Evidence map›Paper›PMID 35386592›Full record

ArticleFrontiers in neuroscience2022

Hypothalamic Nesfatin-1 Resistance May Underlie the Development of Type 2 Diabetes Mellitus in Maternally Undernourished Non-obese Rats.

Máté Durst, Katalin Könczöl, Klementina Ocskay, Klaudia Sípos, Péter Várnai, Anett Szilvásy-Szabó, Csaba Fekete, Zsuzsanna E Tóth

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In one paragraph

Article in Frontiers in neuroscience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.6field-weighted citation impact, top 40% 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

6 citing papers in PubMed, 7 citations in OpenAlex.

  1. 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

8 authors at 2 institutions in 1 country.

Máté DurstLaboratory of Neuroendocrinology and in situ Hybridization, Department of Anatomy, Histology and Embryology, Semmelweis University, Budapest, Hungary.
Katalin KönczölLaboratory of Neuroendocrinology and in situ Hybridization, Department of Anatomy, Histology and Embryology, Semmelweis University, Budapest, Hungary.
Klementina OcskayLaboratory of Neuroendocrinology and in situ Hybridization, Department of Anatomy, Histology and Embryology, Semmelweis University, Budapest, Hungary.
Klaudia SíposLaboratory of Neuroendocrinology and in situ Hybridization, Department of Anatomy, Histology and Embryology, Semmelweis University, Budapest, Hungary.
Péter VárnaiDepartment of Physiology, Semmelweis University, Budapest, Hungary.
Anett Szilvásy-SzabóLaboratory of Integrative Neuroendocrinology, Institute of Experimental Medicine, Budapest, Hungary.
Csaba FeketeLaboratory of Integrative Neuroendocrinology, Institute of Experimental Medicine, Budapest, Hungary.
Zsuzsanna E TóthLaboratory of Neuroendocrinology and in situ Hybridization, Department of Anatomy, Histology and Embryology, Semmelweis University, Budapest, Hungary.
Semmelweis University · HUHUN-REN Institute of Experimental Medicine · HU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Intrauterine growth retardation (IUGR) poses a high risk for developing late-onset, non-obese type 2 diabetes (T2DM). The exact mechanism underlying this phenomenon is unknown, although the contribution of the central nervous system is recognized. The main hypothalamic nuclei involved in the homeostatic regulation express nesfatin-1, an anorexigenic neuropeptide and identified regulator of blood glucose level. Using intrauterine protein restricted rat model (PR) of IUGR, we investigated, whether IUGR alters the function of nesfatin-1. We show that PR rats develop fat preference and impaired glucose homeostasis by adulthood, while the body composition and caloric intake of normal nourished (NN) and PR rats are similar. Plasma nesfatin-1 levels are unaffected by IUGR in both neonates and adults, but pro-nesfatin-1 mRNA expression is upregulated in the hypothalamus of adult PR animals. We find that centrally injected nesfatin-1 inhibits the fasting induced neuronal activation in the hypothalamic arcuate nucleus in adult NN rats. This effect of nesfatin-1 is not seen in PR rats. The anorexigenic effect of centrally injected nesfatin-1 is also reduced in adult PR rats. Moreover, chronic central nesfatin-1 administration improves the glucose tolerance and insulin sensitivity in NN rats but not in PR animals. Birth dating of nesfatin-1 cells by bromodeoxyuridine (BrDU) reveals that formation of nesfatin-1 cells in the hypothalamus of PR rats is disturbed. Our results suggest that adult PR rats acquire hypothalamic nesfatin-1-resistance, probably due to the altered development of the hypothalamic nesfatin-1 cells. Hypothalamic nesfatin-1-resistance, in turn, may contribute to the development of non-obese type T2DM.

Indexed as

arcuate nucleuscFosIP-GTTIP-ITTnesfatin-1neuronal birth dating

Identifiers

PMID35386592
PMCPMC8978526
OpenAlexW4220869116

What OpenQuestion holds

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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.