Figure 2.

Pathogenesis of the pancreatic beta-cell and renal proximal tubule cell induced by increased mitochondrial heterogeneity. Mitochondrial heterogeneity under the pathological state, such as glucolipotoxicity (GLT), yields various functional readouts. (A) Increased mitochondrial membrane potential (ΔΨ) heterogeneity has been associated with various metabolic defects in both the pancreatic beta-cell and renal proximal tubule cell. Intracellular heterogeneity is observed by an increase in differences in ΔΨ. Reduced ΔΨ is presented as green and increased ΔΨ is presented as red. Mitochondria of normal ΔΨ are presented as pink. (B) Architectural heterogeneity yields mitochondria varying from short to long mitochondrial lengths as a result of varying fusion and fission rates. Increased heterogeneity in mitochondrial morphology, specifically increased short mitochondria due to reduced fusion, is associated with reductions in impaired glucose-stimulated insulin secretion (GSIS) in pancreatic beta-cells and reductions in renal fatty acid oxidation (FAO).