Evidence map›Paper›PMID 32814716›Full record

ArticleJCI insight2020

The impact of antidiabetic treatment on human hypothalamic infundibular neurons and microglia.

Martin Jt Kalsbeek, Samantha Ec Wolff, Nikita L Korpel, Susanne E la Fleur, Johannes A Romijn, Eric Fliers, Andries Kalsbeek, Dick F Swaab, Inge Huitinga, Elly M Hol and 1 more

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In one paragraph

Article in JCI insight, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed, 1 pooled it
1.5field-weighted citation impact, top 21% 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

15 citing papers in PubMed, 1 synthesis or guideline pooled it, 26 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

11 authors at 4 institutions in 1 country.

Martin Jt KalsbeekLaboratory of Endocrinology, and.
Samantha Ec WolffLaboratory of Endocrinology, and.
Nikita L KorpelLaboratory of Endocrinology, and.
Susanne E la FleurLaboratory of Endocrinology, and.
Johannes A RomijnDepartment of Medicine, Amsterdam UMC, University of Amsterdam, Amsterdam, Netherlands.
Eric FliersDepartment of Endocrinology and Metabolism, Amsterdam University Medical Center (UMC), University of Amsterdam, Amsterdam, Netherlands.
Andries KalsbeekLaboratory of Endocrinology, and.
Dick F SwaabNetherlands Institute for Neuroscience, an Institute of the Royal Netherlands Academy of Arts and Sciences, Amsterdam, Netherlands.
Inge HuitingaNetherlands Institute for Neuroscience, an Institute of the Royal Netherlands Academy of Arts and Sciences, Amsterdam, Netherlands.
Elly M HolDepartment of Translational Neuroscience, University Medical Center Utrecht Brain Center, Utrecht University, Utrecht, Netherlands.
Chun-Xia YiLaboratory of Endocrinology, and.
Netherlands Institute for Neuroscience · NLAmsterdam Neuroscience · NLUniversity of Amsterdam · NLUtrecht University · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Animal studies indicate that hypothalamic dysfunction plays a major role in type 2 diabetes mellitus (T2DM) development, and that insulin resistance and inflammation are important mechanisms involved in this disorder. However, it remains unclear how T2DM and antidiabetic treatments affect the human hypothalamus. Here, we characterized the proopiomelanocortin (POMC) immunoreactive (-ir) neurons, the neuropeptide-Y-ir (NPY-ir) neurons, the ionized calcium-binding adapter molecule 1-ir (iba1-ir) microglia, and the transmembrane protein 119-ir (TMEM119-ir) microglia in the infundibular nucleus (IFN) of human postmortem hypothalamus of 32 T2DM subjects with different antidiabetic treatments and 17 matched nondiabetic control subjects. Compared with matched control subjects, T2DM subjects showed a decrease in the number of POMC-ir neurons, but no changes in NPY-ir neurons or microglia. Interestingly, T2DM subjects treated with the antidiabetic drug metformin had fewer NPY-ir neurons and microglia than T2DM subjects not treated with metformin. We found that the number of microglia correlated with the number of NPY-ir neurons, but only in T2DM subjects. These results indicate that different changes in POMC and NPY neurons and microglial cells in the IFN accompany T2DM. In addition, T2DM treatment modality is associated with highly selective changes in hypothalamic neurons and microglial cells.

Indexed as

AgedAged, 80 and overCase-Control StudiesDiabetes Mellitus, Type 2FemaleHumansHypoglycemic AgentsInsulinMaleMembrane ProteinsMetforminMicrogliaNeuronsNeuropeptide YPituitary GlandPro-OpiomelanocortinHypoglycemic AgentsInsulinMembrane ProteinsMetforminNeuropeptide YPro-OpiomelanocortinTmem119 protein, humanDiabetesEndocrinologyInsulinNeuroscienceNPY

Identifiers

PMID32814716
PMCPMC7455135
OpenAlexW3065099489

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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.