title: Zinc deficiency exaggerates diabetic osteoporosis.
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.
authors.affiliation: Department of Medicine, Sumitomo Hospital, Osaka, Japan.
authors.forename: H
authors.initials: H
authors.lastname: Fushimi
authors.forename: T
authors.initials: T
authors.lastname: Inoue
authors.forename: Y
authors.initials: Y
authors.lastname: Yamada
authors.forename: H
authors.initials: H
authors.lastname: Horie
authors.forename: M
authors.initials: M
authors.lastname: Kameyama
authors.forename: K
authors.initials: K
authors.lastname: Inoue
authors.forename: T
authors.initials: T
authors.lastname: Minami
authors.forename: Y
authors.initials: Y
authors.lastname: Okazaki
mesh_terms: D000469:Alkaline Phosphatase / Q000097:blood; D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D001842:Bone and Bones / Q000737:chemistry / Q000187:drug effects / Q000473:pathology*; D002118:Calcium / Q000032:analysis / Q000097:blood; D003921:Diabetes Mellitus, Experimental / Q000150:complications* / Q000188:drug therapy / Q000473:pathology; D005360:Fibula; D007328:Insulin / Q000494:pharmacology; D008297:Male; D010024:Osteoporosis / Q000150:complications / Q000473:pathology / Q000503:physiopathology*; D010281:Parathyroid Hormone / Q000097:blood; D010758:Phosphorus / Q000032:analysis / Q000097:blood; D051381:Rats; D017208:Rats, Wistar; D013054:Spectrophotometry, Atomic; D013977:Tibia; D014131:Trace Elements / Q000032:analysis; D015032:Zinc / Q000032:analysis / Q000097:blood / Q000172:deficiency*
chemical_list: D001786:Blood Glucose; D007328:Insulin; D010281:Parathyroid Hormone; D014131:Trace Elements; D010758:Phosphorus; D000469:Alkaline Phosphatase; D015032:Zinc; D002118:Calcium