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Review
. 2019 Jun 23;20(12):3072.
doi: 10.3390/ijms20123072.

Anti-Obesity Effects of Dietary Calcium: The Evidence and Possible Mechanisms

Fenglin Zhang  1   2 , Jingjing Ye  3   4 , Xiaotong Zhu  5   6 , Lina Wang  7   8 , Ping Gao  9   10 , Gang Shu  11   12 , Qingyan Jiang  13   14 , Songbo Wang  15   16
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Review

Anti-Obesity Effects of Dietary Calcium: The Evidence and Possible Mechanisms

Fenglin Zhang et al. Int J Mol Sci. .
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Abstract

Obesity is a serious health challenge worldwide and is associated with various comorbidities, including dyslipidemia, type 2 diabetes, and cardiovascular disease. Developing effective strategies to prevent obesity is therefore of paramount importance. One potential strategy to reduce obesity is to consume calcium, which has been implicated to be involved in reducing body weight/fat. In this review, we compile the evidence for the anti-obesity roles of calcium in cells, animals, and humans. In addition, we summarize the possible anti-obesity mechanisms of calcium, including regulation of (a) adipogenesis, (b) fat metabolism, (c) adipocyte (precursor) proliferation and apoptosis, (d) thermogenesis, (e) fat absorption and excretion, and (f) gut microbiota. Although the exact anti-obesity roles of calcium in different subjects and how calcium induces the proposed anti-obesity mechanisms need to be further investigated, the current evidence demonstrates the anti-obesity effects of calcium and suggests the potential application of dietary calcium for prevention of obesity.

Keywords: adipogenesis; anti-obesity; calcium; fat metabolism; fecal fat excretion; gut microbiota; proliferation and apoptosis; thermogenesis.

Conflict of interest statement

The authors declare no conflicts of interest.

Figures

Figure 1
The possible mechanisms for the anti-obesity effects of dietary calcium. Calcium may elicit anti-obesity effects through (a) regulation of adipogenesis, with stimulation on mesenchymal stem cells (MSCs) (or commitment stage) and inhibition on preadipocytes (or differentiation stage); (b) modulation of fat metabolism, with decreased fat synthesis (lipogenesis) and increased fat breakdown (lipolysis); (c) promotion of adipocyte (precursor) proliferation and apoptosis; (d) enhancement of thermogenesis, with increased brown adipose tissue (BAT) activation and white adipose tissue (WAT) browning; (e) suppression of fat absorption and promotion of fecal fat excretion; and (f) modification of gut microbiota composition and diversity.
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