Unrestricted Feed Intake Induces β-Cell Death and Impairs Insulin Secretion in Broiler Breeder Hens

SIMPLE SUMMARY: Ad-feed intake caused transient hyperinsulinemia, but ultimately impaired insulin secretion and glucose clearance leading to hyperglycemia in broiler breeder hens. The impairments were operated at insulin gene expression and at pyruvate anaplerosis for ATP supply for insulin release. Lipotoxicity, inflammation, and cell apoptosis in the β-islets contributed to impaired insulin secretion in Ad-hens. ABSTRACT: Past studies regarding to insulin secretion and glucose disposal in chickens were focused on rapidly growing juvenile broilers and may not reflect glucose/insulin physiology in adulthood. The study aimed to assess insulin secretion and glucose disposal in respect to restricted (R) vs. ad libitum (Ad) feed intake for obesity development in broiler breeder hens. Hens at age of 26 weeks were continued on R rations, or allowed Ad-feed intake up to 45 weeks. Results from prandial changes and glucose tolerance test suggested that Ad-feed intake to 45 weeks impaired insulin secretion and glucose clearance, and, thus, caused hyperglycemia in accompany with transient hyperinsulinemia at age of 33 weeks (p < 0.05). The alterations were shown operating at both transcript and protein level of insulin gene expression per se and at ATP supply for insulin release as evidenced by consistent changes of enzyme expression and activity in pyruvate anaplerosis in the β-islets (p < 0.05). Ad-feed intake also increased β-islet triacylglycerol and ceramide accumulation and provoked interleukin-1β (IL-1β) production (p < 0.05), which were further manifested by a detrimental increase of caspase 3/7 activity and cell apoptosis (p < 0.05). Results support the conclusion that release to Ad-feed intake in broiler breeder hens transiently induced hyperinsulinemia along rapid bodyweight gain and adiposity, but later provoked lipotoxicity and inflammation leading to β-cell apoptosis and ultimately impaired insulin secretion and glucose disposal.