Internal medicine

mitochondrial fusion

Receptor

Peroxisome proliferator-activated receptor

Mitochondrial DNA

Bioinformatics

Biology

Gene

Endocrinology

Peroxisome

Mitochondrial biogenesis

Insulin resistance

Insulin

Mitochondrion

Cell biology

Biochemistry

Medicine

Frontiers in Physiology

Mitochondrial dysfunction has been implicated in the pathogenesis of insulin resistance, the hallmark of type 2 diabetes mellitus (T2DM). However, the cause-effect relationship remains to be fully elucidated. Compelling evidence suggest that boosting mitochondrial function may represent a valuable therapeutic tool to improve insulin sensitivity. Mitochondria are highly dynamic organelles which adapt to short- and long-term metabolic perturbations by undergoing fusion and fission cycles, spatial rearrangement of the electron transport chain complexes into supercomplexes as well as biogenesis governed by peroxisome proliferator-activated receptor γ co-activator 1 α (PGC 1α). However, these processes appear to be dysregulated in type 2 diabetic individuals. Herein we describe the mechanistic link between mitochondrial dysfunction and insulin resistance in skeletal muscle alongside the intracellular pathways orchestrating mitochondrial bioenergetics. We then review current evidence on nutritional tools, including fatty acids, amino acids, caloric restriction and food bioactive derivatives which may enhance insulin sensitivity by therapeutically targeting mitochondrial function and biogenesis

Mitochondrial (Dys)function and Insulin Resistance: From Pathophysiological Molecular Mechanisms to the Impact of Diet