Evidence map›Paper›PMID 21536059›Full record

ArticlePhysiology & behavior2011

Apolipoprotein E reduces food intake via PI3K/Akt signaling pathway in the hypothalamus.

Ling Shen, David Q-H Wang, Patrick Tso, Ronald J Jandacek, Stephen C Woods, Min Liu

Open access · greenAbstract read
In one paragraph

Article in Physiology & behavior, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.3field-weighted citation impact, top 24% 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

16 citing papers in PubMed, 26 citations in OpenAlex.

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  15. Apolipoprotein E does not cross the blood-cerebrospinal fluid barrier, as revealed by an improved technique for sampling CSF from mice.American journal of physiology. Regulatory, integrative and comparative physiology · 2012
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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 2 institutions in 1 country.

Ling ShenCincinnati Obesity Research Center, University of Cincinnati College of Medicine, Cincinnati, OH, United States.
David Q-H Wang
Patrick Tso
Ronald J Jandacek
Stephen C Woods
Min Liu
University of Cincinnati Medical Center · USSaint Louis University · US

Funding

INSULIN AND CNS CONTROL OF BODY WEIGHT AND FOOD INTAKER01DK017844 · NIDDK · UNIVERSITY OF WASHINGTON · PI WOODS, STEPHEN C · 1986 to 2013
$3.8M
Regulation of Food Intake and Body Weight by Brain Apo ER01DK070992 · NIDDK · UNIVERSITY OF CINCINNATI · PI LIU, MIN · 2007 to 2011
$1.4M
Brain Apolipoprotein AIV, Food Intake and ObesityR01DK063907 · NIDDK · UNIVERSITY OF CINCINNATI · PI LIU, MIN · 2003 to 2007
$1.3M
INSULIN AND CNS CONTROL OF BODY WEIGHT AND FOOD INTAKER37DK017844 · NIDDK · UNIVERSITY OF WASHINGTON · PI WOODS, STEPHEN C · 1993 to 2000
$382k
NIDDK NIH HHS DK 17844NIDDK NIH HHS DK63907NIDDK NIH HHS DK70992NIDDK NIH HHS R01 DK017844NIDDK NIH HHS R01 DK063907NIDDK NIH HHS R01 DK070992NIDDK NIH HHS R37 DK017844
6 · The paper itself

Abstract

Apolipoprotein E (apoE) is a satiation factor. While central apoE administration reduces food intake, the specific intracellular signaling mechanisms activated by apoE remain largely unknown. Using primary cultured hypothalamic neurons, we demonstrated that apoE treatment (50 nM) elicited rapid activation of the phosphatidylinositol-3-kinase (PI3K)/Akt signaling cascade. Specifically, apoE induced the phosphorylation of Akt, peaking at 30 min, and the increased phosphorylation of Akt was significantly attenuated after pretreatment with LY294002 (50 μM), an inhibitor of the PI3K signaling pathway. To determine whether the activation of PI3K by apoE is required for the ability of apoE to reduce food intake, LY294002 (1 nmol) was infused into the 3rd-cerebral ventricle before injection of an anorectic dose of apoE. Consistent with our previous report, apoE (4 μg) exerted significant reduction of food intake in the 4-h fasted rats, compared with saline. Pretreatment with LY294002 significantly attenuated the potency of exogenous apoE to induce satiation, while the same dose of PI3K inhibitor by itself caused only a slight non-significant decrease of food intake. These results indicate that the activation of the PI3K/Akt pathway is necessary for the acute effects of apoE on food intake.

Indexed as

AnimalsApolipoproteins ECells, CulturedEatingHypothalamusMaleNeuronsPhosphatidylinositol 3-KinasesPhosphorylationProto-Oncogene Proteins c-aktRatsRats, Long-EvansSignal TransductionApolipoproteins EPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-akt

Identifiers

PMID21536059
PMCPMC3160520
OpenAlexW2071290036

What OpenQuestion holds

Textmetadata
LicenceTDM
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.