Figure 2.

Diabetes induces upregulation of NADPH oxidase-dependent ROS production, leading to renal lipid dysmetabolism. In DKD, diabetes inhibits the AMPK pathway, causing upregulation of the mTOR pathway. Subsequently, mTOR activation leads to the activation of NADPH oxidases. NADPH oxidase-induced ROS production has been shown to alter renal lipid metabolism by inhibiting fatty acid β-oxidation and upregulating lipogenesis. ACOX1: acyl-CoA oxidase 1; AMPK; 5’ AMP-activated protein kinase; CPT1: carnitine palmitoyltransferase-1; FAS: fatty acid synthase; mTOR: mechanistic target of rapamycin; SREBP-1c: sterol regulatory element-binding protein 1-c; TSC1: hamartin; TSC2: tuberin.