Evidence map›Paper›PMID 34556771›Full record

ArticleScientific reports2021

Growth hormone promotes hepatic gluconeogenesis by enhancing BTG2-YY1 signaling pathway.

Jeong-Rang Jo, Seungwon An, Swati Ghosh, Balachandar Nedumaran, Yong Deuk Kim

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.0field-weighted citation impact, top 25% 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

9 citing papers in PubMed, 16 citations in OpenAlex.

  1. Trial
  2. Research progress on BTG2 in non‑tumor diseases (Review).International journal of molecular medicine · 2026
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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

5 authors at 3 institutions in 2 countries.

Jeong-Rang Jo *Research Institute of Aging and Metabolism, Kyungpook National University, Daegu, 41566, Republic of Korea.
Seungwon An *Department of Ophthalmology and Visual Sciences, University of Illinois at Chicago, Chicago, IL, 60612, USA.
Swati GhoshDepartment of Pediatrics, School of Medicine, University of Colorado Anschutz Medical Campus, Aurora, CO, 80045, USA.
Balachandar NedumaranBarbara Davis Center for Diabetes, School of Medicine, University of Colorado Anschutz Medical Campus, Aurora, CO, 80045, USA.
Yong Deuk KimResearch Institute of Aging and Metabolism, Kyungpook National University, Daegu, 41566, Republic of Korea. ydkim94@knu.ac.kr.
Kyungpook National University · KRUniversity of Colorado Anschutz Medical Campus · USUniversity of Illinois Chicago · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Growth hormone (GH) is one of the critical factors in maintaining glucose metabolism. B-cell translocation gene 2 (BTG2) and yin yang 1 (YY1) are key regulators of diverse metabolic processes. In this study, we investigated the link between GH and BTG2-YY1 signaling pathway in glucose metabolism. GH treatment elevated the expression of hepatic Btg2 and Yy1 in primary mouse hepatocytes and mouse livers. Glucose production in primary mouse hepatocytes and serum blood glucose levels were increased during GH exposure. Overexpression of hepatic Btg2 and Yy1 induced key gluconeogenic enzymes phosphoenolpyruvate carboxykinase 1 (PCK1) and glucose-6 phosphatase (G6PC) as well as glucose production in primary mouse hepatocytes, whereas this phenomenon was markedly diminished by knockdown of Btg2 and Yy1. Here, we identified the YY1-binding site on the Pck1 and G6pc gene promoters using reporter assays and point mutation analysis. The regulation of hepatic gluconeogenic genes induced by GH treatment was clearly linked with YY1 recruitment on gluconeogenic gene promoters. Overall, this study demonstrates that BTG2 and YY1 are novel regulators of GH-dependent regulation of hepatic gluconeogenic genes and glucose production. BTG2 and YY1 may be crucial therapeutic targets to intervene in metabolic dysfunction in response to the GH-dependent signaling pathway.

Indexed as

AnimalsCell LineGluconeogenesisGlucoseGlucose-6-PhosphataseGrowth HormoneHepatocytesHumansImmediate-Early ProteinsInjections, IntraperitonealIntracellular Signaling Peptides and ProteinsLiverMaleMiceModels, AnimalPhosphoenolpyruvate Carboxykinase (GTP)Btg2 protein, mouseGlucoseGlucose-6-PhosphataseGrowth HormoneImmediate-Early ProteinsIntracellular Signaling Peptides and ProteinsPck1 protein, mousePhosphoenolpyruvate Carboxykinase (GTP)Tumor Suppressor ProteinsYy1 protein, mouseYY1 Transcription Factor

Identifiers

PMID34556771
PMCPMC8460702
OpenAlexW3201314349

What OpenQuestion holds

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LicenceCC BY
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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.