Evidence map›Paper›PMID 19481557›Full record

ArticlePhysiology & behavior2009

Up-regulation of apolipoprotein E by leptin in the hypothalamus of mice and rats.

Ling Shen, Patrick Tso, David Q-H Wang, Stephen C Woods, W Sean Davidson, Randall Sakai, Min Liu

Open access · greenAbstract read
In one paragraph

Article in Physiology & behavior, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
0.9field-weighted citation impact, top 33% 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

17 citing papers in PubMed, 29 citations in OpenAlex.

  1. Review
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  6. Chronic exposure to methylmercury enhances the anorexigenic effects of leptin in C57BL/6J male mice.Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association · 2021
    Article
  7. Sex and Exposure to Postnatal Chlorpyrifos Influence the Epigenetics of Feeding-Related Genes in a TransgenicInternational journal of environmental research and public health · 2020
    Article
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  10. Review
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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 3 institutions in 1 country.

Ling ShenCincinnati Obesity Research Center, USA; Department of Pathology and Laboratory Medicine, USA.
Patrick Tso
David Q-H Wang
Stephen C Woods
W Sean Davidson
Randall Sakai
Min Liu
Boise Kidney & Hypertension Institute · USBeth Israel Deaconess Medical Center · USUniversity of Cincinnati Medical Center · 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
CHOLESTEROL HOMEOSTASIS IN THE INBRED MOUSE.R01DK054012 · NIDDK · BRIGHAM AND WOMEN'S HOSPITAL · PI WANG, DAVID Q · 1999 to 2008
$2.9M
Regulation of Food Intake and Body Weight by Brain Apo ER01DK070992 · NIDDK · UNIVERSITY OF CINCINNATI · PI LIU, MIN · 2007 to 2011
$1.4M
The Role of Dysfunctional CCK-1R in CholelithogenesisR01DK073917 · NIDDK · SAINT LOUIS UNIVERSITY · PI WANG, DAVID Q · 2008 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 DK17844NIDDK NIH HHS DK54012NIDDK NIH HHS DK63907NIDDK NIH HHS DK70992NIDDK NIH HHS DK73917NIDDK NIH HHS R01 DK017844NIDDK NIH HHS R01 DK054012NIDDK NIH HHS R01 DK063907NIDDK NIH HHS R01 DK070992NIDDK NIH HHS R01 DK073917NIDDK NIH HHS R37 DK017844
6 · The paper itself

Abstract

Apolipoprotein E (apoE) is a satiation factor, playing an important role in the regulation of food intake and body weight. We previously reported that apoE was present in the hypothalamus, but it is unclear which type of the cells in this brain area expressing apoE. In addition, hypothalamic apoE mRNA levels were significantly reduced in both genetically obese ob/ob (leptin deficient) mice and high-fat diet-induced obese (leptin resistant) rats, raising the possibility that deficient leptin signaling might be related to the change in apoE gene expression. In the present studies, using double-staining immunohistochemistry, we demonstrated that apoE is mainly present in astrocytes. To characterize the effect of leptin on apoE gene expression, ob/ob and db/db mice were treated with recombinant mouse leptin (3 microg/g daily, i.p.) or vehicle for 5 days. We found that the increased hypothalamic apoE mRNA levels occurred only in leptin-treated ob/ob, but not in pair-fed ob/ob, or db/db, mice, indicating that leptin up-regulated hypothalamic apoE gene expression depends upon an intact leptin receptor, and this effect is not related to the changes in food intake and body weight. The reduced apoE gene expression caused by fasting, which also results in relatively lower leptin level, is restored by intracerebroventricular administration of leptin. In addition, leptin was significantly less efficacious in apoE KO mice because these animals consumed more food and lost less weight following leptin treatment, compared with wild-type controls. These observations imply that apoE signaling, at least partially, mediates the inhibitory effects of leptin on feeding.

Indexed as

AnimalsApolipoproteins EAstrocytesBody WeightEatingHypothalamusImmunohistochemistryInjections, IntraventricularLeptinMaleMiceMice, Inbred C57BLMice, KnockoutMice, ObeseObesityRatsApolipoproteins ELeptinRNA, Messenger

Identifiers

PMID19481557
PMCPMC2757054
OpenAlexW1995947477

What OpenQuestion holds

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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.