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Summary  The autoregulation of insulin secretion was studied using perifused and incubated pancreatic islets of normal (obOb) mice and of their obese-hyperglycemic (obob) littermates. Islets secreted more insulin when they were perifused than when they were incubated and insulin was allowed to accumulate in the medium. When rat insulin was added to the incubation medium in the concentration of 250 μU/ml, the secretory activity of the normal islets was suppressed almost completely. The concentration of exogenous insulin required to inhibit the islets of obese mice was higher and increased with the age of the animals, until it reached a value that was 20 to 30 times greater than that found in the circulating blood. Similar concentrations may well exist in the extracellular fluid of the pancreatic islets. It is possible that while insulin resistance of the peripheral tissues may be responsible for the hyperglycemia of the obob mice, the progressive loss of insulin sensitivity of their pancreatic islets and, consequently, of the normal autoregulation of insulin secretion, may play a role in the progressive hyperinsulinism and, hence, of the obesity characteristic of these animals.

The autoregulation of insulin secretion in the isolated pancreatic islets of lean (obOb) and obese-hyperglycemic (obob) mice