Increased free intracellular calcium ([Ca(2+)](i)) in adipocytes blunts the lipolytic response to catecholamines by activating phosphodiesterase 3B - the same enzyme that mediates the antilipolytic effect of insulin - while also compromising the efficiency of insulin-stimulated glucose uptake. Physiological increases in parathyroid hormone (PTH) have been shown to increase [Ca(2+)](i) in adipocytes. These considerations may rationalize recent evidence that high dietary intakes of calcium and/or dairy products may reduce risk for obesity, diabetes, and insulin-resistance syndrome, and they predict that other dietary measures which down-regulate PTH - such as good vitamin D status, and moderation in phosphate and salt intakes - may likewise be beneficial in these respects. Consistent with this position are reports that body weight is elevated in elderly subjects with both primary and secondary hyperparathyroidism; furthermore, insulin resistance is a well-known complication of both forms of hyperparathyroidism. The fact that regular alcohol consumption is associated with decreased PTH secretion may help to explain why moderate drinkers are less prone to insulin resistance, diabetes, and - in women - obesity. Down-regulation of PTH cannot be expected to promote dramatic weight loss, but in the long-term it may lessen risk for significant weight gain and diabetes, and conceivably may potentiate the fat loss achievable with caloric restriction and/or exercise.