Event Title

CIGARETTE SMOKE AND INSULIN RESISTANCE

Location

Atrium

Start Date

14-2-2014 12:00 AM

Description

Objective. This study was conducted to determine the effect of cigarette smoke/oxidative stress on the development of Insulin Resistance, as well as, the regulation of SOCS3 by cigarette smoke in vivo. Background. Oxidative stress through reactive oxygen species (ROS) production has been associated with the etiology of insulin resistance, primarily in skeletal muscle tissue. Skeletal muscle is the major site of dietary glucose disposal. Many cytokines stimulate the tissue-specific expression of suppressor of cytokine signaling (SOCSs) proteins, a group of signaling proteins characterized by their ability to down-regulate cytokine signaling. Moreover, it has been demonstrated that SOCS3 is implicated in the pathogenesis of IR. Methods. C57B/6 mice were exposed to cigarette smoke for 12 weeks. After 8 and 12 weeks of treatment, fed blood glucose and plasma insulin levels were determined using a glucometer and an insulin rat insulin ELISA kit respectively. At the end of the experimental period, animals were sacrificed and skeletal muscle collected. Total protein were extracted and quantified. SOCS3 expression was determined by Western blot analysis. Animals exposed to cigarette smoke for 12 weeks developed IR and subsequent induction of SOCS3 expression. Results. Our results showed that mice that were exposed to cigarette smoke had upregulation of the SOCS3 signaling protein relative to control mice that were unexposed. Conclusion. Our data support the hypothesis that cigarette smoke, through SOCS3, may induce IR, suggesting a pathogenic mechanism to explain the link between cigarette smoke and IR. Grants. NIH center core grant, Research to Prevent Blindness Grant, and Department of Defense.

This document is currently not available here.

Share

COinS
 
Feb 14th, 12:00 AM

CIGARETTE SMOKE AND INSULIN RESISTANCE

Atrium

Objective. This study was conducted to determine the effect of cigarette smoke/oxidative stress on the development of Insulin Resistance, as well as, the regulation of SOCS3 by cigarette smoke in vivo. Background. Oxidative stress through reactive oxygen species (ROS) production has been associated with the etiology of insulin resistance, primarily in skeletal muscle tissue. Skeletal muscle is the major site of dietary glucose disposal. Many cytokines stimulate the tissue-specific expression of suppressor of cytokine signaling (SOCSs) proteins, a group of signaling proteins characterized by their ability to down-regulate cytokine signaling. Moreover, it has been demonstrated that SOCS3 is implicated in the pathogenesis of IR. Methods. C57B/6 mice were exposed to cigarette smoke for 12 weeks. After 8 and 12 weeks of treatment, fed blood glucose and plasma insulin levels were determined using a glucometer and an insulin rat insulin ELISA kit respectively. At the end of the experimental period, animals were sacrificed and skeletal muscle collected. Total protein were extracted and quantified. SOCS3 expression was determined by Western blot analysis. Animals exposed to cigarette smoke for 12 weeks developed IR and subsequent induction of SOCS3 expression. Results. Our results showed that mice that were exposed to cigarette smoke had upregulation of the SOCS3 signaling protein relative to control mice that were unexposed. Conclusion. Our data support the hypothesis that cigarette smoke, through SOCS3, may induce IR, suggesting a pathogenic mechanism to explain the link between cigarette smoke and IR. Grants. NIH center core grant, Research to Prevent Blindness Grant, and Department of Defense.