Evidence map›Paper›PMID 19039651›Full record

ArticleMolecular and cellular biochemistry2009

Peroxisome proliferator-activated receptor-alpha modulates insulin gene transcription factors and inflammation in adipose tissues in mice.

Akadiri Yessoufou, Jean-Marc Atègbo, Eugène Attakpa, Aziz Hichami, Kabirou Moutairou, Karim L Dramane, Naim A Khan

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Article in Molecular and cellular biochemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.2field-weighted citation impact, top 22% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

14 citing papers in PubMed, 35 citations in OpenAlex.

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  11. Opposing actions of Per1 and Cry2 in the regulation of Per1 target gene expression in the liver and kidney.American journal of physiology. Regulatory, integrative and comparative physiology · 2013
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 2 countries.

Akadiri YessoufouLaboratory of Cell Biology and Physiology, Department of Biochemistry and Cellular Biology, Faculty of Sciences and Techniques, Institute of Biomedical and Applied Sciences (ISBA-Cotonou), University of Abomey-Calavi, Cotonou, Benin.
Jean-Marc Atègbo
Eugène Attakpa
Aziz Hichami
Kabirou Moutairou
Karim L Dramane
Naim A Khan
Université d'Abomey-Calavi · BJUniversité de Bourgogne · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We have recently reported that PPAR alpha deficiency leads to hypoglycaemia and hypoinsulinemia in mice (Yessoufou et al. Endocrinology 147:4410-4418, 2006). Besides, these mice exhibited high adiposity with an inflammatory state. We, therefore, assessed, in this study, the effects of PPAR alpha deficiency on the expression of mRNA encoding for the insulin gene transcription factors in pancreatic beta-cells along with those implicated in inflammation in adipose tissues. On fasting, the adult PPAR alpha-null mice were hypoglycemic. Serum insulin concentrations and its pancreatic mRNA transcripts were downregulated in PPAR alpha-null mice, suggesting that PPAR alpha gene deletion contributes to low insulin gene transcription. The PPAR alpha gene deletion downregulates the mRNA expression of insulin gene transcription factors, i.e., Pdx-1, Nkx6.1, and MafA. Besides, the pancreatic function was diminished by PPAR alpha deficiency as PPAR alpha-null mice expressed low pancreatic Glut2 and glucokinase mRNA. PPAR alpha-null mice also expressed high adiponectin and leptin mRNA levels compared to wild type animals. Adipose tissues of PPAR alpha-null mice exhibited upregulation of CD14 and CD68 mRNA, generally expressed by macrophages. PPAR alpha gene deletion downregulates the adipocyte mRNA of certain pro-inflammatory agents, like MCP-1, TNF-alpha, IL-1 beta, IL-6, and RANTES, though pro-inflammatory TLR-2 and TLR-4 mRNAs were upregulated in the adipose tissues. Our results suggest that PPAR alpha deficiency, in mice, is implicated in the modulation of insulin gene transcription and inflammatory status in adipose tissues.

Indexed as

Adipose TissueInsulinAdiponectinAnimalsBlood GlucoseBody WeightFatty AcidsGene Expression RegulationInflammationInsulin-Secreting CellsInterleukin-6LeptinMaleMiceMice, Inbred C57BLMice, KnockoutAdiponectinBlood GlucoseFatty AcidsInsulinInterleukin-6LeptinPPAR alphaRNA, MessengerTlr2 protein, mouseTlr4 protein, mouseToll-Like Receptor 2Toll-Like Receptor 4Transcription FactorsTriglyceridesTumor Necrosis Factor-alpha

Identifiers

PMID19039651
OpenAlexW2037194385

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.