Evidence mapPaperPMID 39201336Full record

ReviewInternational journal of molecular sciences2024

Adipose Tissue: A Novel Target of the Incretin Axis? A Paradigm Shift in Obesity-Linked Insulin Resistance.

Michelantonio De Fano, Massimo Malara, Cristiana Vermigli, Giuseppe Murdolo

Abstract readReview
In one paragraph

Review in International journal of molecular sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
field-weighted citation impact
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

5 citing papers in PubMed.

  1. Review
  2. Review
  3. Article
  4. Review
  5. Spotlight on the Mechanism of Action of Semaglutide.Current issues in molecular biology · 2024
    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.

Michelantonio De FanoComplex Structure of Endocrinology and Metabolism, Department of Medicine, Azienda Ospedaliera Santa Maria Misericordia, Ospedale di Perugia, 06081 Perugia, Italy.ORCID 0000-0002-2657-5991
Massimo MalaraComplex Structure of Endocrinology and Metabolism, Department of Medicine, Azienda Ospedaliera Santa Maria Misericordia, Ospedale di Perugia, 06081 Perugia, Italy.
Cristiana VermigliComplex Structure of Endocrinology and Metabolism, Department of Medicine, Azienda Ospedaliera Santa Maria Misericordia, Ospedale di Perugia, 06081 Perugia, Italy.ORCID 0000-0003-0005-6541
Giuseppe MurdoloComplex Structure of Endocrinology and Metabolism, Department of Medicine, Azienda Ospedaliera Santa Maria Misericordia, Ospedale di Perugia, 06081 Perugia, Italy.ORCID 0000-0001-5654-1760

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Adipose tissue (AT) represents a plastic organ that can undergo significant remodeling in response to metabolic demands. With its numerous checkpoints, the incretin system seems to play a significant role in controlling glucose homeostasis and energy balance. The importance of the incretin hormones, namely the glucagon-like peptide-1 (GLP-1) and the glucose-dependent insulinotropic peptide (GIP), in controlling the function of adipose cells has been brought to light by recent studies. Notably, a "paradigm shift" in reevaluating the role of the incretin system in AT as a potential target to treat obesity-linked metabolic disorders resulted from the demonstration that a disruption of the GIP and GLP-1 signaling axis in fat is associated with adiposity-induced insulin-resistance (IR) and/or type 2 diabetes mellitus (T2D). We will briefly discuss the (patho)physiological functions of GLP-1 and GIP signaling in AT in this review, emphasizing their potential impacts on lipid storage, adipogenesis, glucose metabolism and inflammation. We will also address the conundrum with the perturbation of the incretin axis in white or brown fat tissue and the emergence of metabolic disorders. In order to reduce or avoid adiposity-related metabolic complications, we will finally go over a potential scientific rationale for suggesting AT as a novel target for GLP-1 and GIP receptor agonists and co-agonists.

Indexed as

Adipose TissueGlucagon-Like Peptide 1IncretinsInsulin ResistanceObesityAnimalsDiabetes Mellitus, Type 2Gastric Inhibitory PolypeptideHumansSignal TransductionGastric Inhibitory PolypeptideGlucagon-Like Peptide 1Incretinsadipose tissue (AT)glucagon-like peptide-1 (GLP-1)glucose-dependent insulinotropic peptide (GIP)inflammationobesitytype 2 diabetes mellitus (T2D)

Identifiers

PMID39201336
PMCPMC11354636

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.