Mitochondrial dysfunction in diabetes and the regulatory roles of antidiabetic agents on the mitochondrial function

• Published in: Journal of cellular physiology 2019-06, Vol.234 (6), p.8402-8410
• Main Authors: Yaribeygi, Habib, Atkin, Stephen L., Sahebkar, Amirhossein
• Format: Article
• Language: English
• Subjects: Adipokines - genetics; antidiabetic agents; Antidiabetics; Apoptosis; Apoptosis - genetics; Beta cells; Chemical compounds; Diabetes; Diabetes mellitus; Diabetes mellitus (non-insulin dependent); Diabetes Mellitus, Type 2 - drug therapy; Diabetes Mellitus, Type 2 - genetics; Diabetes Mellitus, Type 2 - pathology; diabetic complications; Glucose; Humans; Hypoglycemic Agents - therapeutic use; Inflammation; Inflammation - drug therapy; Inflammation - genetics; Insulin; Insulin Resistance - genetics; Insulin-Secreting Cells - drug effects; Insulin-Secreting Cells - pathology; Mitochondria; Mitochondria - drug effects; Mitochondria - genetics; Mitochondria - pathology; mitochondrial dysfunction; Morbidity; Oxidation resistance; Oxidative stress; Oxidative Stress - drug effects; Pharmacology
• ISSN: 0021-9541; 1097-4652
• DOI: 10.1002/jcp.27754

The prevalence of type 2 diabetes mellitus (T2DM) is increasing rapidly with its associated morbidity and mortality. Many pathophysiological pathways such as oxidative stress, inflammatory responses, adipokines, obesity‐induced insulin resistance, improper insulin signaling, and beta cell apoptosis are associated with the development of T2DM. There is increasing evidence of the role of mitochondrial dysfunction in the onset of T2DM, particularly in relation to the development of diabetic complications. Here, the role of mitochondrial dysfunction in T2DM is reviewed together with its modulation by antidiabetic therapeutic agents, an effect that may be independent of their hypoglycemic effect. The prevalence of type 2 diabetes mellitus (T2DM) is increasing rapidly with its associated morbidity and mortality; many pathophysiological pathways such as oxidative stress, inflammatory responses, adipokines, obesity‐induced insulin resistance, improper insulin signaling, and beta cell apoptosis are associated with the development of T2DM. There is increasing evidence of the role of mitochondrial dysfunction in the onset of T2DM, particularly in relation to the development of diabetic complications. Here, the role of mitochondrial dysfunction in T2DM is reviewed together with its modulation by antidiabetic therapeutic agents, an effect that may be independent of their hypoglycemic effect.