Evidence map›Paper›PMID 29398616›Full record

ArticleMolecular metabolism2018

Hypothalamic miR-219 regulates individual metabolic differences in response to diet-induced weight cycling.

Mariana Schroeder, Yonat Drori, Yair J Ben-Efraim, Alon Chen

Open access · goldAbstract read
In one paragraph

Article in Molecular metabolism, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.7field-weighted citation impact, top 35% 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

7 citing papers in PubMed, 11 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

4 authors at 2 institutions in 2 countries.

Mariana SchroederDepartment of Neurobiology, Weizmann Institute of Science, Rehovot, 76100, Israel; Department of Stress Neurobiology and Neurogenetics, Max-Planck Institute of Psychiatry, Munich, 80804, Germany. Electronic address: schatzyo@gmail.com.
Yonat DroriDepartment of Neurobiology, Weizmann Institute of Science, Rehovot, 76100, Israel; Department of Stress Neurobiology and Neurogenetics, Max-Planck Institute of Psychiatry, Munich, 80804, Germany.
Yair J Ben-EfraimDepartment of Neurobiology, Weizmann Institute of Science, Rehovot, 76100, Israel; Department of Stress Neurobiology and Neurogenetics, Max-Planck Institute of Psychiatry, Munich, 80804, Germany.
Alon ChenDepartment of Neurobiology, Weizmann Institute of Science, Rehovot, 76100, Israel; Department of Stress Neurobiology and Neurogenetics, Max-Planck Institute of Psychiatry, Munich, 80804, Germany. Electronic address: alon.chen@weizmann.ac.il.
Max Planck Institute of Neurobiology · DEMax Planck Institute of Psychiatry · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Consumption of a low calorie diet is the most common approach to lose weight. While generally effective at first, it is frequently followed by a relapse where the pre-diet weight is regained, and often exceeded. This pattern of repeated weight loss/regain is referred to as weight cycling and the resulting metabolic response varies greatly between individuals.

objectiveWe attempted to address the issue of individual differences in the response to weight cycling in male mice.

methodsWe first exposed adult wild type mice to repeated cycles of high/low fat food. Next, using a lentiviral approach, we knocked-down or over-expressed miR-219 in the ventromedial hypothalamus (VMH) of an additional mouse cohort and performed a full metabolic assessment.

resultsExposure of wild type males to weight cycling resulted in the division of the cohort into subsets of resistant versus metabolic-syndrome-prone (MS) animals, which differed in their metabolic profile and hypothalamic miR-219 levels. Lentiviral knock-down of miR-219 in the VMH led to exacerbation of metabolic syndrome. In contrast, over-expression of miR-219 resulted in moderation of the metabolic syndrome phenotype.

conclusionsOur results suggest a role for miR-219 in the mediation of the metabolic phenotype resulting from repeated weight cycling.

Indexed as

Weight GainWeight LossAnimalsCaloric RestrictionCell Line, TumorDiet, High-FatFemaleGenetic VariationHumansHypothalamusMaleMetabolic SyndromeMiceMice, Inbred C57BLMice, Inbred ICRMicroRNAsMicroRNAsMIRN219 microRNA, mouseDiabetesHigh fat dietMetabolic syndromemiRNAsVentromedial hypothalamusWeight cycling

Identifiers

PMID29398616
PMCPMC5870106
OpenAlexW2791796044

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.