Repository of Research and Investigative Information

Repository of Research and Investigative Information

Ilam University of Medical Sciences

Rosiglitazone, a PPARγ agonist, ameliorates palmitate-induced insulin resistance and apoptosis in skeletal muscle cells

Sun Oct 2 23:39:29 2022

(2014) Rosiglitazone, a PPARγ agonist, ameliorates palmitate-induced insulin resistance and apoptosis in skeletal muscle cells. Cell Biochemistry and Function. pp. 683-691. ISSN 02636484 (ISSN)

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Official URL: https://www.scopus.com/inward/record.uri?eid=2-s2....

Abstract

Palmitate induces insulin resistance and apoptosis in insulin target tissues. Rosiglitazone (RSG), a peroxisome proliferator-activated receptor γ (PPARγ) agonist, can activate both pro-apoptotic and anti-apoptotic pathways in different cells; however, its effect on palmitate-induced apoptosis in skeletal muscle cells remains to be elucidated. After differentiation of C2C12 cells, myotubes were treated with palmitate, RSG and GW9662 (PPARγ antagonist). MTT and terminal deoxynucleotide transferase dUTP nick end labelling (TUNEL) assays and caspase-3 activity were used to investigate the apoptosis. To study the underlying mechanism, glucose uptake, gene expression and protein levels were evaluated. A total of 0.75mM palmitate reduced cell viability by 43 and increased TUNEL-positive cells and caspase-3 activity by 15-fold and 6.6-fold, respectively. RSG (10μM) could markedly decrease the level of TUNEL-positive cells and caspase-3 activity in palmitate-treated cells. The protective effect of RSG on apoptosis was abrogated by GW9662. To investigate the molecular mechanism of this effect, gene expression and protein level of protein tyrosine phosphatase 1B (PTP1B) were evaluated. Palmitate and RSG individually increased the expression and protein level of PTP1B, whereas combined treatment (palmitate and RSG) were able to further increase the expression of PTP1B in C2C12 cells. We also evaluated the effect of RSG on palmitate-induced insulin resistance in muscle cells. RSG could significantly improve glucose uptake by 0.4-fold in myotubes treated with palmitate. Moreover, RSG could restore the phosphorylation of Akt in palmitate-treated cells. These data suggest that RSG protects skeletal muscle cells against palmitate-induced apoptosis and this effect appears to be mediated via the PPARγ-dependent and PTP1B-independent mechanisms. © 2014 John Wiley & Sons, Ltd.

Item Type: Article
Creators:
CreatorsEmail
Meshkani, R.UNSPECIFIED
Sadeghi, A.UNSPECIFIED
Taheripak, G.UNSPECIFIED
Zarghooni, M.UNSPECIFIED
Gerayesh-Nejad, S.UNSPECIFIED
Bakhtiyari, S.UNSPECIFIED
Keywords: Apoptosis C2C12 Palmitate PTP1B Rosiglitazone Skeletal muscle cells 2 chloro 5 nitrobenzanilide caspase 3 palmitic acid protein kinase B protein tyrosine phosphatase 1B 2,4 thiazolidinedione derivative 2-chloro-5-nitrobenzanilide anilide antidiabetic agent enzyme inhibitor palmitic acid derivative peroxisome proliferator activated receptor gamma Ptpn1 protein, mouse animal cell Article cell differentiation cell viability gene expression glucose transport insulin resistance mouse myotube nick end labeling nonhuman priority journal protein expression protein phosphorylation skeletal muscle agonists animal cell line cell survival drug effects metabolism myoblast Anilides Animals Enzyme Inhibitors Hypoglycemic Agents Mice Myoblasts, Skeletal Palmitates PPAR gamma Protein Tyrosine Phosphatase, Non-Receptor Type 1 Thiazolidinediones
Divisions:
Page Range: pp. 683-691
Journal or Publication Title: Cell Biochemistry and Function
Journal Index: Scopus
Volume: 32
Number: 8
Identification Number: https://doi.org/10.1002/cbf.3072
ISSN: 02636484 (ISSN)
Depositing User: مهندس مهدی شریفی
URI: http://eprints.medilam.ac.ir/id/eprint/1502

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