1984American Journal of Physiology-Endocrinology and MetabolismRequires access

Glucose-induced insulin secretion by perfused pancreas of 2- and 12-mo-old Fischer 344 rats

D. L. Curry, G M Reaven, Eve Reaven

Open publisher page 13 citations

Abstract

Previous studies have shown that cells from older Sprague-Dawley rats secrete insulin less efficiently in response to a maximal glucose challenge than do beta-cells from young animals. In the current study we have asked whether this change in beta-cell response occurs in another strain of rat, and, if so, whether the secretory defect occurs at submaximal as well as maximal glucose stimulatory levels. Pancreas perfusions were carried out on 2- and 12-mo-old Fischer 344 rats at perfusate glucose concentrations of 150 and 300 mg/dl. The secretory data for each pancreas was subsequently corrected for differences in islet cell mass and expressed as insulin secretion per unit islet cell. The results show that 12-mo-old Fischer rats release more insulin per total pancreas than do 2-mo-old animals at both glucose concentrations. However when corrected for islet cell mass, the amount of insulin secretion per islet cell is actually reduced in the older Fischer rat. These data are comparable to those seen previously in the 12-mo-old Sprague-Dawley rat and indicate that the insulin secretory defect seen as rats grow older is not species specific.

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What this paper is about

Previous studies have shown that cells from older Sprague-Dawley rats secrete insulin less efficiently in response to a maximal glucose challenge than do beta-cells from young animals. In the current study we have asked whether this change in beta-cell response occurs in another strain of rat, and, if so, whether the secretory defect occurs at submaximal as well as maximal glucose stimulatory levels. Pancreas perfusions were carried out on 2- and 12-mo-old Fischer 344 rats at perfusate glucose concentrations of 150 and 300 mg/dl. The secretory data for each pancreas was subsequently corrected for differences in islet cell mass and expressed as insulin secretion per unit islet cell. The results show that 12-mo-old Fischer rats release more insulin per total pancreas than do 2-mo-old animals at both glucose concentrations. However when corrected for islet cell mass, the amount of insulin secretion per islet cell is actually reduced in the older Fischer rat. These data are comparable to those seen previously in the 12-mo-old Sprague-Dawley rat and indicate that the insulin secretory defect seen as rats grow older is not species specific.

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Available abstract

Previous studies have shown that cells from older Sprague-Dawley rats secrete insulin less efficiently in response to a maximal glucose challenge than do beta-cells from young animals. In the current study we have asked whether this change in beta-cell response occurs in another strain of rat, and, if so, whether the secretory defect occurs at submaximal as well as maximal glucose stimulatory levels. Pancreas perfusions were carried out on 2- and 12-mo-old Fischer 344 rats at perfusate glucose concentrations of 150 and 300 mg/dl. The secretory data for each pancreas was subsequently corrected for differences in islet cell mass and expressed as insulin secretion per unit islet cell. The results show that 12-mo-old Fischer rats release more insulin per total pancreas than do 2-mo-old animals at both glucose concentrations. However when corrected for islet cell mass, the amount of insulin secretion per islet cell is actually reduced in the older Fischer rat. These data are comparable to those seen previously in the 12-mo-old Sprague-Dawley rat and indicate that the insulin secretory defect seen as rats grow older is not species specific.

Key concepts: Internal medicine, Islet, Endocrinology, Pancreas, Insulin, Secretion, Beta cell, Insulin oscillation

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