Evidence map›Paper›PMID 40627229›Full record

ReviewCurrent nutrition reports2025

Microbiota-Gut-Brain Axis and Impaired Satiety in Individuals with Obesity: A Potentially Bidirectional Association.

Mariana de Moura E Dias, Madalena Geralda Cupertino Ribeiro, Ana Claudia Pelissari Kravchychyn, Helen Hermana Miranda Hermsdorff

Abstract readReview
PubMed Publisher
In one paragraph

Review in Current nutrition reports, 2025. 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. Review
  4. Article
  5. 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.

Mariana de Moura E DiasLaboratory of Clinical Analysis and Genomics, Department of Nutrition and Health, Universidade Federal de Viçosa, Viçosa, Minas Gerais, 36570-900, Brazil.ORCID http://orcid.org/0000-0003-0822-0721
Madalena Geralda Cupertino RibeiroLaboratory of Clinical Analysis and Genomics, Department of Nutrition and Health, Universidade Federal de Viçosa, Viçosa, Minas Gerais, 36570-900, Brazil.ORCID https://orcid.org/0000-0002-2658-6519
Ana Claudia Pelissari KravchychynLaboratory of Clinical Analysis and Genomics, Department of Nutrition and Health, Universidade Federal de Viçosa, Viçosa, Minas Gerais, 36570-900, Brazil.ORCID https://orcid.org/0000-0002-2919-2806
Helen Hermana Miranda HermsdorffLaboratory of Clinical Analysis and Genomics, Department of Nutrition and Health, Universidade Federal de Viçosa, Viçosa, Minas Gerais, 36570-900, Brazil. helenhermana@ufv.br.ORCID https://orcid.org/0000-0002-4441-6572

Funding

Fundação de Amparo à Pesquisa do Estado de Minas Gerais BPD-00069-22
6 · The paper itself

Abstract

purpose of reviewThis review aimed to discuss the mechanisms of satiety control related to the neuroendocrine pathways and gut microbiota metabolites, especially in the obesity condition. Physiologically, hormones produced in the cells of the gastrointestinal tract and adipocytes provide feedback to the brain to regulate food consumption. In turn, people living with obesity can present resistance to hormones like leptin and insulin and low-grade inflammation, altering their pre-conditioned functions. RECENT

findingsIn obesity, there is an imbalance in gut microbiota composition and low-grade chronic inflammation, which alters satiety control mechanisms, leading to increased intestinal permeability, resistance to leptin and insulin, ghrelin dysfunction, and dysregulation of dopamine, serotonin and neuropeptides (inclusing increased orexigenic NPY, and AgRP). Altogether, these disorders result in excessive food consumption and consequent weight gain, generating a causal bidirectional relationship. Short-chain fatty acids (SCFAs), a recognized microbiota metabolite, interact with enteroendocrine L cells, inducing the production of GLP-2, which contributes to the maintenance of tight junctions between intestinal epithelial cells. Additionally, SCFAs activate receptors such as GPR109A, which increases the expression of proteins responsible for tight junctions, thereby preserving the integrity of the intestinal barrier and controlling its permeability. This receptor also participates in immune responses, favouring the release of interleukin-10 (IL-10), a cytokine with anti-inflammatory effects. Nutritional strategies for the treatment of obesity should be focused not only on reducing calories and consequent adipose tissue but also on modulating neuroendocrine satiety. Foods that modulate the gut microbiota, reducing low-grade chronic inflammation and stimulating the production of intestinal metabolites such as SCFAs, favour satiety control and obesity management not only through the balance of the gut microbiota but also through the activation of intestinal hormones and neuropeptides.

Indexed as

BrainBrain-Gut AxisGastrointestinal MicrobiomeGastrointestinal TractObesitySatiationAnimalsGhrelinHumansInflammationIntestinal Barrier FunctionGhrelinAppetiteInflammationIntestinal hormonesMicrobiotaSatiety

Identifiers

PMID40627229

What Socratic holds

Textmetadata
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.