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The Durk Pearson & Sandy Shaw®
Life Extension NewsTM
Volume 5 No. 6 • December 2002

Tea Enhances Insulin Activity

Green tea has been reported to have antidiabetic effects, but human studies have failed to detect consistent effects in changes in blood glucose.1 Streptozotocin mice, a model of human diabetes, treated with various types of green, oolong, and black tea show lowered levels of blood glucose.

Tea catechins inhibit alpha-amylase

The active components in tea that cause the reduced glucose levels in animals are not known, but epicatechin gallate was shown to have the greatest activity of the catechins in lowering glucose uptake by Caco-2 cells. Epicatechin gallate was also reported to inhibit glucose uptake in the brush border membrane vesicles from rabbit small intestine. Most interesting, however, is the fact that catechins have been shown to inhibit enzymes that hydrolyze carbohydrates, including alpha-amylase, a major starch-digestive enzyme that converts starch to glucose. This may explain at least in part why a mixture of green tea catechins suppressed increases in blood glucose and insulin following carbohydrate ingestion in rats.1 Moreover, in another study cited in this paper, humans ingesting 50 grams of starch following consumption of 200–500 mg of tea catechins had a suppression of the elevation of glucose and insulin levels. Intestinal glucose uptake is reported to be markedly inhibited by green tea polyphenols, especially those polyphenols having galloyl residues.

The authors1 performed a rat study on the effects of green tea on insulin activity. They evaluated the insulin-potentiating activity of approximately 40 black, green, and oolong teas and found all to enhance insulin activity in the insulin-potentiating epididymal fat-cell assay. Instant teas were not found to have such activity except for one brand (not named). They found the most active green tea constituent in potentiating insulin action to be epigallocatechin, but tannins, theaflavins, and epicatechin gallate were also found to have insulin-enhancing activity and to account, the authors stated, for the number of fractions of black tea that had insulin-enhancing activity.

Milk added to tea inhibited in vitro insulin potentiation

Milk (2%) was found to inhibit the tea insulin potentiation when used at about 1 teaspoon per cup (237 ml), decreasing activity by roughly 33%. Nondairy creamers also decreased insulin-enhancing activity. The decreased insulin-enhancing effects of milk and nondairy creamers was due to the precipitation of epigallocatechin, gallocatechin gallate, and epicatechin gallate. However, the researchers also cited another paper2 in which it was reported that drinking a mixture of tea and milk did not reduce the bioavailability of the tea catechins. They suggest that perhaps the catechin-milk complexes dissociate and allow the tea catechins to be absorbed. Yet another paper3 reported that the antioxidant potential of tea alone or tea plus lemon was greater than that observed when milk was added to tea.

The authors propose that one possible reason why previous studies of humans drinking tea have not found reduced glucose levels is that more effective insulin could lead to lower levels of insulin with no changes in glucose. They note that in a recent study they performed using chromium, they observed no changes in glucose clearance but a very significant effect on circulating insulin. They also note that polyphenols are very rapidly cleared from the blood; hence, measuring glucose levels after an overnight fast would likely yield no effect of tea consumption because the half-life in humans for epigallocatechin gallate is less than 6 hours, and those for epigallocatechin and epicatechin are less than 4 hours.


  1. Anderson, Polansky. Tea enhances insulin activity. J Agric Food Chem 50:7182-6 (2002).
  2. van het Hof et al. Bioavailability of catechins from tea: the effect of milk. Eur J Clin Nutr 52:356-9 (1998).
  3. Tewari et al. Comparative study of antioxidant potential of tea with and without additives. Indian J Physiol Pharmacol 44:215-9 (2000).

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