ZINC-DEFICIENCY EXAGGERATES DIABETIC OSTEOPOROSIS

Streptozotocin diabetic rats showed an increase of bone fragility (11. 9 +/- 2.1 kg/cm2 vs. 16.8 = 2.0, P < 0.005) which was normalized by in sulin treatment (18.3 +/- 4.2), indicating that osteoporosis was induc ed in diabetic rats. The rats were fed a zinc-deficient diet (0.16 mg/ 100 g) or a control diet (5.2 mg/100 g). This mild zinc-deficient diet did not lower the serum zinc level. The cortical bone of diabetic rat s was shown to be markedly thinner by microscopic examination of groun d cross-sections of the tibia. Zinc deficiency induced a reduction in the calcium content of diabetic bone when compared with the rats on a control diet. Urinary excretion of calcium and phosphorus was signific antly increased in diabetic rats, and increased further when the rats were fed a zinc-deficient diet. Moreover, the bone calcium and phospho rus concentrations were significantly lower in these animals. These ch anges in the zinc-deficiency rats were not reversed by insulin treatme nt. Our findings suggest that osteoporosis in the diabetic rats was du e to thinning of the bone cortex secondary to mineral loss and can be reversed by insulin treatment, and that these skeletal changes are gre atly enhanced by mild zinc deficiency. In addition, the effects of zin c deficiency cannot be completely reversed by insulin treatment.