Durk Pearson & Sandy Shaw’s®
Life Extension NewsTM
Volume 15 No. 7 • November 2012

Gamma Tocopherol Protects Healthy Young Men From Glucose Induced Increases in Postprandial Methylglyoxal

Postprandial hyperglycemia is recognized as a risk factor in many diseases—including diabetes and atherosclerosis—in part because of the oxidative stress and endoplasmic reticulum stress that is caused by it. The reactive dicarbonyl methyglyoxal, a precursor to AGEs (advanced glycation end products) is created as a result of glucose metabolism and increased via oxidative stress in vitro. Additionally, oxidative stress reduces the glutathione-dependent detoxification of methylglyoxal.1

Researchers tested the hypothesis that gamma tocopherol would, as a result of its potent antioxidative properties, decrease hyperglycemia-mediated postprandial increases in plasma methylglyoxal (MGO) after ingesting glucose.1 The participants were 12 healthy college-age men (22.3 ± 1.0 years old with mean BMI of 29.3 ± 2.4 kg/m2). The subjects fasted 10–12 hours and then received an oral dose of 75 g of glucose prior to and following 5 day ingestion of a vitamin E supplement of mixed tocopherols enriched in gamma tocopherol (containing 500 mg/day of gamma tocopherol and 60 mg/day alpha tocopherol, 170 mg/day delta tocopherol, and 9 mg/day of beta tocopherol).1 Blood samples were collected at several time points: 0, 15, 30, 45, 60, 120, 150, and 180 minutes after glucose ingestion.

MGO was significantly reduced (p < 0.05) with the supplementation of gamma tocopherol than without (778 ±1010 vs. 2277 ± 705). Plasma concentrations of gamma-carboxyethylhydroxychroman, reduced glutathione, and markers of total antioxidant capacity increased after supplementation and these markers and plasma gamma-tocopherol were inversely correlated with plasma MGO (r = 20.48 to 20.67, p < .05). The authors conclude that “[t]hese data suggest tht short-term supplementation of gamma-tocopherol abolishes the oral glucose-mediated increases in postprandial MGO through its direct and indirect antioxidant properties and may reduce hyperglycemia-mediated cardiovascular disease risk.”1 The authors also claim that “[t]o our knowledge, this investigation provides the first evidence that improvements in gamma-tocopherol status attenuates glucose-induced postprandial increases in MGO, without altering postprandial hyperglycemia.”

Postprandial oxidative stress following glucose consumption contributes to endothelial dysfunction, a failure of arterial vasodilation in response to acetylcholine signaling.2 Moreover, increased levels of methylglyoxal induces significant generation of nitric oxide and superoxide anion in rat vascular smooth muscle cells, which chemically react to form the potent oxidant peroxynitrite.3 The increased reactive oxygen species and reactive nitrogen species (ROS/RNS) resulting from elevated methylglyoxal contributes to insulin resistance.3

As we have written before [See “Reducing Glycation Reactions for Better Health and Longer Life” in the February 2008 issue of Life Enhancement], advanced glycation endproducts (AGEs) are risk factors in aging, cardiovascular disease, diabetes, some types of cancer, insulin resistance and other aspects of the metabolic syndrome, as well as other diseases. Increased circulating levels of methylglyoxal is one pathway that leads to higher levels of AGEs.


  1. Masterjohn et al. Gamma-tocopherol abolishes postprandial increases in plasma methylglyoxal following an oral dose of glucose in healthy, college-aged men. J Nutr Biochem 23:292-8 (2012).
  2. Dhar et al. Methylglyoxal scavengers attenuate endothelial dysfunction induced by methylglyoxal and high concentrations of glucose. Br J Pharmacol 161:1843-56 (2010).
  3. Chang et al. Methylglyoxal-induced nitric oxide and peroxynitrite production in vascular smooth muscle cells. Free Radic Biol Med 38:286-93 (2005).

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