The metabolic and molecular pathways accounting for these phenomena involve increased availability of substrates such as glucose (owing to hepatic insulin resistance) and fatty acids (resulting from adipose tissue insulin resistance) while activating those transcription factors: Carbohydrate Response Element Binding Protein (ChREBP) and Sterol Response Element Binding Protein 1c (SREBP-1c), in the liver. Here, MLXIPL is linked to Insulin resistance.