Fuel selection in human skeletal muscle in insulin resistance: a reexamination.
By D. Kelley, Lawrence J. Mandarino. Diabetes, 2000
1,054 citations recorded by the source corpus.
Subfields: Cell Biology, Physiology
View Paper: https://www.semanticscholar.org/paper/7d3e13d5abd4d7a6fea66a1e0538662de7f49bcc
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Citations in the corpus
- From the Triumvirate to the Ominous Octet: A New Paradigm for the Treatment of Type 2 Diabetes Mellitus (2009, background): “Although there clearly is substrate competition between FFA and glucose with respect to oxidative metabolism (196,197), FFAs have been shown to have independent effects to inhibit glycogen synthase (198,199) and both glucose transport and glucose phosphorylation (192,200).”
- Metformin: An Update (2002, background): “Increased fatty acid oxidation inhibits key enzymes of the glycolytic pathway by accumulation of acetyl coenzyme A and citrate, by-products of free fatty acid oxidation (51).”
- Mitochondrial dynamics in mammalian health and disease. (2009, background): “The switch between glucose and lipid oxidation, depending on energy requirements, is referred to as “metabolic flexibility” (162).”
- Disordered fat storage and mobilization in the pathogenesis of insulin resistance and type 2 diabetes. (2002, background): “This phenotype is hypothesized to be characterized by low oxidative or fat oxidative capacity and a tendency toward a positive energy balance (154).”
- Targeting the RAS/RAF/MAPK pathway for cancer therapy: from mechanism to clinical studies (2023, background): “273,274 The metabolites sapienate, generated by fatty acid desaturase 2, and palmitoleate, generated by stearoyl-CoA desaturase-1, are mono-unsaturated fatty acids involved in the metabolic fl exibility of primary tumors.”
- Membrane fatty acid transporters as regulators of lipid metabolism: implications for metabolic disease. (2010, result): “This increase in intracellular lipid accumulation would not seem to be simply attributable to a concomitant reduction in (mitochondrial) fatty acid oxidation as has been speculated (238), since there is no consistent evidence in support of this notion (for review, see Ref.”
- Effects of Dietary Fiber and Its Components on Metabolic Health (2010, background): “According to Kelley and Mandarino [53], increases in FFA in the blood can inhibit glucose metabolism through the inhibition of GLUT 4 transporters.”
- Interdependence of AMPK and SIRT1 for metabolic adaptation to fasting and exercise in skeletal muscle (2010, background): “The lack of metabolic flexibility to correctly adapt to energy demands and nutrient availability constitutes a burden on energy homeostasis, ultimately leading to metabolic disease (Kelley and Mandarino, 2000).”
- Role of the adipocyte, free fatty acids, and ectopic fat in pathogenesis of type 2 diabetes mellitus: peroxisomal proliferator-activated receptor agonists provide a rational therapeutic approach. (2004, background): “However, it is the decrease in intracellular concentration of metabolites of muscle triglycerides (FA-CoAs, DAG, ceramides, etc.) that best predicts the improvement in muscle sensitivity to insulin (71–82, 86–89), and these metabolites were not measured in this study (268).”