Evidence map›Paper›PMID 20881243›Full record

ArticleEndocrinology2010

Hypothalamic responses to fasting indicate metabolic reprogramming away from glycolysis toward lipid oxidation.

Michal M Poplawski, Jason W Mastaitis, Xue-Jun Yang, Charles V Mobbs

Open access · bronzeAbstract read
In one paragraph

Article in Endocrinology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.1field-weighted citation impact, top 14% 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

30 citing papers in PubMed, 49 citations in OpenAlex.

  1. Article
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  6. Thyroid hormone receptor phosphorylation regulates acute fasting-induced suppression of the hypothalamic-pituitary-thyroid axis.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  7. Review
  8. Physiological Effect of Ghrelin on Body Systems.International journal of endocrinology · 2020
    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

4 authors at 2 institutions in 1 country.

Michal M PoplawskiFishberg Center for Neurobiology, Mount Sinai School of Medicine, New York, New York 10029, USA.
Jason W Mastaitis
Xue-Jun Yang
Charles V Mobbs
Icahn School of Medicine at Mount Sinai · USYale University · US

Funding

Hypothalamic glucokinase in obesity and diabetesR56DK072033 · NIDDK · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI MOBBS, CHARLES V · 2009 to 2010
$509k
NIDDK NIH HHS 1R56DK072033-01A1NIDDK NIH HHS R56 DK072033
6 · The paper itself

Abstract

Nutrient-sensitive hypothalamic neurons regulate energy balance and glucose homeostasis, but the molecular mechanisms mediating hypothalamic responses to nutritional state remain incompletely characterized. To address these mechanisms, the present studies used quantitative PCR to characterize the expression of a panel of genes the hypothalamic expression by nutritional status of which had been suggested by DNA microarray studies. Although these genes regulate a variety of function, the most prominent set regulate intermediary metabolism, and the overall pattern clearly indicated that a 48-h fast produced a metabolic reprogramming away from glucose metabolism and toward the utilization of alternative fuels, particularly lipid metabolism. This general reprogramming of intermediary metabolism by fasting was observed both in cortex and hypothalamus but most prominently in hypothalamus. The effect of fasting on the expression of these genes may be mediated by reduction in plasma glucose or glucose metabolism, rather than leptin, because they were generally recapitulated by hypoglycemia even in the presence of elevated insulin and in vitro by low glucose but were not recapitulated in ob/ob mice. These studies suggest that fasting reduces glucose metabolism and thus minimizes the production of hypothalamic malonyl-coenzyme A. However, because the reprogramming of glucose metabolism by fasting was also observed in cortex, this apparent substrate competition may mediate more general responses to nutritional deprivation, including those responsible for the protective effects of dietary restriction. The present studies also provide a large panel of novel glucose-regulated genes that can be used as markers of glucose action to address mechanisms mediating hypothalamic responses to nutritional state.

Indexed as

Analysis of VarianceAnimalsCerebral CortexFastingGene ExpressionGlycolysisHypothalamusInsulinLeptinLipid MetabolismMaleMiceNeuronsNutritional StatusReverse Transcriptase Polymerase Chain ReactionRNA, MessengerInsulinLeptinRNA, Messenger

Identifiers

PMID20881243
PMCPMC2954726
OpenAlexW2027867105

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.