Review: Insulin resistance and mitochondrial dysfunction following severe burn injury

• Published in: Peptides (New York, N.Y. : 1980) N.Y. : 1980), 2020-04, Vol.126, p.170269-170269, Article 170269
• Main Authors: Berlanga-Acosta, Jorge, Iglesias-Marichal, Ileidys, Rodríguez-Rodríguez, Nadia, Mendoza-Marí, Yssel, García-Ojalvo, Ariana, Fernández-Mayola, Maday, Playford, Raymond J.
• Format: Article
• Language: English
• Subjects: Animals; Burn injury; Burns - metabolism; Humans; Hyperglycemia; Hyperglycemia - metabolism; Hyperglycemia - pathology; Insulin; Insulin receptor; Insulin Resistance; Mitochondria; Mitochondria - pathology
• ISSN: 0196-9781; 1873-5169
• DOI: 10.1016/j.peptides.2020.170269

•Insulin resistance occurs commonly following severe injury.•Mechanisms include increased stress hormones, catecholamines and cytokines.•Serine phosphylation of IRS-1 is an important regulatory element.•Mitochondrial dysfunction and lysis contribute to the inflammatory cascade.•Understanding pathophysiology of IR provides new therapeutic opportunities. The insulin signaling pathway plays a pivotal role in glucose metabolism and metabolic homeostasis. Disruption of this pathway is commonly seen in critical illness such as following severe burn injuries where homeostatic control is lost, leading to “insulin resistance” with poor blood glucose control. The aberrant signaling pathways involved in insulin resistance following burn injury include increases in hyperglycemic stress hormones, pro-inflammatory cytokines and free radical production. Leakage of mitochondrial sequestered self-antigens and signaling between mitochondria and endoplasmic reticulum also contribute to insulin resistance. Greater understanding of molecular processes involved in burn-related insulin resistance could potentially lead to the development of novel therapeutic approaches to improve patient management.