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Research Article Free access | 10.1172/JCI118678

Effects of a change in the pattern of insulin delivery on carbohydrate tolerance in diabetic and nondiabetic humans in the presence of differing degrees of insulin resistance.

A Basu, A Alzaid, S Dinneen, A Caumo, C Cobelli, and R A Rizza

Endocrine Research Unit, Mayo Clinic, Rochester, Minnesota 55905, USA.

Find articles by Basu, A. in: JCI | PubMed | Google Scholar

Endocrine Research Unit, Mayo Clinic, Rochester, Minnesota 55905, USA.

Find articles by Alzaid, A. in: JCI | PubMed | Google Scholar

Endocrine Research Unit, Mayo Clinic, Rochester, Minnesota 55905, USA.

Find articles by Dinneen, S. in: JCI | PubMed | Google Scholar

Endocrine Research Unit, Mayo Clinic, Rochester, Minnesota 55905, USA.

Find articles by Caumo, A. in: JCI | PubMed | Google Scholar

Endocrine Research Unit, Mayo Clinic, Rochester, Minnesota 55905, USA.

Find articles by Cobelli, C. in: JCI | PubMed | Google Scholar

Endocrine Research Unit, Mayo Clinic, Rochester, Minnesota 55905, USA.

Find articles by Rizza, R. in: JCI | PubMed | Google Scholar

Published May 15, 1996 - More info

Published in Volume 97, Issue 10 on May 15, 1996
J Clin Invest. 1996;97(10):2351–2361. https://doi.org/10.1172/JCI118678.
© 1996 The American Society for Clinical Investigation
Published May 15, 1996 - Version history
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Abstract

While it is well established that people with non-insulin dependent diabetes mellitus have defects in both insulin secretion and action, the relative contribution of each to glucose intolerance is not known. Therefore, nondiabetic (lean and obese) and non-insulin dependent diabetes mellitus subjects were studied on two occasions. On each occasion, insulin secretion was inhibited with somatostatin and glucose was infused in a pattern and amount that mimicked the systemic delivery rate normally observed after ingestion of 50 g of glucose. Insulin also was infused so as to mimic postprandial insulin profiles observed in separate groups of diabetic and nondiabetic subjects after food ingestion. Glucose turnover was measured using the isotope dilution method. A delayed pattern of insulin delivery (i.e., a "diabetic" insulin profile) led to higher (P < 0.05) glucose concentrations in all groups; however, the effects were transient, resulting in only a modest increase in the integrated glycemic responses. An isolated defect in insulin action had little effect on peak glucose concentration; however, it prolonged the duration of hyperglycemia, leading to a 2.5-4.2-fold increase (P < 0.05) in the integrated glycemic response. A combined defect in the pattern of insulin secretion and action was additive rather than synergistic. Both defects caused hyperglycemia by altering suppression of endogenous glucose release and stimulation of glucose disposal. Whereas obese diabetic and nondiabetic subjects had comparable defects in glucose clearance, non-insulin dependent diabetes mellitus subjects also had defects in hepatic insulin action. Thus, abnormalities in the pattern of insulin secretion and action alone or in combination impair glucose tolerance. An isolated defect in insulin action has a more pronounced and prolonged effect than does an isolated change in the pattern of insulin secretion. Hepatic and extrahepatic insulin resistance results in marked and sustained hyperglycemia.

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