Evidence map›Paper›PMID 23159624›Full record

ArticleBiochemical and biophysical research communications2013

Insulin suppression of apolipoprotein B in McArdle RH7777 cells involves increased sortilin 1 interaction and lysosomal targeting.

Jeffrey M Chamberlain, Colleen O'Dell, Charles E Sparks, Janet D Sparks

Open access · greenAbstract read
In one paragraph

Article in Biochemical and biophysical research communications, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.0field-weighted citation impact, top 16% 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

22 citing papers in PubMed, 44 citations in OpenAlex.

  1. Molecular Regulation and Therapeutic Targeting of VLDL Production in Cardiometabolic Disease.Cellular and molecular gastroenterology and hepatology · 2025
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  14. Sortilin facilitates VLDL-B100 secretion by insulin sensitive McArdle RH7777 cells.Biochemical and biophysical research communications · 2016
    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

4 authors at 1 institution in 1 country.

Jeffrey M ChamberlainDepartment of Pathology & Laboratory Medicine, University of Rochester School of Medicine & Dentistry, Box 626, 601 Elmwood Avenue, Rochester, NY 14642, USA.
Colleen O'Dell
Charles E Sparks
Janet D Sparks
University of Rochester · US

Funding

Insulin regulated hepatic apo B lipoprotein biogenesisR01DK050376 · NIDDK · UNIVERSITY OF ROCHESTER · PI SPARKS, JANET DEHOFF · 1995 to 2005
$1.3M
Hepatic Steatosis Modulation by Apo B Gene TranscriptionR01DK078131 · NIDDK · UNIVERSITY OF ROCHESTER · PI SPARKS, JANET DEHOFF · 2008 to 2010
$883k
Postprandial insulin regulation of B100 and importance to VLDL1 secretionR01DK100163 · NIDDK · UNIVERSITY OF ROCHESTER · PI SPARKS, JANET DEHOFF · 2014 to 2015
$614k
NIDDK NIH HHS R01 DK050376NIDDK NIH HHS R01 DK078131NIDDK NIH HHS R01 DK100163
6 · The paper itself

Abstract

Insulin suppresses secretion of very low density lipoprotein (VLDL) apolipoprotein (apo) B in primary rodent hepatocytes (RH) by favoring the degradation of B100, the larger form of apo B, through post-endoplasmic reticulum proteolysis. Sortilin 1 (sort1), a multi-ligand sorting receptor, has been proposed as a mediator of lysosomal B100 degradation by directing B100 in pre-VLDL to lysosomes rather than allowing maturation to VLDL and secretion. The purpose of our studies was to investigate the role of sort1 in insulin-dependent degradation of apo B. Using liver derived McArdle RH7777 (McA) cells, we demonstrate that insulin suppresses VLDL B100 secretion via a phosphatidylinositide 3-kinase (PI3K) dependent process that is inhibitable by wortmannin in a fashion similar to RH. Using McA cells and in situ cross-linking, we demonstrate that insulin acutely (30min) stimulates the interaction of B100 with sort1. The insulin-induced interaction of sort1-B100 is markedly enhanced when lysosomal degradation is inhibited by Bafilomycin A1 (BafA1), an inhibitor of lysosomal acidification. As BafA1 also prevents insulin suppressive effects on apo B secretion, our results suggest that sort1-B100 interaction stimulated by insulin transiently accumulates with BafA1 and favors B100 secretion by default.

Indexed as

Adaptor Proteins, Vesicular TransportAnimalsApolipoproteins BCell LineHepatocytesInsulinLipoproteins, VLDLLysosomesMacrolidesRatsSortilinAdaptor Proteins, Vesicular TransportApolipoproteins Bbafilomycin A1InsulinLipoproteins, VLDLMacrolidesSortilin

Identifiers

PMID23159624
PMCPMC3544973
OpenAlexW1973925201

What OpenQuestion holds

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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.