Insulin secretion by perfused islets from the obese Zucker rat.
The dynamics of insulin secretion from pancreatic islets of the Zucker-obese rat were studied by in vitro perfusion of individual islets. Glucose and L-leucine were used as insulinogenic stimuli. Control pancreatic islets were obtained from both normal weight Zucker-thin littermates and equivalent weight Sprague-Dawley rats. Our results demonstrate that pancreatic islets from 13-wk-old Zucker-obese rats hypersecrete insulin in the basal state and in response to both glucose and amino acid (L-leucine) stimuli. Neither pancreatic islets from control Zucker-thin littermate animals (matched with the Zucker-obese animals for age or for total body weight), nor islets from Sprague-Dawley rats of comparable age and weight demonstrate comparable hypersecretion of insulin. These findings; i.e., hypersecretion of insulin from obese pancreatic islets, suggest that the plasma hyperinsulinism characteristic of the obese state is maintained, at least in part, by an inherent abnormality of beta cell secretion. Whether this abnormality in beta cell secretion results from a genetic trait in the Zucker-obese strain or is induced by the insulin resistance of the obese animal is not resolved by this study. In any case, the observed in vitro hyperinsulin secretion from these islets supports the postulation that in vivo peripheral insulin resistance characteristic of obesity may be a physiological response that protects the animal from insulin-induced hypoglycemia.
D000818:Animals; D005947:Glucose / Q000494:pharmacology; D006946:Hyperinsulinism / Q000209:etiology; D066298:In Vitro Techniques; D007328:Insulin / Q000378:metabolism*; D000078790:Insulin Secretion; D007515:Islets of Langerhans / Q000378:metabolism*; D007930:Leucine / Q000494:pharmacology; D008297:Male; D009765:Obesity / Q000235:genetics / Q000378:metabolism / Q000503:physiopathology*; D010477:Perfusion; D051381:Rats; D013268:Stimulation, Chemical
D007328:Insulin; D007930:Leucine; D005947:Glucose