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Agonist-induced activation releases peroxisome proliferator-activated receptor beta/delta from its inhibition by palmitate-induced nuclear factor-kappaB in skeletal muscle cells.
Biochim Biophys Acta. 2005 May 01; 1734(1):52-61.BB

Abstract

The mechanisms by which elevated levels of free fatty acids cause insulin resistance are not well understood, but there is a strong correlation between insulin resistance and intramyocellular lipid accumulation in skeletal muscle. In addition, accumulating evidence suggests a link between inflammation and type 2 diabetes. The aim of this work was to study whether the exposure of skeletal muscle cells to palmitate affected peroxisome proliferator-activated receptor (PPAR) beta/delta activity. Here, we report that exposure of C2C12 skeletal muscle cells to 0.75 mM palmitate reduced (74%, P<0.01) the mRNA levels of the PPARbeta/delta-target gene pyruvatedehydrogenase kinase 4 (PDK-4), which is involved in fatty acid utilization. This reduction was not observed in the presence of the PPARbeta/delta agonist L-165041. This drug prevented palmitate-induced nuclear factor (NF)-kappaB activation. Increased NF-kappaB activity after palmitate exposure was associated with enhanced protein-protein interaction between PPARbeta/delta and p65. Interestingly, treatment with the PPARbeta/delta agonist L-165041 completely abolished this interaction. These results indicate that palmitate may reduce fatty acid utilization in skeletal muscle cells by reducing PPARbeta/delta signaling through increased NF-kappaB activity.

Authors+Show Affiliations

Pharmacology Unit, Department of Pharmacology and Therapeutic Chemistry, Faculty of Pharmacy, University of Barcelona, Spain.No affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

15866483

Citation

Jové, Mireia, et al. "Agonist-induced Activation Releases Peroxisome Proliferator-activated Receptor Beta/delta From Its Inhibition By Palmitate-induced Nuclear factor-kappaB in Skeletal Muscle Cells." Biochimica Et Biophysica Acta, vol. 1734, no. 1, 2005, pp. 52-61.
Jové M, Laguna JC, Vázquez-Carrera M. Agonist-induced activation releases peroxisome proliferator-activated receptor beta/delta from its inhibition by palmitate-induced nuclear factor-kappaB in skeletal muscle cells. Biochim Biophys Acta. 2005;1734(1):52-61.
Jové, M., Laguna, J. C., & Vázquez-Carrera, M. (2005). Agonist-induced activation releases peroxisome proliferator-activated receptor beta/delta from its inhibition by palmitate-induced nuclear factor-kappaB in skeletal muscle cells. Biochimica Et Biophysica Acta, 1734(1), 52-61.
Jové M, Laguna JC, Vázquez-Carrera M. Agonist-induced Activation Releases Peroxisome Proliferator-activated Receptor Beta/delta From Its Inhibition By Palmitate-induced Nuclear factor-kappaB in Skeletal Muscle Cells. Biochim Biophys Acta. 2005 May 1;1734(1):52-61. PubMed PMID: 15866483.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Agonist-induced activation releases peroxisome proliferator-activated receptor beta/delta from its inhibition by palmitate-induced nuclear factor-kappaB in skeletal muscle cells. AU - Jové,Mireia, AU - Laguna,Juan C, AU - Vázquez-Carrera,Manuel, Y1 - 2005/03/17/ PY - 2005/01/13/received PY - 2005/02/09/revised PY - 2005/02/09/accepted PY - 2005/5/4/pubmed PY - 2005/6/24/medline PY - 2005/5/4/entrez SP - 52 EP - 61 JF - Biochimica et biophysica acta JO - Biochim Biophys Acta VL - 1734 IS - 1 N2 - The mechanisms by which elevated levels of free fatty acids cause insulin resistance are not well understood, but there is a strong correlation between insulin resistance and intramyocellular lipid accumulation in skeletal muscle. In addition, accumulating evidence suggests a link between inflammation and type 2 diabetes. The aim of this work was to study whether the exposure of skeletal muscle cells to palmitate affected peroxisome proliferator-activated receptor (PPAR) beta/delta activity. Here, we report that exposure of C2C12 skeletal muscle cells to 0.75 mM palmitate reduced (74%, P<0.01) the mRNA levels of the PPARbeta/delta-target gene pyruvatedehydrogenase kinase 4 (PDK-4), which is involved in fatty acid utilization. This reduction was not observed in the presence of the PPARbeta/delta agonist L-165041. This drug prevented palmitate-induced nuclear factor (NF)-kappaB activation. Increased NF-kappaB activity after palmitate exposure was associated with enhanced protein-protein interaction between PPARbeta/delta and p65. Interestingly, treatment with the PPARbeta/delta agonist L-165041 completely abolished this interaction. These results indicate that palmitate may reduce fatty acid utilization in skeletal muscle cells by reducing PPARbeta/delta signaling through increased NF-kappaB activity. SN - 0006-3002 UR - https://www.unboundmedicine.com/medline/citation/15866483/Agonist_induced_activation_releases_peroxisome_proliferator_activated_receptor_beta/delta_from_its_inhibition_by_palmitate_induced_nuclear_factor_kappaB_in_skeletal_muscle_cells_ DB - PRIME DP - Unbound Medicine ER -