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Activation of PPARdelta up-regulates fatty acid oxidation and energy uncoupling genes of mitochondria and reduces palmitate-induced apoptosis in pancreatic beta-cells.
Biochem Biophys Res Commun. 2010 Jan 15; 391(3):1567-72.BB

Abstract

Recent evidence indicates that decreased oxidative capacity, lipotoxicity, and mitochondrial aberrations contribute to the development of insulin resistance and type 2 diabetes. The goal of this study was to investigate the effects of peroxisome proliferator-activated receptor delta (PPARdelta) activation on lipid oxidation, mitochondrial function, and insulin secretion in pancreatic beta-cells. After HIT-T15 cells (a beta-cell line) were exposed to high concentrations of palmitate and GW501516 (GW; a selective agonist of PPARdelta), we found that administration of GW increased the expression of PPARdelta mRNA. GW-induced activation of PPARdelta up-regulated carnitine palmitoyltransferase 1 (CPT1), long-chain acyl-CoA dehydrogenase (LCAD), pyruvate dehydrogenase kinase 4 (PDK4), and uncoupling protein 2 (UCP2); alleviated mitochondrial swelling; attenuated apoptosis; and reduced basal insulin secretion induced by increased palmitate in HIT cells. These results suggest that activation of PPARdelta plays an important role in protecting pancreatic beta-cells against aberrations caused by lipotoxicity in metabolic syndrome and diabetes.

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Authors+Show Affiliations

Wan J
Department of Endocrinology, West China Hospital of Sichuan University, 37 Guoxue Lane, Chengdu, Sichuan 610041, China.
Jiang L
No affiliation info available
Lü Q
No affiliation info available
Ke L
No affiliation info available
Li X
No affiliation info available
Tong N
No affiliation info available

MeSH

Acyl-CoA Dehydrogenase, Long-ChainAnimalsCarnitine O-PalmitoyltransferaseCell LineCricetinaeFatty AcidsGene Expression RegulationGenes, MitochondrialInsulinInsulin-Secreting CellsIon ChannelsMicroscopy, Electron, TransmissionMitochondriaMitochondrial ProteinsOxidation-ReductionPPAR deltaPalmitic AcidProtein KinasesThiazolesUncoupling Protein 2Up-Regulation

Pub Type(s)

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

Language

eng

PubMed ID

20040361

Citation

Wan, Jun, et al. "Activation of PPARdelta Up-regulates Fatty Acid Oxidation and Energy Uncoupling Genes of Mitochondria and Reduces Palmitate-induced Apoptosis in Pancreatic Beta-cells." Biochemical and Biophysical Research Communications, vol. 391, no. 3, 2010, pp. 1567-72.
Wan J, Jiang L, Lü Q, et al. Activation of PPARdelta up-regulates fatty acid oxidation and energy uncoupling genes of mitochondria and reduces palmitate-induced apoptosis in pancreatic beta-cells. Biochem Biophys Res Commun. 2010;391(3):1567-72.
Wan, J., Jiang, L., Lü, Q., Ke, L., Li, X., & Tong, N. (2010). Activation of PPARdelta up-regulates fatty acid oxidation and energy uncoupling genes of mitochondria and reduces palmitate-induced apoptosis in pancreatic beta-cells. Biochemical and Biophysical Research Communications, 391(3), 1567-72. https://doi.org/10.1016/j.bbrc.2009.12.127
Wan J, et al. Activation of PPARdelta Up-regulates Fatty Acid Oxidation and Energy Uncoupling Genes of Mitochondria and Reduces Palmitate-induced Apoptosis in Pancreatic Beta-cells. Biochem Biophys Res Commun. 2010 Jan 15;391(3):1567-72. PubMed PMID: 20040361.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Activation of PPARdelta up-regulates fatty acid oxidation and energy uncoupling genes of mitochondria and reduces palmitate-induced apoptosis in pancreatic beta-cells. AU - Wan,Jun, AU - Jiang,Li, AU - Lü,Qingguo, AU - Ke,Linqiu, AU - Li,Xiaoyu, AU - Tong,Nanwei, Y1 - 2009/12/27/ PY - 2009/12/14/received PY - 2009/12/22/accepted PY - 2009/12/31/entrez PY - 2009/12/31/pubmed PY - 2010/2/23/medline SP - 1567 EP - 72 JF - Biochemical and biophysical research communications JO - Biochem Biophys Res Commun VL - 391 IS - 3 N2 - Recent evidence indicates that decreased oxidative capacity, lipotoxicity, and mitochondrial aberrations contribute to the development of insulin resistance and type 2 diabetes. The goal of this study was to investigate the effects of peroxisome proliferator-activated receptor delta (PPARdelta) activation on lipid oxidation, mitochondrial function, and insulin secretion in pancreatic beta-cells. After HIT-T15 cells (a beta-cell line) were exposed to high concentrations of palmitate and GW501516 (GW; a selective agonist of PPARdelta), we found that administration of GW increased the expression of PPARdelta mRNA. GW-induced activation of PPARdelta up-regulated carnitine palmitoyltransferase 1 (CPT1), long-chain acyl-CoA dehydrogenase (LCAD), pyruvate dehydrogenase kinase 4 (PDK4), and uncoupling protein 2 (UCP2); alleviated mitochondrial swelling; attenuated apoptosis; and reduced basal insulin secretion induced by increased palmitate in HIT cells. These results suggest that activation of PPARdelta plays an important role in protecting pancreatic beta-cells against aberrations caused by lipotoxicity in metabolic syndrome and diabetes. SN - 1090-2104 UR - https://www.unboundmedicine.com/medline/citation/20040361/Activation_of_PPARdelta_up_regulates_fatty_acid_oxidation_and_energy_uncoupling_genes_of_mitochondria_and_reduces_palmitate_induced_apoptosis_in_pancreatic_beta_cells_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0006-291X(09)02513-3 DB - PRIME DP - Unbound Medicine ER -
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