heat exposure.

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Specific Microbial Taxa and Functional Capacity Contribute to Chicken Abdominal Fat Deposition

Cited by 32 publications

References 59 publications

Antibiotic-Induced Dysbiosis of Microbiota Promotes Chicken Lipogenesis by Altering Metabolomics in the Cecum

Antibiotic-Induced Dysbiosis of Microbiota Promotes Chicken Lipogenesis by Altering Metabolomics in the Cecum

Multi-Omics Association Reveals the Effects of Intestinal Microbiome–Host Interactions on Fat Deposition in Broilers

Gut Microbiota and Serum Metabolite Potential Interactions in Growing Layer Hens Exposed to High-Ambient Temperature

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