Evidence map›Paper›PMID 26317058›Full record

ArticleAdipocyte

Role of histone deacetylase 9 in regulating adipogenic differentiation and high fat diet-induced metabolic disease.

Tapan K Chatterjee, Joshua E Basford, Kan Hui Yiew, David W Stepp, David Y Hui, Neal L Weintraub

Open access · goldAbstract read
In one paragraph

Article in Adipocyte. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

24 citing papers in PubMed, 38 citations in OpenAlex.

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  17. Epigenetics of metabolic syndrome.Physiological genomics · 2018
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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

6 authors at 4 institutions in 2 countries.

Tapan K ChatterjeeDepartment of Internal Medicine; Vascular Biology Center; Georgia Regents University ; Augusta, GA USA.
Joshua E BasfordDepartment of Pathology; Metabolic Disease Institute; University of Cincinnati ; Cincinnati, OH USA.
Kan Hui YiewDepartment of Pharmacology; Vascular Biology Center; Georgia Regents University ; Augusta, GA USA.
David W SteppDepartment of Physiology; Vascular Biology Center; Georgia Regents University ; Augusta, GA USA.
David Y HuiDepartment of Pathology; Metabolic Disease Institute; University of Cincinnati ; Cincinnati, OH USA.
Neal L WeintraubDepartment of Internal Medicine; Vascular Biology Center; Georgia Regents University ; Augusta, GA USA.
Augusta University · USOncology Hematology Care · USCenter for Vascular Biology Research · USGeorgia Regents Medical Center · US

Funding

LCenter for Clinical and Translational Science and TrainingUL1TR001425 · NCATS · UNIVERSITY OF CINCINNATI · PI HEUBI, JAMES E., KISSELA, BRETT M · 2015 to 2024
$37.5M
Metabolic Determinants of Cardiovascular Dysfunction in ObesityR01HL092446 · NHLBI · AUGUSTA UNIVERSITY · PI FULTON, DAVID J, STEPP, DAVID W · 2009 to 2013
$2.1M
Perivascular adipose tissue and vascular remodelingR01HL112640 · NHLBI · UNIVERSITY OF CINCINNATI · PI WEINTRAUB, NEAL L · 2012 to 2016
$2.1M
NCATS NIH HHS UL1 TR001425NHLBI NIH HHS R01 HL112640
6 · The paper itself

Abstract

Adipose tissue serves as both a storage site for excess calories and as an endocrine organ, secreting hormones such as adiponectin that promote metabolic homeostasis. In obesity, adipose tissue expands primarily by hypertrophy (enlargement of existing adipocytes) rather than hyperplasia (generation of new adipocytes via adipogenic differentiation of preadipocytes). Progressive adipocyte hypertrophy leads to inflammation, insulin resistance, dyslipidemia, and ectopic lipid deposition, the hallmark characteristics of metabolic disease. We demonstrate that during chronic high fat feeding in mice, adipogenic differentiation is impaired due to the actions of histone deacetylase 9 (HDAC9), a member of the class II family of HDACs. Mechanistically, upregulated HDAC9 expression blocks the adipogenic differentiation program during chronic high fat feeding, leading to accumulation of improperly differentiated adipocytes with diminished expression of adiponectin. These adipocytes are inefficient at storing lipid, resulting in ectopic lipid deposition in the liver. HDAC9 gene deletion prevents the detrimental effects of chronic high fat feeding on adipogenic differentiation, increases adiponectin expression, and enhances energy expenditure by promoting beige adipogenesis, thus leading to reduced body mass and improved metabolic homeostasis. HDAC9 is therefore emerging as a critical regulator of adipose tissue health and a novel therapeutic target for obesity-related disease.

Indexed as

adaptive thermogenesisadipogenic differentiationadipose tissue dysfunctionbeige adipocytesectopic lipid accumulationenergy expenditurefibroblast growth factor 21glucose intolerancehigh fat diethistone deacetylase 9insulin resistancemetabolic diseaseobesity

Identifiers

PMID26317058
PMCPMC4550687
OpenAlexW2060189112

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.