Abstract
BackgroundDecreased expression of glucose transporter protein GLUT4, encoded by the solute carrier 2A4 (Slc2a4) gene, is involved in obesity-induced insulin resistance. Local tissue inflammation, by nuclear factor-κB (NFκB)-mediated pathway, has been related to Slc2a4 repression; a mechanism that could be modulated by statins. Using a model of obesity with insulin resistance, this study investigated whether (1) inflammatory markers and Slc2a4 expression are altered; (2) atorvastatin has beneficial effects on inflammation and Slc2a4 expression; and (3) inhibitor of NFκB (IKK)/NFκB pathway is involved in subcutaneous adipose tissue (SAT).FindingsObese mice showed insulin resistance, decreased expression of Slc2a4 mRNA (66%, P < 0.01) and GLUT4 protein (30%, P < 0.05), and increased expression of interleukin 6 (Il6) mRNA (44%, P < 0.05) in SAT. Obese mice treated with atorvastatin had enhanced in vivo insulin sensitivity, besides increased Slc2a4/GLUT4 expression and reduced Il6 expression in SAT. No alterations of tumor necrosis factor-α, interleukin 1β and adiponectin expression or IKKα/β activity in SAT of obese mice or obese mice treated with atorvastatin were observed.ConclusionsAtorvastatin has beneficial effect upon glycemic homeostasis, which may be related to its positive impact on Il6 and Slc2a4/GLUT4 expression in SAT.
Highlights
The glucose transporter protein Glucose transporter 4 (GLUT4) is responsible for insulin-mediated glucose uptake in adipose tissue and skeletal muscle, and plays an important role in glycemic homeostasis [1]
Atorvastatin has beneficial effect upon glycemic homeostasis, which may be related to its positive impact on interleukin 6 (Il6) and solute carrier 2A4 (Slc2a4)/GLUT4 expression in subcutaneous adipose tissue (SAT)
Results untreated obese mice (OB) and atorvastatintreated obese mice (OBA) showed similar body weight to that observed in control mice (CTL), the significant higher Lee obesity index indicated that both groups were obese (Table 1)
Summary
The glucose transporter protein GLUT4 is responsible for insulin-mediated glucose uptake in adipose tissue and skeletal muscle, and plays an important role in glycemic homeostasis [1]. Obesity is associated with insulin resistance and reduced Slc2a4/GLUT4 expression in both muscle and fat [2,5]. Some studies have reported evidences for antiinflammatory and insulin sensitizing effects of statin in visceral adipose tissue (VAT) of glutamate monosodiuminduced obese mice [2,9]. There are evidences that IKK/NFκB pathway is involved in the Slc2a4 gene expression in VAT [2]. Decreased expression of glucose transporter protein GLUT4, encoded by the solute carrier 2A4 (Slc2a4) gene, is involved in obesity-induced insulin resistance. Using a model of obesity with insulin resistance, this study investigated whether (1) inflammatory markers and Slc2a4 expression are altered; (2) atorvastatin has beneficial effects on inflammation and Slc2a4 expression; and (3) inhibitor of NFκB (IKK)/NFκB pathway is involved in subcutaneous adipose tissue (SAT)
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
