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The Aged Rat Model of Ovarian Hormone Deficiency Bone Loss^*

Department of Physiology, University of Texas Health Science Center (D.N.K., R. R. H.) San Antonio, Texas 78284
Mineral Metabolism Laboratory, Department of Medicine, University of Washington (C.-C.L.J) Tacoma, Washington 98493
Department of Pediatrics, Medical University of South Carolina (B.W.H.) Charleston, South Carolina 29425-2248

Address all correspondence and requests for reprints to: Dr. Dike N. Kalu, Department of Physiology, University of Texas Health Science Center, 7703 Floyd Curl Drive, San Antonio, Texas 78284.

Abstract

Three studies were carried out. First, the effects of aging on the maturation of the female skeleton were assessed. Second, the hypothesis that has linked ovarian hormone deficiency bone loss to hypercalcemic suppression of the parathyroids leading to a decrease in 1,25-dihydroxyvitamin D synthesis and gut absorption of calcium was examined. Third, the effects of ovariectomy and a combination of ovarian hormone deficiency and low dietary calcium on bone and the calcium-regulating hormones were evaluated.

After 6 months, ovariectomy and a low calcium diet independently decreased the density of the ilium, the femur, and the fourth lumbar vertebra as well as the calcium content of the latter two. The effects of the two treatment regimens were additive and more marked in the vertebral bone. Ovariectomy lowered serum calcitonin only in animals fed a normal diet and had no effect on serum PTH and vitamin D metabolites, while a low calcium diet caused a significant increase in serum 1,25- dihydroxyvitamin D. In both dietary regimens ovariectomy resulted in about a 30% decrease in intestinal calcium absorption. A low calcium diet increased morphometric indices of bone formation and bone resorption as did ovariectomy, with resorption exceeding formation. The discussion of our findings led to the conclusion that the aged rat model of ovarian hormone deficiency bone loss qualifies for serious consideration as a practical convenient cost-effective animal model for exploring aspects of the pathogenesis and treatment of postmenopausal bone loss. (Endocrinology 124: 7–16, 1989)

Footnotes

^* This work was supported by Grants AG-07572 and AG-03764.

Received July 26, 1988.

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