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- W4283722268 abstract "<p> </p> <p>Skeletal muscle is a major regulator of glycemic control at rest and glucose utilization increases drastically during exercise. Sustaining a high glucose utilization via glycolysis requires efficient replenishment of NAD+ in the cytosol. Apoptosis-inducing mitochondrion-associated factor 2 (AIFM2) has previously been shown to be a NADH oxidoreductase domain–containing flavoprotein to promote glycolysis for diet and cold-induced thermogenesis. Here, we find that AIFM2 is selectively and highly induced in glycolytic extensor digitorum longus (EDL) muscle during exercise. Overexpression of AIFM2 in myotubes is sufficient to elevate the NAD+/NADH ratio, increasing the glycolytic rate. Thus, overexpression of AIFM2 in skeletal muscle greatly increases exercise capacity, with increased glucose utilization. Conversely, muscle-specific <em>Aifm2</em> depletion via <em>in vivo</em> transfection of hairpins against <em>Aifm2</em> or tamoxifen-inducible haploinsufficiency of <em>Aifm2 </em>in muscles decreases exercise capacity and glucose utilization in mice. Moreover, muscle-specific introduction of NDE1, <em>Saccharomyces cerevisiae</em> external NADH dehydrogenase, NDE, ameliorates impairment in glucose utilization and exercise intolerance of the muscle-specific <em>Aifm2</em> haploinsufficient mice. Together, we show a novel role for AIFM2 as a critical metabolic regulator for efficient utilization of glucose in glycolytic EDL muscles. </p>" @default.
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- W4283722268 date "2022-06-30" @default.
- W4283722268 modified "2023-10-01" @default.
- W4283722268 title "AIFM2 is required for high-intensity aerobic exercise by promoting glucose utilization" @default.
- W4283722268 doi "https://doi.org/10.2337/figshare.20173055" @default.
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