RNA-Seq Analysis of Abdominal Fat in Genetically Fat and Lean Chickens Highlights a Divergence in Expression of Genes Controlling Adiposity, Hemostasis, and Lipid Metabolism
Date
2015-10-07
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Public Library of Science (PLOS)
Abstract
Genetic selection for enhanced growth rate in meat-type chickens (Gallus domesticus) is
usually accompanied by excessive adiposity, which has negative impacts on both feed efficiency
and carcass quality. Enhanced visceral fatness and several unique features of avian
metabolism (i.e., fasting hyperglycemia and insulin insensitivity) mimic overt symptoms of
obesity and related metabolic disorders in humans. Elucidation of the genetic and endocrine
factors that contribute to excessive visceral fatness in chickens could also advance our
understanding of human metabolic diseases. Here, RNA sequencing was used to examine
differential gene expression in abdominal fat of genetically fat and lean chickens, which
exhibit a 2.8-fold divergence in visceral fatness at 7 wk. Ingenuity Pathway Analysis
revealed that many of 1687 differentially expressed genes are associated with hemostasis,
endocrine function and metabolic syndrome in mammals. Among the highest expressed
genes in abdominal fat, across both genotypes, were 25 differentially expressed genes
associated with de novo synthesis and metabolism of lipids. Over-expression of numerous
adipogenic and lipogenic genes in the FL chickens suggests that in situ lipogenesis in
chickens could make a more substantial contribution to expansion of visceral fat mass than
previously recognized. Distinguishing features of the abdominal fat transcriptome in lean
chickens were high abundance of multiple hemostatic and vasoactive factors, transporters,
and ectopic expression of several hormones/receptors, which could control local vasomotor
tone and proteolytic processing of adipokines, hemostatic factors and novel endocrine factors.
Over-expression of several thrombogenic genes in abdominal fat of lean chickens is
quite opposite to the pro-thrombotic state found in obese humans. Clearly, divergent genetic
selection for an extreme (2.5–2.8-fold) difference in visceral fatness provokes a number of
novel regulatory responses that govern growth and metabolism of visceral fat in this unique
avian model of juvenile-onset obesity and glucose-insulin imbalance.
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Resnyk CW, Chen C, Huang H, Wu CH, Simon J, Le Bihan-Duval E, et al. (2015) RNA-Seq Analysis of Abdominal Fat in Genetically Fat and Lean Chickens Highlights a Divergence in Expression of Genes Controlling Adiposity, Hemostasis, and Lipid Metabolism. PLoS ONE 10(10): e0139549. doi:10.1371/journal.pone.0139549