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 alcohol on postprandial metabolic factors in 20 postmenopausal women over 6 h. We measured 1) glucose, insulin, lipids, C-reactive protein, and adiponectin levels; 2) augmentation index by applanation tonometry; and 3) energy expenditure and substrate oxidation by indirect calorimetry. Subjects received low carbohydrate (LC; visits 1 and 2) and high carbohydrate (HC; visits 3 and 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) after the LC meal only. Triglycerides were increased by alcohol after the LC (P = 0.002) and HC (P = 0.008) meals. Total and high-density lipoprotein cholesterol, fatty acids, and total adiponectin responses were unaffected. C-reactive protein levels decreased postprandially; reductions were enhanced by alcohol after the HC meal, but were attenuated after the LC meal. Postprandial reductions in the augmentation index were increased by alcohol after the LC meal only (P = 0.007). Alcohol enhanced the postprandial increase in energy expenditure 30–60 min after the LC meal (increase, 373 ± 49 vs. 236 ± 32 kcal/d; P = 0.02) and HC meal (increase, 362 ± 36 vs. 205 ± 34 kcal/d; P = 0.0009), but suppressed fat and carbohydrate oxidation. Some of our findings may be mechanisms for lower diabetes and cardiovascular risks in moderate drinkers.
Consuming a hypocaloric high fat low carbohydrate diet for 12weeks lowers C-reactive protein, and raises serum adiponectin and high density lipoprotein-cholesterol in obese subjects