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Davis MR, Shamoon H. Impaired glucose disposal following mild hypoglycemia in nondiabetic and type I diabetic humans. Metabolism. 1992;41(2):216-23doi: 10.1016/0026-0495(92)90156-5.
Davis, M. R., & Shamoon, H. (1992). Impaired glucose disposal following mild hypoglycemia in nondiabetic and type I diabetic humans. Metabolism: clinical and experimental, 41(2), 216-23. https://doi.org/10.1016/0026-0495(92)90156-5
Davis, M R, and Shamoon, H. "Impaired glucose disposal following mild hypoglycemia in nondiabetic and type I diabetic humans." Metabolism: clinical and experimental vol. 41,2 (1992): 216-23. doi: https://doi.org/10.1016/0026-0495(92)90156-5
Davis MR, Shamoon H. Impaired glucose disposal following mild hypoglycemia in nondiabetic and type I diabetic humans. Metabolism. 1992 Feb;41(2):216-23. doi: 10.1016/0026-0495(92)90156-5. PMID: 1736045.
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Elsevier Science

Metabolism. 1992 Feb;41(2):216-23. doi: 10.1016/0026-0495(92)90156-5.

Impaired glucose disposal following mild hypoglycemia in nondiabetic and type I diabetic humans.

Metabolism: clinical and experimental

M R Davis, H Shamoon

Affiliations

  1. Department of Medicine, Albert Einstein College of Medicine, New York, NY 10461.

PMID: 1736045 DOI: 10.1016/0026-0495(92)90156-5

Abstract

Insulin-mediated glucose disposal was studied immediately prior to and following moderate hypoglycemia in nondiabetic subjects and subjects with insulin-dependent (type I) diabetes mellitus (IDDM), the latter having varying epinephrine secretory capacities. Plasma insulin concentration was fixed throughout the study at approximately 300 to 400 pmol/L to avoid effects of waning insulin action and plasma glucose was clamped at either 5 mmol/L (euglycemic control) or at 3.1 mmol/L (hypoglycemic) periods of 120 minutes. Baseline (clamp 1) and postexperiment (clamp 2) periods were assessed for net glucose disposal (as a function of the exogenous glucose infusion rate) and glucose kinetics using 3H-glucose. In normal subjects, glucose disposal increased progressively by 132% during control studies but only by 57% with intervening hypoglycemia (P less than .005). Similarly, 33% during hypoglycemia, P less than .025). These changes were mediated by reduction of whole-body glucose uptake (rate of glucose disappearance [Rd], [3H]-3-glucose) and metabolic clearance rates with comparable suppression of hepatic glucose production in both groups. The increase in plasma free-fatty acids (FFA) following hypoglycemia was modest but greater in subjects with IDDM (P less than .01), whereas IDDM had reduced concentrations of epinephrine (P less than .01) and glucagon (P less than .005) during hypoglycemia. In subjects with IDDM but not in normal subjects, the change in posthypoglycemia glucose disposal was inversely correlated with the increase in plasma norepinephrine (R2 = .54, P less than .004) and epinephrine (R2 = .32, P less than .04). Glucose disposal did not correlate with other counterregulatory hormones, plasma FFA, or antecedent glycemic control.(ABSTRACT TRUNCATED AT 250 WORDS)

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