Evidence map›Paper›PMID 26435324›Full record

ArticleInternational journal of obesity (2005)2016

IL-10 gene transfer upregulates arcuate POMC and ameliorates hyperphagia, obesity and diabetes by substituting for leptin.

M Nakata, S Yamamoto, T Okada, D Gantulga, H Okano, K Ozawa, T Yada

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In one paragraph

Article in International journal of obesity (2005), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing 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

22 citing papers in PubMed, 41 citations in OpenAlex.

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  19. Cigarette Smoking Modulation of Saliva Microbial Composition and Cytokine Levels.International journal of environmental research and public health · 2018
    Article
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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 4 institutions in 1 country.

M NakataDepartment of Physiology, Division of Integrative Physiology, Jichi Medical University School of Medicine, Shimotsuke, Japan.
S YamamotoDepartment of Physiology, Division of Integrative Physiology, Jichi Medical University School of Medicine, Shimotsuke, Japan.
T OkadaDivision of Genetic Therapeutics, Center for Molecular Medicine, Jichi Medical University, Shimotsuke, Japan.
D GantulgaDepartment of Physiology, Division of Integrative Physiology, Jichi Medical University School of Medicine, Shimotsuke, Japan.
H OkanoDepartment of Physiology, Keio University School of Medicine, Tokyo, Japan.
K OzawaDivision of Genetic Therapeutics, Center for Molecular Medicine, Jichi Medical University, Shimotsuke, Japan.
T YadaDepartment of Physiology, Division of Integrative Physiology, Jichi Medical University School of Medicine, Shimotsuke, Japan.
Jichi Medical University · JPKeio University · JPNational Institute for Physiological Sciences · JPNippon Medical School · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundObesity and metabolic syndrome are the major risk factors for cardiovascular disease. Obesity is caused by increased food intake and/or decreased energy expenditure. Leptin potently inhibits food intake and promotes energy expenditure. These effects of leptin involve the activation of proopiomelanocortin (POMC) neurons in the hypothalamus arcuate nucleus (ARC). Disruption of leptin signaling in POMC neuron is considered one of the major causes for obesity.

aimsThe present study aimed to examine whether overexpression of interleukin-10 (IL-10) could substitute for the leptin action and ameliorate obesity in leptin-deficient Lep(ob/ob) mice.

designAdeno-associated virus (AAV) expressing murine IL-10 (AAV-mIL-10) was injected into the skeletal muscle to overexpress IL-10 in mice. These mice were subsequently subjected to analysis of body weight, food intake, glucose metabolism and underlying mechanisms.

resultsIn Lep(ob/ob) mice, AAV-IL-10 ameliorated hyperphagia, obesity, glucose intolerance and insulin resistance, as well as attenuated tumor necrosis factor-α expression. The IL-10 treatment also improved glucose-induced insulin release. Furthermore, IL-10 treatment increased POMC mRNA expression in ARC and phosphorylation of signal transducer and activator of transcription-3 (STAT3) in ARC and white adipose tissue (WAT). In neuron-specific STAT3-null mice that exhibited obesity and hyperphagia, AAV-mIL-10 administration failed to affect food intake, body weight and phosphorylation of STAT3 in WAT.

conclusionsThese results demonstrate that peripheral overexpression of IL-10 induces STAT3 phosphorylation in ARC POMC neurons, and thereby ameliorates hyperphagia and obesity caused by leptin deficiency. IL-10 gene transfer may provide an effective approach for preventing progression of metabolic syndrome due to leptin resistance.

Indexed as

AnimalsArcuate Nucleus of HypothalamusDiabetes MellitusDisease Models, AnimalEnergy MetabolismGene Transfer TechniquesHyperphagiaInterleukin-10LeptinMaleMiceObesityPro-OpiomelanocortinUp-RegulationIL10 protein, mouseInterleukin-10LeptinPro-Opiomelanocortin

Identifiers

PMID26435324
OpenAlexW2261774031

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Registered trials

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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.