Evidence map›Paper›PMID 23990408›Full record

ReviewReviews in endocrine & metabolic disorders2013

Brain regulation of energy balance and body weight.

Liangyou Rui

Abstract readReview
In one paragraph

Review in Reviews in endocrine & metabolic disorders, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
77citing papers in PubMed, 2 pooled it
4.8field-weighted citation impact, top 4% 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

77 citing papers in PubMed, 2 syntheses or guidelines pooled it, 163 citations in OpenAlex.

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  9. Brown adipose tissue inactivation exacerbates alcohol-induced liver steatosis, inflammation, and fibrosis.American journal of physiology. Gastrointestinal and liver physiology · 2026
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17 more citing papers are in PubMed but not listed here.

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

1 author at 1 institution in 1 country.

Liangyou RuiDepartment of Molecular & Integrative Physiology, University of Michigan Medical School, Ann Arbor, MI, 48109-0622, USA, ruily@umich.edu.
University of Michigan–Ann Arbor · US

Funding

Regional Pilot And Feasibility Study Grants ProgramP30DK020572 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Mehboob A Hussain · 2013 to 2026
$24.3M
Role of SH2-B in Glucose MetabolismR01DK065122 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI RUI, LIANGYOU · 2004 to 2012
$2.9M
Transcriptional Regulation of MetabolismR01DK094014 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI RUI, LIANGYOU · 2012 to 2015
$1.5M
Role of inflammation and cellular stress in the pathogenesis of type 2 diabetesR01DK091591 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI RUI, LIANGYOU · 2012 to 2015
$1.5M
NIDDK NIH HHS P30 DK020572NIDDK NIH HHS R01 DK 065122NIDDK NIH HHS R01 DK065122NIDDK NIH HHS R01 DK091591NIDDK NIH HHS R01 DK094014
6 · The paper itself

Abstract

Body weight is determined by a balance between food intake and energy expenditure. Multiple neural circuits in the brain have evolved to process information about food, food-related cues and food consumption to control feeding behavior. Numerous gastrointestinal endocrine cells produce and secrete satiety hormones in response to food consumption and digestion. These hormones suppress hunger and promote satiation and satiety mainly through hindbrain circuits, thus governing meal-by-meal eating behavior. In contrast, the hypothalamus integrates adiposity signals to regulate long-term energy balance and body weight. Distinct hypothalamic areas and various orexigenic and anorexigenic neurons have been identified to homeostatically regulate food intake. The hypothalamic circuits regulate food intake in part by modulating the sensitivity of the hindbrain to short-term satiety hormones. The hedonic and incentive properties of foods and food-related cues are processed by the corticolimbic reward circuits. The mesolimbic dopamine system encodes subjective "liking" and "wanting" of palatable foods, which is subjected to modulation by the hindbrain and the hypothalamic homeostatic circuits and by satiety and adiposity hormones. Satiety and adiposity hormones also promote energy expenditure by stimulating brown adipose tissue (BAT) activity. They stimulate BAT thermogenesis mainly by increasing the sympathetic outflow to BAT. Many defects in satiety and/or adiposity hormone signaling and in the hindbrain and the hypothalamic circuits have been described and are believed to contribute to the pathogenesis of energy imbalance and obesity.

Indexed as

Appetite RegulationBody WeightBrainEnergy MetabolismHomeostasisHumansNerve NetSatiety Response

Identifiers

PMID23990408
PMCPMC3817823
OpenAlexW2090476959

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.