ArticleBritish journal of pharmacology2004
Expression and functional activity of PPARgamma in pancreatic beta cells.
Article in British journal of pharmacology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 29 citations in OpenAlex.
- Niacin exacerbates β cell lipotoxicity in diet-induced obesity mice through upregulation of GPR109A and PPARγ2: Inhibition by incretin drugs.Frontiers in endocrinology · 2022Article
- Thiazolidinediones (TZDs) enhance insulin secretory response via GPR40 and adenylate cyclase (AC).Journal of cellular physiology · 2021Article
- Heterozygous deletion of Seipin in islet beta cells of male mice has an impact on insulin synthesis and secretion through reduced PPARγ expression.Diabetologia · 2020Article
- Is the Mouse a Good Model of Human PPARγ-Related Metabolic Diseases?International journal of molecular sciences · 2016Review
- Interleukin-18 increases TLR4 and mannose receptor expression and modulates cytokine production in human monocytes.Mediators of inflammation · 2015Article
- Peroxisome proliferator-activated receptor targets for the treatment of metabolic diseases.Mediators of inflammation · 2013Review
- The effects of Leptin and Adiponectin on Pdx1, Foxm1, and PPARγ Transcription in Rat Islets of Langerhans.Hepatitis monthly · 2013Article
- Rosiglitazone promotes PPARγ-dependent and -independent alterations in gene expression in mouse islets.Endocrinology · 2012Article
- Effects of rosiglitazone on the configuration of action potentials and ion currents in canine ventricular cells.British journal of pharmacology · 2011Article
- The role of peroxisome proliferator-activated receptor γ in pancreatic β cell function and survival: therapeutic implications for the treatment of type 2 diabetes mellitus.Diabetes, obesity & metabolism · 2010Article
- Molecular mechanism by which pioglitazone preserves pancreatic beta-cells in obese diabetic mice: evidence for acute and chronic actions as a PPARgamma agonist.American journal of physiology. Endocrinology and metabolism · 2010Article
- The influence of feeding linoleic, gamma-linolenic and docosahexaenoic acid rich oils on rat brain tumor fatty acids composition and fatty acid binding protein 7 mRNA expression.Lipids in health and disease · 2008Article
- PPARgamma in human and mouse physiology.Biochimica et biophysica acta · 2007Review
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Rosiglitazone is an agonist of peroxisome proliferator activated receptor-gamma (PPARgamma) and ameliorates insulin resistance in type II diabetes. In addition, it may also promote increased pancreatic beta-cell viability, although it is not known whether this effect is mediated by a direct action on the beta cell. We have investigated this possibility. Semiquantitative real-time reverse transcription-polymerase chain reaction analysis (Taqman) revealed that freshly isolated rat islets and the clonal beta-cell line, BRIN-BD11, express PPARgamma, as well as PPARalpha and PPARdelta. The levels of expression of PPARgamma were estimated by reference to adipose tissue and were found to represent approximately 60% (islets) and 30% (BRIN-BD11) of that found in freshly isolated visceral adipose tissue. Western blotting confirmed the presence of immunoreactive PPARgamma in rat (and human) islets and in BRIN-BD11 cells. Transfection of BRIN-BD11 cells with a PPARgamma-sensitive luciferase reporter construct was used to evaluate the functional competence of the endogenous PPARgamma. Luciferase activity was modestly increased by the putative endogenous ligand, 15-deoxy-Delta12,14 prostaglandin J2 (15dPGJ2). Rosiglitazone also caused activation of the luciferase reporter construct but this effect required concentrations of the drug (50-100 microm) that are beyond the expected therapeutic range. This suggests that PPARgamma is relatively insensitive to activation by rosiglitazone in BRIN-BD11 cells. Exposure of BRIN-BD11 cells to the lipotoxic effector, palmitate, caused a marked loss of viability. This was attenuated by treatment of the cells with either actinomycin D or cycloheximide suggesting that a pathway of programmed cell death was involved. Rosiglitazone failed to protect BRIN-BD11 cells from the toxic actions of palmitate at concentrations up to 50 microm. Similar results were obtained with a range of other PPARgamma agonists. Taken together, the present data suggest that, at least under in vitro conditions, thiazolidinediones do not exert direct protective effects against fatty acid-mediated cytotoxicity in pancreatic beta cells.
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