Effects of high calcium/Vit D breakfast on thermogenesis
Posted: Thu Feb 24, 2011 11:14 am
Diet induced thermogenesis, fat oxidation and food intake following sequential meals: Influence of calcium and vitamin D
BACKGROUND & AIMS: The mechanisms linking dietary calcium and vitamin D to body weight regulation require confirmation.
METHODS: Eleven subjects, aged (mean ± SEM) 54 ± 1.2 y and BMI 31 ± 2.4 kg/m(2), participated in a randomised within-subject, sequential meal protocol comparing a low calcium trial (LCT) to an isoenergetic high calcium trial (HCT). Diet induced thermogenesis (DIT), fat oxidation rates (FOR), serum leptin, subjective feelings of hunger/satiety were measured at fasting and hourly over 8 h. Spontaneous food intake at a buffet and over the following 30 h was recorded. Postprandial responses, calculated as change (Δ) from baseline for each meal, were analysed by paired t-tests and 2 × 2 repeated measures ANOVA.
RESULTS: HCT resulted in lesser suppression of ΔFOR (p = 0.02) and a significantly greater DIT (p = 0.01). Further, the buffet to dinner interval was prolonged (p = 0. 083) and reported 24 h energy intake following this trial was significantly reduced (p = 0.017). ∆leptin following HCT but not LCT was negatively related to 24 h fat intake (r = -0.81, p = 0.016).
CONCLUSIONS: Higher calcium and vitamin D intake at a breakfast meal acutely increased postprandial FOR and DIT over two successive meals, and reduced spontaneous energy intake in the subsequent 24 h period.
BACKGROUND & AIMS: The mechanisms linking dietary calcium and vitamin D to body weight regulation require confirmation.
METHODS: Eleven subjects, aged (mean ± SEM) 54 ± 1.2 y and BMI 31 ± 2.4 kg/m(2), participated in a randomised within-subject, sequential meal protocol comparing a low calcium trial (LCT) to an isoenergetic high calcium trial (HCT). Diet induced thermogenesis (DIT), fat oxidation rates (FOR), serum leptin, subjective feelings of hunger/satiety were measured at fasting and hourly over 8 h. Spontaneous food intake at a buffet and over the following 30 h was recorded. Postprandial responses, calculated as change (Δ) from baseline for each meal, were analysed by paired t-tests and 2 × 2 repeated measures ANOVA.
RESULTS: HCT resulted in lesser suppression of ΔFOR (p = 0.02) and a significantly greater DIT (p = 0.01). Further, the buffet to dinner interval was prolonged (p = 0. 083) and reported 24 h energy intake following this trial was significantly reduced (p = 0.017). ∆leptin following HCT but not LCT was negatively related to 24 h fat intake (r = -0.81, p = 0.016).
CONCLUSIONS: Higher calcium and vitamin D intake at a breakfast meal acutely increased postprandial FOR and DIT over two successive meals, and reduced spontaneous energy intake in the subsequent 24 h period.