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Submitted on July 30, 2004
Accepted on October 25, 2004
Diabetes and Obesity Program, Garvan Institute of Medical Research, St. Vincent's Hospital, Sydney, Australia; Diabetes Centre and Department of Cardiology, St. Vincent's Hospital, Sydney, Australia
* To whom correspondence should be addressed.
Lesley V. Campbell, E-mail: l.campbell{at}garvan.org.au
Moderate alcohol consumption protects against type 2 diabetes and cardiovascular disease. Because humans spend most of their time in the postprandial state, we examined the effect of 15 g of alcohol on postprandial metabolic factors in 20 postmenopausal women over 6-hrs. We measured (i) glucose, insulin, lipids, C-reactive protein (CRP) and adiponectin levels; (ii) augmentation index [AIx] by applanation tonometry; (iii) energy expenditure and substrate oxidation by indirect calorimetry. Subjects received low-carbohydrate (LC: visits 1, 2) and high-carbohydrate (HC: visits 3, 4) high-fat meals with and without alcohol. Alcohol augmented the postprandial increment in insulin (P = 0.07) and reduced the postprandial increment in glucose (P = 0.04) following the LC-meal only. Triglycerides were increased by alcohol following the LC- (P = 0.002) and HC- (P = 0.008) meals. Total and HDL-cholesterol, fatty acids and total adiponectin responses were unaffected. CRP levels decreased postprandially; reductions were enhanced by alcohol following the HC-meal but attenuated following the LC-meal. Postprandial reductions in AIx were increased by alcohol following the LC-meal only (P = 0.007). Alcohol enhanced the postprandial increase in energy expenditure 30-60mins after the LC-meal (
373 ± 49 vs. 236 ± 32kcal/d, P = 0.02) and HC-meal (362 ± 36 vs. 205 ± 34kcal/d, P = 0.0009), but suppressed fat and carbohydrate oxidation. Our findings may be mechanisms for lower diabetes and cardiovascular risks in moderate drinkers.
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