Genetic selection for rapid growth results in a propensity for hyperphagia and an obesity-susceptible characteristic in modern broiler chickens. In the present studies, lipopenic dysregulation and following lipotoxicity was proposed as a causative factor to account for obesity-associated reproductive dysfunction in modern broiler hens. Allowance of satiated feeding for 10 days in broiler hens led to poor egg production in association with the presence of ovarian abnormalities, mainly hierarchical follicle atresia. Satiated feed intake also resulted in dramatically enhanced hepatic lipogenesis and adiposity, exacerbated fatty liver syndrome, hyperglycemia, hyperleptinemia, hyperinsulinemia, hyperlipidemia, increased saturated fatty acid fractions in plasma lipids, and metabolic syndrome X-like alterations. These results resembled lipopenic dysregulations in the development of obesity and type-II diabetics in mammals. Hens that developed ovarian abnormalities in response to satiated feed intake exhibited a higher hepatic triacylglycerol accumulation and plasma triacylglycerol concentration, but a lower degree of fatty acid unsaturation in hepatic and plasma lipids, suggesting a genetic divergence of hepatic de novo fatty acid synthesis and triacylglycerol secretion, and adiposity in the susceptibility of ovarian dysfunction to increased feed intake. Satiated feed intake also led to an increase of absolute and relative pancreas weight, pancreatic protein mass, protein/DNA ratio, and phospholipid contents suggesting hypertrophy consequence of pancreatic cells in response to increased glucose and lipid availability. Higher incidences of hierarchical follicle atresia were associated with hyperleptinemia-mediated longer retention of follicles within the hierarchy and delayed ovulation, leading to upregulation of interleukin 1beta and Fas-ligand, an inflammation-like response in hierarchical granulosa cells. In concert with increased interleukin 1beta and Fas-ligand expression, longer retention within the hierarchy increased the exposure of granulosa cells to lipopenic saturated fatty acids, leading to activation of ceramide-related apoptotic machinery, through which serine palmitoyltransferase, sphingomyelinase, inducible nitric oxide synthase, and caspase-3 expression were upregulated, and Bcl-xL expression was decreased. These apoptotic alterations resulted in programmed death of granulosa cells and subsequently follicle atresia, and thereby impaired egg production in broiler hens. Results in the present study suggest lipopenic dysregulation and following lipotoxicity as an upstream event and causative factor in poor reproductive function of modern broiler hens.
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