Evidence map›Paper›PMID 32392909›Full record

ReviewMolecules and cells2020

Cellular Contributors to Hypothalamic Inflammation in Obesity.

Chan Hee Lee, Kyoungho Suk, Rina Yu, Min-Seon Kim

Open access · greenAbstract readReview
In one paragraph

Review in Molecules and cells, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed, 1 pooled it
2.4field-weighted citation impact, top 11% 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

39 citing papers in PubMed, 1 synthesis or guideline pooled it, 53 citations in OpenAlex.

  1. Pooled it
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  16. Review
  17. Effect of ProbioticNutrients · 2024
    Article
  18. Article
  19. Hypothalamic astrocyte NADNature communications · 2024
    Article
  20. Review
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 1 institution in 1 country.

Chan Hee LeeAsan Institute for Life Sciences, Asan Medical Center, University of Ulsan College of Medicine, Seoul 05505, Korea.ORCID https://orcid.org/0000-0001-8791-817X
Kyoungho SukDepartment of Pharmacology, School of Medicine, Kyungpook National University College of Medicine, Daegu 41944, Korea.ORCID https://orcid.org/0000-0002-9555-4203
Rina YuDepartment of Food Science and Nutrition, University of Ulsan, Ulsan 44610, Korea.ORCID https://orcid.org/0000-0002-1965-3891
Min-Seon KimAsan Institute for Life Sciences, Asan Medical Center, University of Ulsan College of Medicine, Seoul 05505, Korea.ORCID https://orcid.org/0000-0002-4881-0390
University of Ulsan · KR

Funding

AMERICAN IMMUNIZATION REGISTRY ASSOC (AIRA) STANDARDS SUPPORT & DEV FOR IMMUNIZATION INFORMATION SYSTEMS TO INCREASE ADHERENCE TO NATL STANDARDSH23IP000855 · IP · AMERICAN IMMUNIZATION REGISTRY ASSN · PI COYLE, REBECCA · 2014 to 2015
$2.0M
NCIRD CDC HHS H23 IP000855
6 · The paper itself

Abstract

The hypothalamus is a crucial organ for the maintenance of appropriate body fat storage. Neurons in the hypothalamic arcuate nucleus (ARH) detect energy shortage or surplus via the circulating concentrations of metabolic hormones and nutrients, and then coordinate energy intake and expenditure to maintain energy homeostasis. Malfunction or loss of hypothalamic ARH neurons results in obesity. Accumulated evidence suggests that hypothalamic inflammation is a key pathological mechanism that links chronic overconsumption of a high-fat diet (HFD) with the development of obesity and related metabolic complications. Interestingly, overnutrition-induced hypothalamic inflammation occurs specifically in the ARH, where microglia initiate an inflammatory response by releasing proinflammatory cytokines and chemokines in response to excessive fatty acid flux. Upon more prolonged HFD consumption, astrocytes and perivascular macrophages become involved and sustain hypothalamic inflammation. ARH neurons are victims of hypothalamic inflammation, but they may actively participate in hypothalamic inflammation by sending quiescence or stress signals to surrounding glia. In this mini-review, we describe the current state of knowledge regarding the contributions of neurons and glia, and their interactions, to HFD-induced hypothalamic inflammation.

Indexed as

Adipose TissueAnimalsCytokinesDiet, High-FatEnergy MetabolismHumansHypothalamusImmunity, CellularInflammationMacrophagesMicrogliaNeurogenic InflammationNeuronsObesityCytokinesgliahypothalamusinflammationneuronsobesity

Identifiers

PMID32392909
PMCPMC7264480
OpenAlexW3028327162

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.