Evidence map›Paper›PMID 27545894›Full record

ArticleCell reports2016

KLF15 Enables Rapid Switching between Lipogenesis and Gluconeogenesis during Fasting.

Yoshinori Takeuchi, Naoya Yahagi, Yuichi Aita, Yuki Murayama, Yoshikazu Sawada, Xiaoying Piao, Naoki Toya, Yukari Oya, Akito Shikama, Ayako Takarada and 20 more

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
9.7field-weighted citation impact, top 1% 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

49 citing papers in PubMed, 94 citations in OpenAlex.

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  19. SREBP1 regulatesMolecular therapy. Nucleic acids · 2022
    Article
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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

30 authors at 2 institutions in 1 country.

Yoshinori TakeuchiNutrigenomics Research Group, Faculty of Medicine, University of Tsukuba, Ibaraki 305-8575, Japan.
Naoya YahagiNutrigenomics Research Group, Faculty of Medicine, University of Tsukuba, Ibaraki 305-8575, Japan. Electronic address: nyahagi-tky@umin.ac.jp.
Yuichi AitaNutrigenomics Research Group, Faculty of Medicine, University of Tsukuba, Ibaraki 305-8575, Japan.
Yuki MurayamaNutrigenomics Research Group, Faculty of Medicine, University of Tsukuba, Ibaraki 305-8575, Japan.
Yoshikazu SawadaNutrigenomics Research Group, Faculty of Medicine, University of Tsukuba, Ibaraki 305-8575, Japan.
Xiaoying PiaoNutrigenomics Research Group, Faculty of Medicine, University of Tsukuba, Ibaraki 305-8575, Japan.
Naoki ToyaNutrigenomics Research Group, Faculty of Medicine, University of Tsukuba, Ibaraki 305-8575, Japan.
Yukari OyaNutrigenomics Research Group, Faculty of Medicine, University of Tsukuba, Ibaraki 305-8575, Japan.
Akito ShikamaNutrigenomics Research Group, Faculty of Medicine, University of Tsukuba, Ibaraki 305-8575, Japan.
Ayako TakaradaNutrigenomics Research Group, Faculty of Medicine, University of Tsukuba, Ibaraki 305-8575, Japan.
Yukari MasudaNutrigenomics Research Group, Faculty of Medicine, University of Tsukuba, Ibaraki 305-8575, Japan.
Makiko NishiNutrigenomics Research Group, Faculty of Medicine, University of Tsukuba, Ibaraki 305-8575, Japan.
Midori KubotaNutrigenomics Research Group, Faculty of Medicine, University of Tsukuba, Ibaraki 305-8575, Japan.
Yoshihiko IzumidaNutrigenomics Research Group, Faculty of Medicine, University of Tsukuba, Ibaraki 305-8575, Japan.
Takashi YamamotoDepartment of Internal Medicine (Endocrinology and Metabolism), Faculty of Medicine, University of Tsukuba, Ibaraki 305-8575, Japan.
Motohiro SekiyaDepartment of Internal Medicine (Endocrinology and Metabolism), Faculty of Medicine, University of Tsukuba, Ibaraki 305-8575, Japan.
Takashi MatsuzakaDepartment of Internal Medicine (Endocrinology and Metabolism), Faculty of Medicine, University of Tsukuba, Ibaraki 305-8575, Japan.
Yoshimi NakagawaDepartment of Internal Medicine (Endocrinology and Metabolism), Faculty of Medicine, University of Tsukuba, Ibaraki 305-8575, Japan.
Osamu UrayamaDepartment of Internal Medicine (Endocrinology and Metabolism), Faculty of Medicine, University of Tsukuba, Ibaraki 305-8575, Japan.
Yasushi KawakamiDepartment of Internal Medicine (Endocrinology and Metabolism), Faculty of Medicine, University of Tsukuba, Ibaraki 305-8575, Japan.
Yoko IizukaDepartment of Internal Medicine, Graduate School of Medicine, University of Tokyo, Tokyo 113-8655, Japan.
Takanari GotodaDepartment of Internal Medicine, Graduate School of Medicine, University of Tokyo, Tokyo 113-8655, Japan.
Keiji ItakaCenter for Disease Biology and Integrative Medicine, Graduate School of Medicine, University of Tokyo, Tokyo 113-8655, Japan.
Kazunori KataokaCenter for Disease Biology and Integrative Medicine, Graduate School of Medicine, University of Tokyo, Tokyo 113-8655, Japan.
Ryozo NagaiDepartment of Internal Medicine, Graduate School of Medicine, University of Tokyo, Tokyo 113-8655, Japan.
Takashi KadowakiDepartment of Internal Medicine, Graduate School of Medicine, University of Tokyo, Tokyo 113-8655, Japan.
Nobuhiro YamadaDepartment of Internal Medicine (Endocrinology and Metabolism), Faculty of Medicine, University of Tsukuba, Ibaraki 305-8575, Japan.
Yuan LuCase Cardiovascular Research Institute, Cleveland, OH 44106, USA.
Mukesh K JainCase Cardiovascular Research Institute, Cleveland, OH 44106, USA.
Hitoshi ShimanoDepartment of Internal Medicine (Endocrinology and Metabolism), Faculty of Medicine, University of Tsukuba, Ibaraki 305-8575, Japan.
University of Tsukuba · JPThe University of Tokyo · JP

Funding

KLF15 in Cardiac MetabolismR01HL119195 · NHLBI · CASE WESTERN RESERVE UNIVERSITY · PI JAIN, MUKESH KUMAR · 2014 to 2017
$1.2M
NHLBI NIH HHS R01 HL119195
6 · The paper itself

Abstract

Hepatic lipogenesis is nutritionally regulated (i.e., downregulated during fasting and upregulated during the postprandial state) as an adaptation to the nutritional environment. While alterations in the expression level of the transcription factor SREBP-1c are known to be critical for nutritionally regulated lipogenesis, upstream mechanisms governing Srebf1 expression remain unclear. Here, we show that the fasting-induced transcription factor KLF15, a key regulator of gluconeogenesis, forms a complex with LXR/RXR, specifically on the Srebf1 promoter. This complex recruits the corepressor RIP140 instead of the coactivator SRC1, resulting in reduced Srebf1 and thus downstream lipogenic enzyme expression during the early and euglycemic period of fasting prior to hypoglycemia and PKA activation. Through this mechanism, KLF15 overexpression specifically ameliorates hypertriglyceridemia without affecting LXR-mediated cholesterol metabolism. These findings reveal a key molecular link between glucose and lipid metabolism and have therapeutic implications for the treatment of hyperlipidemia.

Indexed as

GenomeAnimalsCyclic AMP-Dependent Protein KinasesDNA-Binding ProteinsFastingGenes, ReporterGluconeogenesisHepatocytesKruppel-Like Transcription FactorsLipogenesisLiverLiver X ReceptorsLuciferasesMaleMiceMice, Inbred ICRCyclic AMP-Dependent Protein KinasesDNA-Binding ProteinsKlf15 protein, mouseKruppel-Like Transcription FactorsLiver X ReceptorsLuciferasesNuclear Receptor Co-Repressor 1Retinoid X ReceptorsSrebf1 protein, mouseSterol Regulatory Element Binding Protein 1Transcription Factors

Identifiers

PMID27545894
PMCPMC5031553
OpenAlexW2515431384

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.