Pharmacologic doses of vitamin E improve insulin action in healthy subjects and non-insulin-dependent diabetic patients

Abstract

Ten control (healthy) subjects and 15 non-insulin-dependent diabetics underwent an oral glucose-tolerance test and a euglycemic hyperinsulinemic glucose clamp before and after vitamin E supplementation (900 mg/d for 4 mo). In control subjects (placebo-treated vs vitamin E-supplemented subjects, respectively) vitamin E reduced the area under the curve for glucose (344 +/- 21 vs 287 +/- 13 mmol.L-1 x min-1; P < 0.05) and increased total body glucose disposal (39.0 +/- 0.3 vs 47.6 +/- 0.4 mumol.kg lean body mass-1 x min-1; P < 0.05) and non-oxidative glucose metabolism (23.4 +/- 0.2 vs 30.8 +/- 0.3 mumol.kg lean body mass-1 x min-1; P < 0.05). In diabetics (placebo-treated vs vitamin E-supplemented subjects, respectively) vitamin E supplementation reduced glucose area under the curve (614 +/- 129 vs 544 +/- 98 mmol.L-1 x min-1; P < 0.03) and increased glucose disappearance (19.4 +/- 0.4 vs 26.4 +/- 0.7 mumol.kg lean body mass-1.min-1; P < 0.03), total glucose disposal (19.0 +/- 0.7 vs 28.1 +/- 0.4 mumol.kg lean body mass-1 x min-1; P < 0.02), and nonoxidative glucose metabolism (8.5 +/- 0.3 vs 13.9 +/- 0.3 mumol.kg lean body mass-1 x min-1; P < 0.02). Therefore we conclude that administration of pharmacologic doses of vitamin E is a useful tool to reduce oxidative stress and improve insulin action.

Protective influence of vitamin E on the antioxidant defence system in the whole blood and liver of normal and alloxan-induced diabetic rats

“…The results obtained from this study have revealed that there is a relationship between vitamin E and glucose metabolism, as there was an increase in insulin sensitivity in diabetic rats treated with vitamin E. This was in agreement with the results of previous studies that antioxidant like vitamin E improves insulin sensitivity in diabetics (26). The reduction in the glucose levels of the diabetic control animals may also be due to partial recovery.…”

Serum antioxidants and risk of non‐insulin dependent diabetes mellitus

“…It has not usually been thought that free radicals affect the ef®cacy of insulin on peripheral cells. Interestingly, however, pharmacological doses of tocopherol, one of the most important exogenous antioxidants, have recently been reported to enhance the action of insulin (Paolisso et al, 1993a). Although not much is known about the contribution made by free radicals to the pathogenesis of NIDDM, more is known about their role in the pathogenesis of diabetic complications.…”

“…Tocopherol in pharmacological doses reduces indicators of oxidative stress (Ka Èhler et al, 1993) and protein glycosylation (Ceriello et al, 1991) in diabetic patients, and thus could therefore be bene®cial in preventing diabetic complications (Baynes, 1991). Pharmacological doses of vitamin E have also been shown to reduce insulin resistance (Paolisso et al, 1993a(Paolisso et al, , 1994 and improve metabolic control in NIDDM patients (Paolisso et al, 1993b). In the ®rst prospective population study involving Serum antioxidants and risk of non-IDDM A Reunanen et al middle-aged men, high serum concentrations of a-tocopherol were shown to protect against development of NIDDM (Salonen et al, 1995).…”

Glycemic index in chronic disease: a review

“…Recent findings suggest that metabolic processes following a meal may increase oxidative stress (Ceriello et al, 1999;Rao & Agarwal, 1999). A direct link has been found between postprandial glycemia and the induction of oxidative stress (Ceriello et al, 1998a(Ceriello et al, ,1999) that can be reversed by antioxidants (Paolisso et al, 1993(Paolisso et al, ,1994Sharma et al, 2000). In this respect, possible mechanisms of action of low-GI diets include reduction of: (i) glucose toxicity, ie the effect of high glucose levels in depressing pancreatic function through free radical damage of pancreatic b cells; and (ii) glycosylation of proteins and key enzymes responsible for metabolic processes (advanced glycosylation end products -AGE, Paolisso et al, 1992;Ceriello, 2000).…”