Obesity
The linkage of obesity to low calcium intake has only recently become apparent. At least four sets of clinical observations have shown that children and adolescents with high milk intakes weigh less and have less body fat than nonmilk drinkers. Moreover, Zemel and associates have shown, using the NHANES-III database, that risk of obesity exhibits a highly significant stepwise, inverse correlation with dietary calcium intake. In other work, the same authors have demonstrated that low calcium intake incre'ases cytosolic [Ca2+] in the adipocyte (whether through increased PTH or 1, 25(OH)2D is unclear).
The result of this cell biologic effect is to switch adipose cell metabolism from lipolysis to lipogenesis. This change means a higher average fat content per fat cell in the presence of high PTH levels and provides a plausible mechanism to explain the clinical and epidemiological observations. In transgenic mice expressing the ago-uti gene, low calcium diets provoke obesity, whereas high calcium diets suppress the obesity and elevate core body temperature. Rather than an untoward response (as with blood pressure), this effect may well reflect a primitive adaptation to food shortage. With the primitive diet naturally rich in calcium, low levels of absorbed calcium would signal low food intake and possibly, therefore, impending starvation.
Under such circumstances, a shift from fat breakdown to fat synthesis and a reduction in thermogenesis would help conserve critical energy reserves. It is still unclear how large the effect may be at a population level. Nor are there randomized clinical trial data showing the extent to which high calcium intakes will reduce weight gain or augment weight loss. So the ultimate significance of the observations cited remains uncertain. At very least, this linkage may simply be a fortuitous instance illustrating how PTH can affect the function of cells and tissues not usually considered a part of the calcium homeostatic regulatory system.
