INS and Insulin resistance: For example, MS-based metabolomic profiling of amino acids, fatty acids, and acylcarnitines [20] has provided support for the hypothesis that lipid-induced insulin resistance is explained in part by overload of mitochondrial lipid oxidation, accumulation of incompletely oxidized fats, and depletion of TCA intermediates, thereby leading to a condition of mitochondrial stress that activates signaling pathways that interfere with insulin action [21].