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Objective: Increased per capita consumption of sweeteners may be responsible in part for the rising prevalence of obesity in the United States. Recent studies suggest that consumption of honey is not associated with this same obesogenic effect and may have beneficial effects neuro on body weight. The purpose of this study was to evaluate whether the meal-induced responses of ghrelin and peptide YY(3-36) (PYY(3-36)) and/or meal-induced thermogenesis differ following a honey- versus a sucrose-containing meal., Methods: In a double-blind randomly assigned study, appetite hormones (ghrelin, PYY(3-36), leptin) and glycemic and thermic responses were evaluated following isoglucidic ∼450 kcal honey- or sucrose-containing breakfasts in 14 healthy, nonobese women (22 ± 3 y). Blood samples and hunger ratings were obtained at baseline and every 30 minutes for 240 minutes following the meal. Meal-induced thermogenesis was measured by indirect calorimetry. Ad libitum food intake was evaluated from a free-choice meal following the test meal., Results: Honey consumption delayed the postprandial ghrelin response (p = 0.037), enhanced the total PYY (p = 0.007) response, and blunted the glucose response (p = 0.039) compared with consumption of the sucrose-containing meal. Meal-induced insulin response, hunger ratings, thermogenesis, and subsequent ad libitum food intake, however, did not differ (p > 0.10) between diet treatments., Conclusions: Alterations in meal-induced responses of ghrelin and PYY(3-36) but not meal-induced thermogenesis may be responsible in part for the potential "obesity protective" effect(s) of honey consumption. A blunted glycemic response may be beneficial for reducing glucose intolerance. Further research is required to determine if these findings hold true for obese individuals, for males, or with habitual consumption.

To determine whether fasting and meal-induced appetite-regulating hormones are altered during lactation and associated with body weight retention after childbearing, we studied 24 exclusively breastfeeding women (BMI = 25.2 ± 3.6 kg/m2) at 4-5 weeks postpartum and 20 never-pregnant controls (BMI = 24.0 ± 3.1 kg/m2). Ghrelin, PYY, GLP-1, and appetite ratings were measured before/and 150 minutes after a standardized breakfast and 60 minutes after an ad libitum lunch. Body weight/composition were measured at 6 and 12 months. Fasting and area under-the-curve responses for appetite-regulating hormones did not differ between lactating and control groups; ghrelinacyl, however, tended to track higher after the standardized breakfast in lactating women and was higher (p<0.05) after the ad libitum lunch despite a 24% higher energy intake (p < 0.05). By 12 months, lactating women lost 5.3 ± 2.2 kg (n=18), whereas control women (n=15) remained weight stable (p=0.019); fifteen of the lactating women returned to within ±2.0 kg of prepregnancy weight but three retained >6.0 kg. The retainers had greater (p<0.05) postmeal ghrelin rebound responses following breakfast. Overall these studies do not support the hypothesis that appetite-regulating hormones are altered during lactation and associated with postpartum weight retention. Altered ghrelin responses, however, deserve further exploration. [ABSTRACT FROM AUTHOR]