Obesity and Trace Elements.
It is the second most abundant intracellular cation, approximately 50% of total body magnesium is found in bones. The other 50% is found inside cells of body tissues and only 1% is found in blood. Magnesium is essential for absorption and utilization of nutrients; carbohydrates, fats and proteins. It is a critical cofactor for hundreds of enzymes especially those involved in glucose metabolism and a direct antagonist of intracellular calcium. Moreover, it is associated with insulin sensitivity. As hypomagnesaemia results in reduced insulin sensitivity of peripheral tissue through reduced auto-phosphorylation of tyrosine kinase, a component of the β-subunit of the insulin receptor for which magnesium is a co-factor. Also, hypomagnesaemia may be associated with reduced β-cells proliferation and thus affecting insulin production. Therefore, serum magnesium levels are negatively correlated with Insulin Resistance (HOMAIR).
The exact mechanism of hypomagnesaemia in obese patients is unclear but may be related to eating habits; as increased intake of carbonated soft drinks, which are rich in phosphorous and thereby interfere with magnesium absorption, or increased intake of caffeine resulting in increased magnesium excretion.
Copper imbalance often results in a reduced desire for protein, especially animal protein. Also high tissue copper aggravates obesity. It is always associated with high serum leptin. In addition, its excess tends to raise tissue sodium levels while lowering tissue potassium levels. High sodium level subsequently results in water retention. Low potassium results in hypoglycemia and sweet cravings.
It is an essential trace element and is a key component of several selenoproteins required for normal health as Glutathione peroxidase. It plays an important role as an anti-oxidant, especially when combined with vitamin E.
Obes Res Open J. 2015; 2(3): 98-100. doi: 10.17140/OROJ-2-115
