ArticleActa pharmacologica Sinica2010
AMPK enhances the expression of pancreatic duodenal homeobox-1 via PPARalpha, but not PPARgamma, in rat insulinoma cell line INS-1.
Article in Acta pharmacologica Sinica, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 9 citations in OpenAlex.
- The Perfect Cup? Coffee-Derived Polyphenols and Their Roles in Mitigating Factors Affecting Type 2 Diabetes Pathogenesis.Molecules (Basel, Switzerland) · 2024Review
- Association Between the Trajectories of the Atherogenic Index of Plasma and Prediabetes Progression to Diabetes: A Retrospective Cohort Study.Diabetes, metabolic syndrome and obesity : targets and therapy · 2024Article
- PPARs at the crossroads of T cell differentiation and type 1 diabetes.Frontiers in immunology · 2023Review
- SIRT6 regulates SREBP1c-induced glucolipid metabolism in liver and pancreas via the AMPKα-mTORC1 pathway.Laboratory investigation; a journal of technical methods and pathology · 2022Article
- PPARs and the Development of Type 1 Diabetes.PPAR research · 2020Review
- Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimTo investigate whether AMP-activated protein kinase (AMPK) regulates the expression of pancreatic duodenal homeobox-1 (PDX-1), a beta-cell-specific transcription factor and whether PPARalpha/gamma is involved in the regulation of pancreatic beta-cell lines after acute stimulation.
methodsRat insulinoma cell line INS-1 was treated with an activator (AICAR) or inhibitor (Compound C) of AMPK as well as inhibitors of PPARs (MK886 to PPARalpha and BADGE to PPARgamma). The mRNA levels of PDX-1, PPARalpha and PPARgamma were measured using real-time RT-PCR, and Western blotting was used to detect the protein expression of these factors.
resultsActivation of AMPK by AICAR induced significantly increased the expression of PDX-1, and this increase was abrogated when AMPK was inactivated by Compound C. Similarly, the expression of PPARalpha and PPARgamma was also increased by AICAR or decreased by Compound C. However AMPK activation did not increase nuclear PDX-1 protein levels when PPARalpha was inhibited. In contrast, AMPK activation still up-regulated PDX-1 protein levels during PPARgamma inhibition. Additionally, PPARalpha activation induced by fenofibrate significantly enhanced nuclear PDX-1 protein expression.
conclusionAMPK regulates the expression of PDX-1 at both the transcriptional and protein levels, and PPARalpha may be acutely involved in the regulation of INS-1 cells.
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Registered trials
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