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.
Highlights
The domestic chicken (Gallus domesticus) serves a dual purpose as a world-wide source of high-quality dietary protein and as an important model organism for developmental biology and genomics research [1,2,3,4]
Scheme A provided an average of 32.5 M mapped reads for the fat line (FL) (N = 3) and 36 M mapped reads for the lean line (LL) (N = 3), which allowed detection of 73% genes and 65% of transcripts across the FL and LL genotypes
The average number of reads mapped across Scheme A, B and C was greater for the LL (41.6 M) than the FL (35.4 M), which is reflected in the slightly higher number of expressed genes found in abdominal fat of the LL cockerels
Summary
The domestic chicken (Gallus domesticus) serves a dual purpose as a world-wide source of high-quality dietary protein and as an important model organism for developmental biology and genomics research [1,2,3,4]. Chickens naturally exhibit hyperglycemia (>200 mg/dL during fasting) and survive large doses of exogenous insulin, indicating an innate insensitivity to insulin, in adipose tissue where insulin exerts only marginal effects on the uptake of glucose by isolated adipocytes [5,6]. Another unique feature of metabolic regulation in the chicken is the disruption of syntenic genomic loci of five major mammalian adipokines [leptin (LEP) [7], plasminogen activator inhibitor–1 (PAI–1), tissue necrosis factor alpha (TNFA), resistin and omentin [8]]. Abdominal fatness is a highly-heritable polygenic trait regulated by multiple behavioral, environmental and hormonal factors [14,15,16,17,18,19,20,21]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
