Green tea extract and catechol-O-methyltransferase genotype modify the post-prandial serum insulin response in a randomised trial of overweight and obese post-menopausal women.
Ontology highlight
ABSTRACT: BACKGROUND:Green tea extract (GTE) may be involved in a favourable post-prandial response to high-carbohydrate meals. The catechol-O-methyltransferase (COMT) genotype may modify these effects. We examined the acute effects of GTE supplementation on the post-prandial response to a high-carbohydrate meal by assessing appetite-associated hormones and glucose homeostasis marker concentrations in women who consumed 843 mg of (-)-epigallocatechin-3-gallate (EGCG) or placebo capsules for 11-12 months. METHODS:Sixty Caucasian post-menopausal women (body mass index ? 25.0 kg m-2 ) were included in a randomised, double-blind feeding study. GTE was consumed with a breakfast meal [2784.0 kJ (665.4 kcal); 67.2% carbohydrate]. Blood samples were drawn pre-meal, post-meal, and every 30 min for 4 h. Participants completed six satiety questionnaires. RESULTS:Plasma leptin, ghrelin and adiponectin did not differ between GTE and placebo at any time point; COMT genotype did not modify these results. Participants randomised to GTE with the high-activity form of COMT (GTE-high COMT) had higher insulin concentrations at time 0, 0.5 and 1.0 h post-meal compared to all COMT groups randomised to placebo. Insulin remained higher in the GTE-high COMT group at 1.5, 2.0 and 2.5 h compared to Placebo-low COMT (P < 0.02). GTE-high COMT had higher insulin concentrations at times 0, 0.5, 1.0, 1.5 and 2.0 h compared to the GTE-low COMT (P ? 0.04). Area under the curve measurements of satiety did not differ between GTE and placebo. CONCLUSIONS:GTE supplementation and COMT genotype did not alter acute post-prandial responses of leptin, ghrelin, adiponectin or satiety, although it may be involved in post-meal insulinaemic response of overweight and obese post-menopausal women.
SUBMITTER: Dostal AM
PROVIDER: S-EPMC5340619 | biostudies-literature | 2017 Apr
REPOSITORIES: biostudies-literature
ACCESS DATA