Evidence map›Paper›PMID 25695641›Full record

ArticleThe Biochemical journal2015

Regulation of IGFBP-2 expression during fasting.

Hye Suk Kang, Mi-Young Kim, Seung-Jae Kim, Jae-Ho Lee, Yong-Deuk Kim, Young-Kyo Seo, Jae-Hoon Bae, Goo-Taeg Oh, Dae-Kyu Song, Yong-Ho Ahn and 1 more

Open access · hybridAbstract read
In one paragraph

Article in The Biochemical journal, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed, 1 pooled it
1.6field-weighted citation impact, top 16% 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

11 citing papers in PubMed, 1 synthesis or guideline pooled it, 15 citations in OpenAlex.

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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

11 authors at 4 institutions in 1 country.

Hye Suk Kang*Department of Physiology, Keimyung University School of Medicine, Daegu 704-701, Republic of Korea.
Mi-Young Kim†Department of Biochemistry and Molecular Biology, Yonsei University College of Medicine, Seoul 120-752, Republic of Korea.
Seung-Jae Kim*Department of Physiology, Keimyung University School of Medicine, Daegu 704-701, Republic of Korea.
Jae-Ho Lee*Department of Physiology, Keimyung University School of Medicine, Daegu 704-701, Republic of Korea.
Yong-Deuk Kim*Department of Physiology, Keimyung University School of Medicine, Daegu 704-701, Republic of Korea.
Young-Kyo Seo‡School of Life Sciences, UNIST, Ulsan 689-798, Republic of Korea.
Jae-Hoon Bae*Department of Physiology, Keimyung University School of Medicine, Daegu 704-701, Republic of Korea.
Goo-Taeg Oh§Division of Life and Pharmaceutical Sciences, Ewha Womans University, Seoul 120-750, Republic of Korea.
Dae-Kyu Song*Department of Physiology, Keimyung University School of Medicine, Daegu 704-701, Republic of Korea.
Yong-Ho Ahn†Department of Biochemistry and Molecular Biology, Yonsei University College of Medicine, Seoul 120-752, Republic of Korea.
Seung-Soon Im*Department of Physiology, Keimyung University School of Medicine, Daegu 704-701, Republic of Korea.
Keimyung University · KRYonsei University · KREwha Womans University · KRUlsan National Institute of Science and Technology · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Insulin-like growth factor (IGF)-binding protein-2 (IGFBP-2), one of the most abundant circulating IGFBPs, is known to attenuate the biological action of IGF-1. Although the effect of IGFBP-2 in preventing metabolic disorders is well known, its regulatory mechanism remains unclear. In the present study, we demonstrated the transcriptional regulation of the Igfbp-2 gene by peroxisome-proliferator-activated receptor (PPAR) α in the liver. During fasting, both Igfbp-2 and PPARα expression levels were increased. Wy14643, a selective PPARα agonist, significantly induced Igfbp-2 gene expression in primary cultured hepatocytes. However, Igfbp-2 gene expression in Pparα null mice was not affected by fasting or Wy14643. In addition, through transient transfection and chromatin immunoprecipitation assay in fasted livers, we determined that PPARα bound to the putative PPAR-responsive element between -511 bp and -499 bp on the Igfbp-2 gene promoter, indicating that the Igfbp-2 gene transcription is activated directly by PPARα. To explore the role of PPARα in IGF-1 signalling, we treated primary cultured hepatocytes with Wy14643 and observed a decrease in the number of IGF-1 receptors (IGF-1Rs) and in Akt phosphorylation. No inhibition was observed in the hepatocytes isolated from Pparα null mice. These results suggest that PPARα controls IGF-1 signalling through the up-regulation of hepatic Igfbp-2 transcription during fasting and Wy14643 treatment.

Indexed as

AnimalsCells, CulturedFastingGene Expression RegulationHepatocytesInsulin-Like Growth Factor Binding Protein 2Insulin-Like Growth Factor ILiverMaleMiceMice, Inbred C57BLMice, KnockoutPeroxisome ProliferatorsPhosphorylationPPAR alphaPPAR gammaInsulin-Like Growth Factor Binding Protein 2Insulin-Like Growth Factor IPeroxisome Proliferatorspirinixic acidPPAR alphaPPAR gammaProto-Oncogene Proteins c-aktPyrimidinesRNA, MessengerRosiglitazoneThiazolidinediones

Identifiers

PMID25695641
PMCPMC4403943
OpenAlexW2099419747

What OpenQuestion holds

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Registered trials

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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.