Abstract

This study was undertaken to determine whether increased oxidation of intracellular muscle lipids could explain the impaired carbohydrate metabolism of that tissue following growth hormone (GH) administration. Pieces of diaphragm from either hypophysectomized (hypox) rats injected for 10 days with saline or 1 mg bovine GH or animals of similar weight with intact pituitary glands were studied. In hypox rats, GH administration increased both weight gain and plasma glucose concentrations at sacrifice and impaired glucose uptake by diaphragms in vitro. Tissue triglyceride (TG) content was markedly decreased in hypox muscle compared to diaphragms removed from animals with intact pituitary glands. GH administration lowered TG levels even further. Initial phospholipid (PL) content was similar in all groups and fell significantly during the second hour of incubation only in hypox muscle. GH administration had no effect on PL changes. The differences in TG- and PL-specific activities strongly suggested that most of the C 14O 2 produced in the second hour of incubation was derived from TG. Approximately 25% of diaphragm TG was oxidized to CO 2 in all three groups of animals. Changes in lipid-specific activities during the second hour indicated that in tissue from hypox animals, TG-fatty acids were converted to PL-fatty acids, whereas no such exchange occurred in muscle from intact rats. In conclusion: (1) enhanced oxidation of intracellular muscle lipids does not explain the effect of GH on carbohydrate metabolism; (2) diaphragm TG content is markedly decreased in hypox animals and is not secondary to GH deficiency; (3) diaphragms incubated in vitro will utilize PL for energy only if TG levels are low; and (4) as PI content falls, some TG-fatty acids are shifted into PL, possibly in an attempt to maintain the important “structural-functional elements” of muscle.

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