esearch implicates vitamin D and calcium insufficiency in the development of metabolic syndrome and subsequent deterioration of the condition to type 2 diabetes. Metabolic syndrome is characterised by insulin resistance, abdominal obesity, hyperglycaemia, inflammation and β-cell dysfunction, which suggests that calcium and vitamin D may be important anti-obesity nutrients that can regulate blood sugar. A review and meta-analysis of the Medline database has confirmed that low intakes of calcium and vitamin D may play a role in the development of metabolic syndrome and type 2 diabetes1. The review reported that observational studies show a consistent association between low vitamin D, calcium or dairy intake and the prevalence of metabolic syndrome or type 2 diabetes. Evidence from clinical trials also supports a role for high vitamin D and calcium intakes in the prevention of type 2 diabetes, particularly in populations at high risk.
A number of mechanisms can explain the requirement for adequate intakes of calcium and vitamin D in the prevention of metabolic syndrome. Vitamin D is pivotal in raising the plasma calcium concentrations in humans, through increased absorption in the gastrointestinal tract and increased resorption in the kidney. Long-term low intakes of calcium are therefore exacerbated by a low plasma level of vitamin D. When plasma calcium levels are low, a calcium paradox can occur, whereby the intracellular levels of calcium rise. This causes an imbalance of the intracellular to extracellular calcium ratio which may cause metabolic disturbances and have subsequent implications for calcium signalling. In adipocytes for example, the high intracellular calcium may cause decreased lipolysis and increase de novo lipogensis. This leads to abdominal visceral fat accumulation, which is thought to causes systemic inflammation through influx of macrophages.
Some evidence also implicates an imbalance in the intracellular to extracellular calcium ratio in modifications to normal β-cell function. Insulin secretion is calcium dependent and changes in the intracellular levels of calcium may interfere with the degree of insulin release through alterations to calcium signalling. Intracellular calcium is also required for the insulin signal cascade following activation of insulin receptors by insulin. Intracellular calcium must be maintained within a very narrow window for correct insulin receptor function and low plasma calcium levels may therefore have a substantial impact on signalling. Disruption to calcium homeostasis may therefore also prevent correct receptor function, and this may be a cause of the insulin resistance in skeletal muscle seen in metabolic syndrome. The combination of dysfunctional insulin release and the resistance of skeletal muscle to insulin, explains the glycaemic disruption associated with metabolic syndrome.
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