Lipid oxidation is reduced in obese human skeletal muscle.

By Jong-Yeon Kim, R. Hickner, Ronald L. Cortright, G. Dohm, Joseph A. Houmard. American Journal of Physiology. Endocrinology and Metabolism, 2000

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Membrane fatty acid transporters as regulators of lipid metabolism: implications for metabolic disease. (2010, background): “In obese individuals, the reduction in fatty acid oxidation appears to be correlated with the extent of obesity (BMI) (430) and has also been attributed to a reduced mitochondrial content (202, 246, 384), as fatty acid oxidation by isolated mitochondria of obese individuals was normal (202) and not ”
Disordered fat storage and mobilization in the pathogenesis of insulin resistance and type 2 diabetes. (2002, neutral): “palmitoyl-transferase-1 (CPT-1) and post-CPT-1 levels (106).”
Deficiency of subsarcolemmal mitochondria in obesity and type 2 diabetes. (2005, background): “The mechanism by which mitochondrial dysfunction causes insulin resistance remains unclear, although one attractive hypothesis is a disposition to lipid accumulation caused by impaired capacity for lipid oxidation (10,40).”
Metabolic Syndrome and Insulin Resistance: Underlying Causes and Modification by Exercise Training (2013, neutral): “LCFA entry into the mitochondria, carnitine palmitoyltransferase-1 (CPT1), and impaired mitochondrial function (decreased mitochondrial number, lower levels of oxidative enzymes, and lower ATP synthetic rates) are found in insulin-resistant skeletal muscle and coincide with muscle lipid accumulation”