Document Type
Article
Publication Date
2-1-1996
Abstract
TNFα is overexpressed in the adipose tissue of obese rodents and humans, and is associated with insulin resistance. To more closely link TNF expression with whole body insulin action, we examined the expression of TNF by muscle, which is responsible for the majority of glucose uptake in vivo. Using RT-PCR, TNF was detected in human heart, in skeletal muscle from humans and rats, and in cultured human myocytes. Using competitive RT-PCR, TNF was quantitated in the muscle biopsy specimens from 15 subjects whose insulin sensitivity had been characterized using the glucose clamp technique. TNF expression in the insulin resistant subjects and the diabetic patients was fourfold higher than in the insulin sensitive subjects, and there was a significant inverse linear relationship between maximal glucose disposal rate and muscle TNF (r = -0.60, P < 0.02). In nine subjects, muscle cells from vastus lateralis muscle biopsies were placed into tissue culture for 4 wk, and induced to differentiate into myotubes. TNF was secreted into the medium from these cells, and cells from diabetic patients expressed threefold more TNF than cells from nondiabetic subjects. Thus, TNF is expressed in human muscle, and is expressed at a higher level in the muscle tissue and in the cultured muscle cells from insulin resistant and diabetic subjects. These data suggest another mechanism by which TNF may play an important role in human insulin resistance.
Recommended Citation
Saghizadeh, Mehrnoosh; Ong, John M.; Garvey, W. Timothy; Henry, Robert R.; and Kern, Philip A., "The Expression of TNFα by Human Muscle: Relationship to Insulin Resistance" (1996). MUSC Faculty Journal Articles. 27.
https://medica-musc.researchcommons.org/facarticles/27
Comments
Article written by researchers from the Department of Medicine, Cedars-Sinai Medical Center and University of California, Los Angeles;Department of Medicine, Medical University of South Carolina;Department of Medicine, VA Medical Center and University of California, San Diego;and Department of Medicine, VA Medical Center, Little Rock, Arkansas, and University of Arkansas for Medical Sciences. Published in the Journal of Clinical Investigation, February 1996, volume 97, number 4, pages 1111-1116. Includes abstract, references, tables, and diagrams.