|Kalupahana, Nishan -|
|Moustaid-Moussa, Naima -|
Submitted to: Molecular Aspects of Medicine
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: October 14, 2011
Publication Date: February 9, 2012
Repository URL: http://handle.nal.usda.gov/10113/58076
Citation: Kalupahana, N.S., Moustaid-Moussa, N., Claycombe, K.J. 2012. Immunity as a link between obesity and insulin resistance. Molecular Aspects of Medicine . 33:26-34. Interpretive Summary: In recent decades, the prevalence of obesity in the U.S. has increased at an alarming rate. Obesity increases the risk for development of type II diabetes mellitus. The elevated risk has been suggested to be mediated, in part, by increased chronic inflammation. Studies have shown an elevated secretion of pro-inflammatory cytokines during onset obesity is significantly reduced with weight loss, particularly with decreased body fat. These findings suggest that adipose tissue is an important source of obesity-associated inflammation. As a result, this review focuses on how immunes cells that are found in adipose tissue of obese animals and human have altered numbers as well as function to increase adipose tissue inflammation and development of type II diabetes mellitus.
Technical Abstract: Type-2 diabetes mellitus (T2DM) is a major health problem in the United States and worldwide. Obesity is causally linked to the pathogenesis of insulin resistance, metabolic syndrome and T2DM. A chronic low-grade inflammation occurring in adipose tissue is at least in part responsible for the obesity-induced insulin resistance. This adipose tissue inflammation is characterized by changes in immune cell populations giving rise to altered adipokine profiles, which in turn induces skeletal muscle and hepatic insulin resistance. Detailed molecular mechanisms of insulin resistance, adipose tissue inflammation and the implications of these findings on therapeutic strategies are discussed in this review.