The Effect of Ingested Glucose Dose on the Suppression of Endogenous Glucose Production in Humans.

Autor: Kowalski GM; Institute for Physical Activity and Nutrition, School of Exercise and Nutrition Science, Deakin University, Burwood, Victoria, Australia greg.kowalski@deakin.edu.au., Moore SM; Institute for Physical Activity and Nutrition, School of Exercise and Nutrition Science, Deakin University, Burwood, Victoria, Australia., Hamley S; Institute for Physical Activity and Nutrition, School of Exercise and Nutrition Science, Deakin University, Burwood, Victoria, Australia., Selathurai A; Institute for Physical Activity and Nutrition, School of Exercise and Nutrition Science, Deakin University, Burwood, Victoria, Australia., Bruce CR; Institute for Physical Activity and Nutrition, School of Exercise and Nutrition Science, Deakin University, Burwood, Victoria, Australia clinton.bruce@deakin.edu.au.
Jazyk: angličtina
Zdroj: Diabetes [Diabetes] 2017 Sep; Vol. 66 (9), pp. 2400-2406. Date of Electronic Publication: 2017 Jul 06.
DOI: 10.2337/db17-0433
Abstrakt: Insulin clamp studies have shown that the suppressive actions of insulin on endogenous glucose production (EGP) are markedly more sensitive than for stimulating glucose disposal ( R d ). However, clamp conditions do not adequately mimic postprandial physiological responses. Here, using the variable infusion dual-tracer approach, we used a threefold range of ingested glucose doses (25, 50, and 75 g) to investigate how physiological changes in plasma insulin influence EGP in healthy subjects. Remarkably, the glucose responses were similar for all doses tested, yet there was a dose-dependent increase in insulin secretion and plasma insulin levels. Nonetheless, EGP was suppressed with the same rapidity and magnitude (∼55%) across all doses. The progressive hyperinsulinemia, however, caused a dose-dependent increase in the estimated rates of R d , which likely accounts for the lack of a dose effect on plasma glucose excursions. This suggests that after glucose ingestion, the body preferentially permits a transient and optimal degree of postprandial hyperglycemia to efficiently enhance insulin-induced changes in glucose fluxes, thereby minimizing the demand for insulin secretion. This may represent an evolutionarily conserved mechanism that not only reduces the secretory burden on β-cells but also avoids the potential negative consequences of excessive insulin release into the systemic arterial circulation.
(© 2017 by the American Diabetes Association.)
Databáze: MEDLINE
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