Evidence map›Paper›PMID 33547367›Full record

ArticleScientific reports2021

Domeless receptor loss in fat body tissue reverts insulin resistance induced by a high-sugar diet in Drosophila melanogaster.

Fernanda Lourido, Daniela Quenti, Daniela Salgado-Canales, Nicolás Tobar

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
3.8field-weighted citation impact, top 6% 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

24 citing papers in PubMed, 47 citations in OpenAlex.

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  2. Scientifica · 2026
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  15. The Intestinal Immune Defense System in Insects.International journal of molecular sciences · 2022
    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

4 authors at 1 institution in 1 country.

Fernanda LouridoCellular Biology Laboratory, Institute of Nutrition and Food Technology (INTA), University of Chile, Av. El Líbano, 5524, Macul, Santiago, Chile.
Daniela QuentiCellular Biology Laboratory, Institute of Nutrition and Food Technology (INTA), University of Chile, Av. El Líbano, 5524, Macul, Santiago, Chile.
Daniela Salgado-CanalesCellular Biology Laboratory, Institute of Nutrition and Food Technology (INTA), University of Chile, Av. El Líbano, 5524, Macul, Santiago, Chile.
Nicolás TobarCellular Biology Laboratory, Institute of Nutrition and Food Technology (INTA), University of Chile, Av. El Líbano, 5524, Macul, Santiago, Chile. ntobar@inta.uchile.cl.
University of Chile · CL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Insulin resistance is a hallmark of type 2 diabetes resulting from the confluence of several factors, including genetic susceptibility, inflammation, and diet. Under this pathophysiological condition, the dysfunction of the adipose tissue triggered by the excess caloric supply promotes the loss of sensitivity to insulin at the local and peripheral level, a process in which different signaling pathways are involved that are part of the metabolic response to the diet. Besides, the dysregulation of insulin signaling is strongly associated with inflammatory processes in which the JAK/STAT pathway plays a central role. To better understand the role of JAK/STAT signaling in the development of insulin resistance, we used a simple organism, Drosophila melanogaster, as a type 2 diabetes model generated by the consumption of a high-sugar diet. In this model, we studied the effects of inhibiting the expression of the JAK/STAT pathway receptor Domeless, in fat body, on adipose metabolism and glycemic control. Our results show that the Domeless receptor loss in fat body cells reverses both hyperglycemia and the increase in the expression of the insulin resistance marker Nlaz, observed in larvae fed a high sugar diet. This effect is consistent with a significant reduction in Dilp2 mRNA expression and an increase in body weight compared to wild-type flies fed high sugar diets. Additionally, the loss of Domeless reduced the accumulation of triglycerides in the fat body cells of larvae fed HSD and also significantly increased the lifespan of adult flies. Taken together, our results show that the loss of Domeless in the fat body reverses at least in part the dysmetabolism induced by a high sugar diet in a Drosophila type 2 diabetes model.

Indexed as

Insulin ResistanceAnimalsDiabetes Mellitus, Type 2Diet, Carbohydrate LoadingDisease Models, AnimalDrosophila melanogasterDrosophila ProteinsFat BodyGene DeletionInsulinReceptors, Interleukindome protein, DrosophilaDrosophila ProteinsInsulinReceptors, Interleukin

Identifiers

PMID33547367
PMCPMC7864986
OpenAlexW3127389595

What OpenQuestion holds

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LicenceCC BY
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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.