Research Article

The acute effects of different sources of dietary calcium on postprandial energy metabolism

Nicola K. Cummingsa1, Anthony P. Jamesa1 and Mario J. Soaresa1 c1

a1 Program of Nutrition, Dietetics and Food Science, School of Public Health, Curtin University of Technology, GPO Box U1987, Perth, WA 6845, Australia


Dairy Ca intake has been shown to be superior to elemental Ca in increasing the loss of body fat during energy restriction. We questioned whether the mechanisms involved an increase in postprandial energy expenditure, fat oxidation and/or a greater lipolysis. The acute effects of different sources of Ca were examined in eight subjects, aged 47–66 years and BMI 27·6–36·1kg/m2, in a three-way cross-over study. Subjects were randomly provided breakfast meals either low in dairy Ca and vitamin D (LD; control), high in non-dairy Ca (calcium citrate) but low in vitamin D (HC) or high in dairy Ca and vitamin D (HD). Diet-induced thermogenesis, fat oxidation rates (FOR), carbohydrate oxidation rates (COR), insulin, glucose, ΔNEFA and glycerol were measured hourly over a 6h postprandial period. Postprandial data were calculated as a change (Δ) from the fasting value. Results showed that ΔNEFA was significantly different between meals (LD −1·50 (sem 0·26), HC −1·22 (sem 0·32), HD −0·94 (sem 0·27) mmol/l×6h; P=0·035), with a lesser suppression following both high-Ca meals. ΔFOR was significantly higher following the two high-Ca meals (LD −6·5 (sem 2·2), HC 2·93 (sem 2·34), HD 3·3 (sem 2·5) g×6;h; P=0·005), while reciprocally ΔCOR was significantly lower. ΔGlycerol was less suppressed following the high-Ca meals but statistical significance was not achieved. No differences in diet-induced thermogenesis, insulin or glucose were observed. Regardless of source, Ca intake acutely stimulated postprandial fat oxidation; and there was a lesser suppression of NEFA following these meals.

(Received October 18 2005)

(Revised March 02 2006)

(Accepted March 13 2006)


c1 *Corresponding author: Dr Mario J. Soares, fax +61 8 9266 2958, email