Notice: Users may be experiencing issues with displaying some pages on stanfordhealthcare.org. We are working closely with our technical teams to resolve the issue as quickly as possible. Thank you for your patience.
 

Learn about the flu shot, COVID-19 vaccine, and our masking policy »

Stanford Health Care

Mitochondrial dysfunction, insulin resistance and potential genetic implications. Endocrinology Sangwung, P. n., Petersen, K. F., Shulman, G. I., Knowles, J. W. 2020

Abstract

Insulin resistance, IR, is fundamental to the development type 2 diabetes (T2D) and is present in most prediabetic (preDM) individuals. IR has both heritable and environmental determinants centered on energy storage and metabolism. Recent insights from human genetic studies, coupled with comprehensive in vivo and ex vivo metabolic studies in humans and rodents have highlighted the critical role of reduced mitochondrial function as a predisposing condition for ectopic lipid deposition and IR. These studies support the hypothesis that reduced mitochondrial function, particularly in insulin responsive tissues such as skeletal muscle, white adipose tissue, and liver is inextricably linked to tissue and whole body IR through effects on cellular energy balance. Here we discuss these findings as well as address potential mechanisms that serve as the nexus between mitochondrial malfunction and IR.

View details for DOI 10.1210/endocr/bqaa017

View details for PubMedID 32060542