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A Mixed Meal Potentiates the Insulin Sensitivity of Glucose Transport and Metabolism in Adipocytes from Patients with Type 2 Diabetes Mellitus
Author(s) -
Lange A.,
Bak J.,
Andersen P. H.,
Richelsen B.,
Pedersen O.
Publication year - 1988
Publication title -
diabetic medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.474
H-Index - 145
eISSN - 1464-5491
pISSN - 0742-3071
DOI - 10.1111/j.1464-5491.1988.tb01104.x
Subject(s) - medicine , endocrinology , insulin , lipogenesis , diabetes mellitus , carbohydrate metabolism , meal , adipocyte , glucose uptake , basal (medicine) , glucose transporter , insulin resistance , metabolism , adipose tissue
Post‐glucose enhancement of insulin action may represent a physiological mechanism for the acute regulation of insulin sensitivity of target tissues. To clarify whether a similar mechanism is operative in the insulin‐resistant diabetic state we have investigated the effects of a mixed meal on adipocyte insulin action in eight patients with Type 2 diabetes mellitus. Ninety minutes after ingestion of breakfast insulin binding to fat cells increased by 21% ( p <0.05). In the fasting state 6 patients had a significant response of glucose transport and lipogenesis to insulin whereas two exhibited non‐responsiveness. In the 6 responders insulin sensitivity, as estimated by the insulin concentration at which half‐maximal effect was achieved, increased for glucose transport (before, 260±46 pmol ***l −1 ; after, 105±21 pmol l −1 ; p <0.05) and for lipogenesis (before, 36±9pmol l −1 ; after, 9±2 pmol l −1 ; p <0.05). No significant changes occurred in basal or maximal glucose transport or lipogenesis. In the two primary non‐responders intake of the meal was associated with average increases in maximal insulin responsiveness of 51% for glucose transport and 28% for lipogenesis. Intake of a mixed meal is associated with a slight increase of insulin binding to adipocytes from patients with Type 2 diabetes mellitus but a marked increase of adipocyte insulin sensitivity at the post‐binding levels of glucose transport and metabolism.