Calcium is an important macromineral that in its ionic form (Ca2+) plays an important role as an intracellular signal molecule. The main source of calcium in most Western diets is dairy produce, with sources including milk, yogurt and cheese. Traditionally, calcium has been researched in relation to bone health, but more recently research has identified a role for calcium in weight control. The benefits of calcium with regard to the maintenance of correct body weight were discovered by researchers accidently during a study investigating blood pressure in 2000. During the study, those given calcium in the form of a yogurt drink had a reduction in blood pressure but also lost 4.9kg over the course of the 1 year study. In addition, epidemiological evidence dating back almost 2 decades has reported an inverse relationship between weight and calcium intake, but little interest has been generated from this data.
The calcitrophic hormones, parathyroid hormone and 1,25(OH)2D, can both raise intracellular levels of calcium ions (Ca2+). In vitro evidence suggests that when Ca2+ increase in adipocytes, changes occur that cause the accumulation of lipids and the inhibition of lipolysis. Intracellular Ca2+ increases expression of fatty acid synthase, which results in an increase in de novo lipogenesis. At the same time lipolysis is inhibited, and this causes an increase in fat storage within the adipocyte and an expansion of the adipose tissue. Evidence suggests that of the calcitrophic hormones, it is 1,25(OH)2D which is the key regulator of adipocyte lipid metabolism via the membrane vitamin D receptor, that when activated by 1,25(OH)2D, results in a rapid increase in intracellular Ca2+. Dietary calcium is able to suppress levels of both parathyroid hormone and 1,25(OH)2D, which results in a shift from lipid storage to lipid oxidation and thermogenesis.
As well as activating the membrane bound vitamin D receptor, 1,25(OH)2D also activates a nuclear vitamin D receptor which is known in mice to inhibit expression of uncoupling protein 2. Increasing the dietary calcium of mice suppresses the concentration of 1,25(OH)2D and results in increased expression of UCP-2 in adipose tissue and increased thermogenesis. In addition, mice fed high calcium diets show increased rates of adipocyte apoptosis via suppression of 1,25(OH)2D. High concentrations of 1,25(OH)2D are able to inhibit apoptosis through inhibition of UCP-2 expression which results in an increase in mitochondrial potential that disrupts function and initiates cell death. Although the mechanisms of calcium influencing weigh loss described here are based on in vitro and animal studies, it should be remembered that clinical and epidemiological evidence supports a role for high dairy and calcium intakes on correct body weight maintenance.
Figure 1. Possible mechanisms by which dietary calcium may influence adipocyte metabolism.
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