Evidence map›Paper›PMID 19020660›Full record

ArticlePloS one2008

ApoB100-LDL acts as a metabolic signal from liver to peripheral fat causing inhibition of lipolysis in adipocytes.

Josefin Skogsberg, Andrea Dicker, Mikael Rydén, Gaby Aström, Roland Nilsson, Hasanuzzaman Bhuiyan, Sigurd Vitols, Aline Mairal, Dominique Langin, Peteris Alberts and 5 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
0.6field-weighted citation impact, top 27% 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

18 citing papers in PubMed, 37 citations in OpenAlex.

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  12. An apolipoprotein B100 mimotope prevents obesity in mice.Clinical science (London, England : 1979) · 2016
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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

15 authors at 5 institutions in 2 countries.

Josefin SkogsbergThe Computational Medicine Group, Karolinska Institutet, Karolinska University Hospital, Solna, Stockholm, Sweden. josefin.skogsberg@ki.se
Andrea Dicker
Mikael Rydén
Gaby Aström
Roland Nilsson
Hasanuzzaman Bhuiyan
Sigurd Vitols
Aline Mairal
Dominique Langin
Peteris Alberts
Erik Walum
Jesper Tegnér
Anders Hamsten
Peter Arner
Johan Björkegren
Karolinska University Hospital · SEKarolinska Institutet · SEInserm · FRLinköping University · SESwedish Orphan Biovitrum (Sweden) · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundFree fatty acids released from adipose tissue affect the synthesis of apolipoprotein B-containing lipoproteins and glucose metabolism in the liver. Whether there also exists a reciprocal metabolic arm affecting energy metabolism in white adipose tissue is unknown. METHODS AND

findingsWe investigated the effects of apoB-containing lipoproteins on catecholamine-induced lipolysis in adipocytes from subcutaneous fat cells of obese but otherwise healthy men, fat pads from mice with plasma lipoproteins containing high or intermediate levels of apoB100 or no apoB100, primary cultured adipocytes, and 3T3-L1 cells. In subcutaneous fat cells, the rate of lipolysis was inversely related to plasma apoB levels. In human primary adipocytes, LDL inhibited lipolysis in a concentration-dependent fashion. In contrast, VLDL had no effect. Lipolysis was increased in fat pads from mice lacking plasma apoB100, reduced in apoB100-only mice, and intermediate in wild-type mice. Mice lacking apoB100 also had higher oxygen consumption and lipid oxidation. In 3T3-L1 cells, apoB100-containing lipoproteins inhibited lipolysis in a dose-dependent fashion, but lipoproteins containing apoB48 had no effect. ApoB100-LDL mediated inhibition of lipolysis was abolished in fat pads of mice deficient in the LDL receptor (Ldlr(-/-)Apob(100/100)).

conclusionsOur results show that the binding of apoB100-LDL to adipocytes via the LDL receptor inhibits intracellular noradrenaline-induced lipolysis in adipocytes. Thus, apoB100-LDL is a novel signaling molecule from the liver to peripheral fat deposits that may be an important link between atherogenic dyslipidemias and facets of the metabolic syndrome.

Indexed as

3T3-L1 CellsAdipocytesAdipose Tissue, WhiteAdultAgedAnimalsApolipoprotein B-100GlucoseHumansLipolysisLipoproteins, LDLLiverMaleMetabolic SyndromeMiceMiddle AgedApolipoprotein B-100GlucoseLipoproteins, LDL

Identifiers

PMID19020660
PMCPMC2582480
OpenAlexW2090448497

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.