Magnesium deficiency-induced anorexia in hyperphagic obese Zucker rats.

In clinical practice diabetes mellitus is the most significant cause of hypomagnesemia and Mg depletion. The obese Zucker rat approaches non-insulin-dependent type II diabetes; lean Zucker rats being suitable controls. Using this disease model the influence of dietary Mg deficiency was studied: animals received a diet providing only approximately 25 per cent of the Mg requirement; controls received drinking water fortified with Mg (16 mmol/L). During 125 days ad libitum feeding, Mg-deficient obese rats consumed nearly 50 per cent less feed pellets and gained 50 per cent less body weight than their obese counterparts. This effect was not fully reversible indicating Mg depletion. Blood glucose reflected food consumption, no glucosuria was detectable using test strips. In the heart muscle Mg was decreased and Ca increased in Mg-deficient rats indicating increased cardiac risk. When the rats were pair fed with lean Mg-deficient controls the development of obesity was prevented. Despite pronounced Mg deficiency blood glucose remained unaffected and no glucosuria was detectable. In future experiments the production of marginal Mg deficiency not inducing anorexia should be applied to study the pathogenetic role of Mg depletion in obese Zucker rats.

Increase of streptozocin toxicity by magnesium deficiency in the diabetic rat model.

To study interactions between magnesium (Mg) and diabetes mellitus, female SD-rats weighing ca. 230 g were rendered Mg-deficient by offering a diet providing only 20% of the rat's requirement. After 14 days the animals were injected 75 mg streptozocin (STZ) per kg body weight intraperitoneally. Placebo-treated controls received the same diet, however their drinking-water was enriched with 20 mmol/l Mg as the magnesium-L-aspartate hydrochloride. Mg deficiency remarkably increased STZ-induced lethality from 3.8% to 61.1% on day 35. Pronounced hyperglycemia and necrosis of pancreatic beta cells also suggest an increased effect of STZ on the pancreas during Mg deficiency. The underlying mechanisms are discussed. Food consumption was decreased in Mg-deficient animals and steeply increased 7 days following STZ treatment. Similarly consumption of drinking-water also increased. Since diabetic rats lost body weight, relative and absolute Mg intake via food or drinking-water increased. In this way further Mg depletion of diabetic rats was prevented.