Scholarlink

Purpose of Review <p>This 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.</p> Recent Findings <p>In 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.</p> Summary <p>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.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

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

  • 期刊论文

  • 发表日期：

    2025年7月8日

查看全文
  • Mariana de Moura e Dias,
  • Madalena Geralda Cupertino Ribeiro,
  • Ana Claudia Pelissari Kravchychyn,
  • Helen Hermana Miranda Hermsdorff

摘要

Purpose of Review

This 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 Findings

In 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.

Summary

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.