In order to determine the effects of hypoinsulinaemia or hyperinsulinaemia on
nephrocalcinosis induced by the interaction between
fructose and
magnesium (Mg) deficiency, we compared kidney calcification in obese versus lean, and non-diabetic versus diabetic female Zucker rats fed a
magnesium-deficient
fructose diet. One half of the obese and lean animals, respectively, was injected with
streptozotocin to produce diabetes, and the other half was injected with
citrate buffer alone. Diabetic, non-diabetic, obese, and lean animals were divided into two dietary groups, consisting of high
starch or high
fructose without added Mg. After a four week period, 24 hour urine was collected for urinary output,
protein,
oxalate,
citrate, MG, and
calcium (Ca) measurements. The animals were then decapitated, and blood was collected for
glucose, Mg, and Ca determinations, and kidneys were removed to determine their Mg and Ca contents. All
fructose-fed animals exhibited significantly more kidney Ca then the
starch-fed animals. Lean non-diabetic rats fed
fructose showed the greatest kidney Ca along with the greatest urinary
protein excretion among all experimental groups. The significant finding in the present study is that diabetes or
obesity reduced
nephrocalcinosis regardless of the
insulin status of the rats. Diuresis and hypercitraturia in diabetic and/or obese animals may cause a reduction in
nephrocalcinosis induced by the interaction between
fructose and
magnesium deficiency. Hyperproteinuria (
uromucoid) in combination with
hypercalciuria and hypomagnesuria may be responsible for greater
nephrocalcinosis in the
fructose than the
starch group. The possible mechanisms for this interaction on
nephrocalcinosis have been discussed.