Literature DB >> 8404452

Zinc deficiency exaggerates diabetic osteoporosis.

H Fushimi1, T Inoue, Y Yamada, H Horie, M Kameyama, K Inoue, T Minami, Y Okazaki.   

Abstract

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 insulin treatment (18.3 +/- 4.2), indicating that osteoporosis was induced 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 rats was shown to be markedly thinner by microscopic examination of ground 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 significantly increased in diabetic rats, and increased further when the rats were fed a zinc-deficient diet. Moreover. the bone calcium and phosphorus concentrations were significantly lower in these animals. These changes in the zinc-deficiency rats were not reversed by insulin treatment. Our findings suggest that osteoporosis in the diabetic rats was due to thinning of the bone cortex secondary to mineral loss and can be reversed by insulin treatment, and that these skeletal changes are greatly enhanced by mild zinc deficiency. In addition the effects of zinc deficiency cannot be completely reversed by insulin treatment.

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Year:  1993        PMID: 8404452     DOI: 10.1016/0168-8227(93)90077-i

Source DB:  PubMed          Journal:  Diabetes Res Clin Pract        ISSN: 0168-8227            Impact factor:   5.602


  8 in total

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Authors:  T Minami; Y Okazaki; H Komiya; Y Horiuchi; T Inoue; Y Yamada; H Fushimi
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7.  Dietary zinc modifies diabetic-induced renal pathology in rats.

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8.  Zinc is essential for the transcription function of Nrf2 in human renal tubule cells in vitro and mouse kidney in vivo under the diabetic condition.

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  8 in total

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