Evidence map›Paper›PMID 18332095›Full record

ArticleDiabetes2008

Central nervous system neuropeptide Y signaling modulates VLDL triglyceride secretion.

John M Stafford, Fang Yu, Richard Printz, Alyssa H Hasty, Larry L Swift, Kevin D Niswender

Open access · bronzeAbstract read
In one paragraph

Article in Diabetes, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
1.9field-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

40 citing papers in PubMed, 81 citations in OpenAlex.

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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.

John M StaffordDivision of Diabetes, Endocrinology, and Metabolism, Department of Internal Medicine, Vanderbilt University School of Medicine, Nashville, Tennessee, USA.
Fang Yu
Richard Printz
Alyssa H Hasty
Larry L Swift
Kevin D Niswender
Vanderbilt University · USVA Tennessee Valley Healthcare System · US

Funding

Vanderbilt Diabetes Research CenterP30DK020593 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI ALVIN C POWERS · 2012 to 2026
$29.3M
TRANSGENIC MOUSE/ ES CELL SHARES RESOURCESP60DK020593 · NIDDK · VANDERBILT UNIVERSITY · PI POWERS, ALVIN C · 1986 to 2011
$28.1M
Vanderbilt Mouse Metabolic Physiology CenterU24DK059637 · NIDDK · VANDERBILT UNIVERSITY · PI WASSERMAN, DAVID H · 2001 to 2015
$14.9M
Vanderbilt Mouse Metabolic Phenotyping CenterU2CDK059637 · NIDDK · VANDERBILT UNIVERSITY · PI WASSERMAN, DAVID H · 2016 to 2021
$6.3M
Brain insulin and leptin resistance in obesityR01DK069927 · NIDDK · VANDERBILT UNIVERSITY · PI NISWENDER, KEVIN D · 2004 to 2008
$1.5M
Leptin and insulin action in the brain;role in obesityK08DK064857 · NIDDK · VANDERBILT UNIVERSITY · PI NISWENDER, KEVIN D · 2003 to 2007
$622k
Role of the CNS in the Metabolic SyndromeF32DK076344 · NIDDK · VANDERBILT UNIVERSITY · PI STAFFORD, JOHN MICHAEL · 2006 to 2008
$82k
NIDDK NIH HHS DK-064857NIDDK NIH HHS DK-069927NIDDK NIH HHS DK-20593NIDDK NIH HHS DK-59637NIDDK NIH HHS F32 DK076344NIDDK NIH HHS F32 DK-076344-0NIDDK NIH HHS K08 DK064857NIDDK NIH HHS P30 DK020593NIDDK NIH HHS P60 DK020593NIDDK NIH HHS R01 DK069927NIDDK NIH HHS U24 DK059637
6 · The paper itself

Abstract

objectiveElevated triglyceride (TG) is the major plasma lipid abnormality in obese and diabetic patients and contributes to cardiovascular morbidity in these disorders. We sought to identify novel mechanisms leading to hypertriglyceridemia. Resistance to negative feedback signals from adipose tissue in key central nervous system (CNS) energy homeostatic circuits contributes to the development of obesity. Because triglycerides both represent the largest energy depot in the body and are elevated in both the plasma and adipose in obesity and diabetes, we hypothesized that the same neural circuits that regulate energy balance also regulate the secretion of TGs into plasma. RESEARCH DESIGN AND

methodsIn normal fasting rats, the TG secretion rate was estimated by serial blood sampling after intravascular tyloxapol pretreatment. Neuropeptide Y (NPY) signaling in the CNS was modulated by intracerebroventricular injection of NPY, receptor antagonist, and receptor agonist.

resultsA single intracerebroventricular injection of NPY increased TG secretion by 2.5-fold in the absence of food intake, and this was determined to be VLDL by fast performance liquid chromatography (FPLC). This effect was recapitulated by activating NPY signaling in downstream neurons with an NPY-Y5 receptor agonist. An NPY-Y1 receptor antagonist decreased the elevated TGs in the form of VLDL secretion rate by 50% compared with vehicle. Increased TG secretion was due to increased secretion of VLDL particles, rather than secretion of larger particles, because apolipoprotein B100 was elevated in FPLC fractions corresponding to VLDL.

conclusionsWe find that a key neuropeptide system involved in energy homeostasis in the CNS exerts control over VLDL-TG secretion into the bloodstream.

Indexed as

Acyl Coenzyme AAnimalsCerebral VentriclesCholesterolGlucagonInjections, IntraventricularInsulinLeptinLipoproteinsLipoproteins, VLDLLiverMaleNeuropeptide YRatsRats, Long-EvansSignal TransductionAcyl Coenzyme ACholesterolGlucagonInsulinLeptinLipoproteinsLipoproteins, VLDLNeuropeptide YTriglyceridesvery low density lipoprotein triglyceride

Identifiers

PMID18332095
PMCPMC3968924
OpenAlexW2152052175

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.