A theoretical argument to support the biological benefits for insulin stimulating mitochondrial oxidative phosphorylation. Issue 25 (February 2022)

• Record Type: Journal Article
• Authors: Brunetta, Henver S; Holloway, Graham P
• Is Part Of: Current opinion in physiology. Issue 25(2022)
• Publication Date: 2022-02
• Subjects: Physiology -- Periodicals; Physiological Phenomena; Periodical; Fulltext; Internet Resources; Periodicals; 571
• DOI: 10.1016/j.cophys.2022.100491
• Languages: English
• ISSNs: 2468-8673

Abstract

Abstract : Insulin is a key hormone involved in diverse processes that directly impact whole-body metabolic control. One theory behind the etiology of reduced insulin signaling, known as insulin resistance, is compromised mitochondrial bioenergetics. Mitochondria are small organelles located within almost all cells in the body, producing the vast majority of ATP and representing a key location for reactive oxygen species production. Although there is considerable controversy surrounding the notion that mitochondrial respiratory dysfunction causes insulin resistance, more recently, studies have highlighted that insulin acutely regulates mitochondrial bioenergetics, raising the possibility that insulin resistance contributes to the development of mitochondrial 'dysfunction'. Here, we briefly discuss what is known about the effects of insulin on mitochondrial biology within skeletal muscle. We offer a theoretical perspective on why it would be advantageous for insulin signaling to acutely improve mitochondrial bioenergetics, as well as the implications of this crosstalk in health and insulin-resistant conditions.