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Consumption of a Glucose Diet Enhances the Sensitivity of Pancreatic Islets from Adrenalectomized Genetically Obese (ob/ob) Mice to Glucose-Induced Insulin Secretion^1,2,3,

Department of Food Science and Human Nutrition, Michigan State University, East Lansing, MI 48824-1224

Consumption of a glucose diet for 4 d markedly elevates plasma insulin concentrations in adrenalectomized ob/ob mice. The present study examined regulation of insulin secretion from perifused pancreatic islets of female adrenalectomized genetically obese (ob/ob) and lean mice fed a glucose diet for 4 d. These mice were fed a high carbohydrate commercial diet for 21 d, or the high carbohydrate commercial diet for 17 d and a purified high glucose diet for the last 4 d of the 21-d feeding period. Adrenalectomy equalized plasma insulin concentrations, pancreatic islet size, rates of insulin secretion in response to 20 mmol/L glucose and insulin mRNA relative abundance in ob/ob and lean mice fed the commercial diet, but the threshold for glucose-induced insulin secretion determined by a linear glucose gradient remained lower in islets from adrenalectomized ob/ob mice than in those from lean mice (3.8 ± 0.1 vs. 4.9 ± 0.2 mmol/L glucose), and addition of acetylcholine to the perifusate lowered the threshold to only 2.0 ± 0.1 mmol/L glucose in islets from ob/ob mice vs. 3.3 ± 0.1 mmol/L glucose in lean mice. Switching from the commercial diet to the glucose diet for 4 d increased plasma insulin concentrations 10-fold in islets from adrenalectomized ob/ob mice without affecting islet size, 20 mmol/L glucose-induced insulin secretion or insulin mRNA abundance. Consumption of the glucose diet did, however, markedly lower the threshold for glucose-induced insulin secretion in islets from adrenalectomized ob/ob mice to approximate the abnormally low glucose thresholds in intact ob/ob mice. Islets from lean mice were unaffected by the diet switch. The signaling pathway that sensitizes islets to glucose-induced insulin secretion seems to be persistently altered in ob/ob mice.

KEY WORDS: • pancreatic islets • insulin secretion • genetically obese (ob/ob) mice • adrenalectomy • dietary glucose

¹ Supported by NIH grant DK-15847 and the Michigan Agricultural Experiment Station.

² Anahita M. Mistry and Neng-Guin Chen contributed equally to the conduct of the research. Young-Soon Lee was on leave from Keimyung Junior College in Korea when this research was conducted.

³ The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 USC section 1734 solely to indicate this fact.

⁴ To whom correspondence should be addressed.

Manuscript received 23 May 1994. Revision accepted 15 August 1994.