Abstract

The osteopetrotic bone of the grey-lethal mouse has been shown to have an abnormal citrate metabolism. Increased levels of this metabolite are found in bone and in the circulation. High bone values may be due in part to apparent decreased amounts of NADP available for the oxidative decarboxylation of citrate. However, an increased O2 uptake by osteopetrotic bone fragments suggests that some at least of the increased citrate is being further metabolised along an oxidative pathway. Increased stimulation of parathyroid hormone secretion in response to overproduction of thyrocalcitonin has been suggested to account for the findings.

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