Regulation of Mitochondrial Fatty Acid Oxidation By Endothelial Nitric Oxide Synthase-Derived Nitric Oxide
Faust, Michael A. Jr.
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production in the heart under physiological conditions and is an indispensable energy source during fasting, exposure to cold, and exercise. Genetic or acquired deficiencies within the mFAO pathway result in a spectrum of metabolic and cardiovascular disorders. In addition, deficiencies in endothelial nitric oxide synthase (eNOS)-derived nitric oxide (NO) have also been linked to these disorders, and evidence suggests that NO may regulate mFAO. However, the mechanism(s) linking eNOS-NO and mFAO remain unclear. A systematic approach aiming to elucidate these mechanisms was the main goal of this study. NO may regulate mFAO via two pathways, either the activation of soluble guanalyl cyclase (sGC) or protein S-nitrosylation of mFAO enzymes. Thus, a series of assays were performed on fasted wildtype mice, eNOS knockout (eNOS KO) mice, and eNOS KO mice treated with either sodium nitrate (NaNO2) or the sGC activator BAY 41-2272. The data indicated that eNOS KO mice had impaired ability to undergo mFAO as compared to wildtype mice, and also that the lack of eNOS resulted in non-detectable S-nitrosylated mFAO enzymes in the livers of fasted mice. The treatment of eNOS KO mice with NaNO2 resulted in the restoration of S-nitrosylation of mFAO enzymes in these eNOS KO mice. In addition, the mFAO efficiency was corrected in NaNO2-treated mice but only partially restored in BAY 41- 2272-treated animals. The data suggests that NO regulates mFAO mainly via protein Snitrosylation.
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