Evidence map›Paper›PMID 21750268›Full record

ArticleAmerican journal of physiology. Endocrinology and metabolism2011

Homocysteine suppresses lipolysis in adipocytes by activating the AMPK pathway.

Zhigang Wang, Maria Pini, Tong Yao, Zhanxiang Zhou, Changhao Sun, Giamila Fantuzzi, Zhenyuan Song

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Endocrinology and metabolism, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
1.9field-weighted citation impact, top 15% 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

23 citing papers in PubMed, 1 synthesis or guideline pooled it, 52 citations in OpenAlex.

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  14. Homocysteine regulates fatty acid and lipid metabolism in yeast.The Journal of biological chemistry · 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

7 authors at 4 institutions in 2 countries.

Zhigang WangDepartment of Kinesiology and Nutrition, University of Illinois at Chicago, USA.
Maria Pini
Tong Yao
Zhanxiang Zhou
Changhao Sun
Giamila Fantuzzi
Zhenyuan Song
University of Illinois Chicago · USHarbin Medical University · CNUniversity of Chicago Medical Center · USUniversity of North Carolina at Greensboro · US

Funding

Homocysteine, Adiponectin, and Alcoholic Liver DiseaseR01AA017442 · NIAAA · UNIVERSITY OF ILLINOIS AT CHICAGO · PI SONG, ZHENYUAN · 2009 to 2013
$1.4M
Acute pancreatitis and obesityR01DK083328 · NIDDK · UNIVERSITY OF ILLINOIS AT CHICAGO · PI FANTUZZI, GIAMILA · 2010 to 2013
$1.4M
Mechanisms of Sensitization to TNF hepatotoxicity in ALDK01AA015344 · NIAAA · UNIVERSITY OF LOUISVILLE · PI SONG, ZHENYUAN · 2005 to 2009
$526k
NIAAA NIH HHS K01-AA-015344NIAAA NIH HHS R01-AA-017442NIDDK NIH HHS R01 DK083328
6 · The paper itself

Abstract

Hyperhomocysteinemia (HHcy) is an independent risk factor for coronary artery disease. Emerging evidence suggests that HHcy is also associated with adipocyte tissue dysfunction. One of the principal functions of adipose tissue is to provide energy substrate via lipolysis. In the present study, we investigated the effects of homocysteine (Hcy) on lipolysis in adipocytes. We found that Hcy inhibited release of glycerol and fatty acids, two typical indicators of the lipolytic response, in primary adipocytes and fully differentiated 3T3-L1 adipocytes in a dose-dependent manner under both basal and isoproterenol-stimulated conditions. In differentiated 3T3-L1 adipocytes, decreased glycerol and free fatty acid (FFA) release was associated with elevation of intracellular TG content. Further studies showed that Hcy-mediated antilipolytic responses were independent of the cyclic AMP-PKA and MEK-ERK1/2 pathways. However, Hcy increased phosphorylation levels of AMP-activated protein kinase (AMPK) and its downstream enzyme acetyl-CoA carboxylase. Compound C, an AMPK inhibitor, abolished Hcy-induced reduction of glycerol and FFA release under both basal and isoproterenol-stimulated conditions. Furthermore, AMPKα1 siRNA reversed Hcy-inhibited glycerol release. Supplementation of exogenous Hcy in the diet for 2 wk lowered circulating glycerol and FFA levels. Moreover, Hcy supplementation was associated with elevated leptin levels and reduced adiponectin levels in plasma. These results show that Hcy inhibits lipolysis through a pathway that involves AMPK activation.

Indexed as

3T3-L1 CellsAcetyl-CoA CarboxylaseAdenylate KinaseAdipocytesAnimalsCells, CulturedCyclic AMPHomocysteineLipolysisMicePhosphorylationSignal TransductionAcetyl-CoA CarboxylaseAdenylate KinaseCyclic AMPHomocysteine

Identifiers

PMID21750268
PMCPMC3191546
OpenAlexW2124189385

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.