The release of insulin from the pancreas is caused in part by interaction with glucose to receptors on the cell membrane and the activation of ATP-sensitive potassium ion (K+) channels. In this respect, depolarisation of the cell membrane results in closure of the potassium ion channels, the activation of calcium (Ca2+) sensitive ion channels and the resulting influx of calcium causes the exocytotic release of vesicles which contain insulin. One of the main regulatory mechanisms that maintains the stability of the potassium ions and regulates the potassium ion channels is the intracellular concentrations of magnesium ions (Mg2+). Low cellular magnesium ion concentration can cause changes in the potassium channel homeostasis and this may in turn affect the release of insulin. There are two main ways to affect the magnesium content of the cells. One is through dietary changes to the magnesium intake. Another is through the genetic expression of magnesium ion channels in the cell membrane.
Studies have investigated the association between genetic variants in genes related to magnesium homeostasis and the risk of type 2 diabetes in human subjects. For example, in one study1, researchers identified 17 magnesium-related ion channel genes and examined their association to type 2 diabetes in African and hispanic American women. The results showed that expression of a number of magnesium channel genes was associated with a change in the risk of type 2 diabetes. Interestingly, those women with magnesium intakes in the lowest 30 % showed an increased signal strength for the genes that were associated with type 2 diabetes. This suggest that magnesium intake epigenetically may regulate the expression of the channels, leading to changes in the magnesium ion channel numbers on the cell membranes. These results show that nutritional factors that affect blood sugar control are very complex and difficult to quantify, and this highlights the importance of a well balanced diet that supplies all the essential nutrient.
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