Abstract
Recent studies have demonstrated the release from isolated crude plasma membranes of a putative undefined mediator(s) of insulin's molecular action. This messenger is generated after insulin-receptor binding. Rat liver particulate cell membranes (4 mg/ml prot) were incubated with physiologic[insulin] or saline; the mediator was prepared as described (Proc Natl Acad Sci, 1982; 79:3513). To study its effect on ketogenesis and pyruvate dehydrogenase (PDH), suspensions of either the crude lyophylized extract (C) or the ethanol-separated stimulatory (S)/inhibitory (I) fractions were added to freshly-prepared liver mitochondria or mitoplasts. Our mediator had similiar effects on PDH as reported previously (above ref) and was <12,000 daltons. The S fraction (ethanol nonextractable) did not modify ketogenesis; however, both the undiluted and 1:10 C (data below) and I fractions (data not shown) were inhibitory (p <.025). Results are expressed as 7. inhibition of ketogenesis by mediator prepared from insulin (10−8M) vs saline-treated membranes (mean ± S.E.; n=12); the control mitochondria ketogenic rate was 1.8 ± 0.3 nmol/min/mg prot.
Preliminary data suggest that the addition of ATP with insulin may faciliate the generation of mediator (? receptor or membrane phosphorylation). We conclude that insulin's mediator suppresses fatty acid oxidation in intact mitochondria.
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McCormick, K., Williams, M., Steinberg, J. et al. 1236 INSULIN'S INTRACELLULAR MESSENGER: EFFECT ON MITOCHONDRIAL FATTY ACID OXIDATION. Pediatr Res 19, 316 (1985). https://doi.org/10.1203/00006450-198504000-01266
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DOI: https://doi.org/10.1203/00006450-198504000-01266