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Plasma and dietary vitamin E in relation to insulin secretion and sensitivity
Author(s) -
Costacou T.,
Ma B.,
King I. B.,
MayerDavis E. J.
Publication year - 2008
Publication title -
diabetes, obesity and metabolism
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.445
H-Index - 128
eISSN - 1463-1326
pISSN - 1462-8902
DOI - 10.1111/j.1463-1326.2006.00683.x
Subject(s) - insulin resistance , medicine , endocrinology , insulin , diabetes mellitus , vitamin e , vitamin , insulin sensitivity , chemistry , antioxidant , biochemistry
Aim: In the Insulin Resistance and Atherosclerosis Study (IRAS), we have previously shown a protective effect of plasma α‐tocopherol concentration against diabetes incidence among persons not taking vitamin E supplements. The biologic mechanism for such a protective effect could involve improvement in either insulin sensitivity (S I ), insulin secretion or both. Thus, we examined vitamin E in relation to insulin secretion and S I among persons not taking vitamin E supplements. Methods: This analysis included 457 adults aged 40–69 years without a previous diabetes diagnosis or vitamin E supplement use at baseline and seen at the 5‐year follow‐up examination. Baseline nutrient intake was estimated from a validated 1‐year food frequency questionnaire; plasma levels of α‐tocopherol were also assessed. At follow up, a frequently sampled intravenous glucose tolerance test determined S I , acute insulin response to glucose (AIR), and the disposition index (DI) was calculated as the sum of the log‐transformed AIR and S I to reflect pancreatic compensation for insulin resistance. Results: In multivariable regression analyses, no relationship was observed for vitamin E intake and either S I , AIR or DI. However, plasma α‐tocopherol concentration was positively associated with log‐transformed S I (β= 0.27 ± 0.09, p < 0.01) and DI (β= 0.41 ± 0.14, p < 0.01), but not with log‐transformed AIR. Conclusions: Plasma concentration of α‐tocopherol may improve S I and pancreatic compensation for insulin resistance, although it does not seem to be related to acute insulin response.