RESUMEN
In recent years, a paradigm shift in the bidirectional interactions within the gut-brain axis in normal and pathologic conditions has been evidenced. Although the causal relationship is not completely known, the application of new therapeutic tools such as physical exercise has been described in several studies. However, there are caveats to consider when interpreting the effect of exercise training on the axis. Therefore, an integrative perspective of the gut and the brain's communication pathway is discussed and the role of exercise on influencing this communication highway is explained in this review.
Asunto(s)
Encéfalo/metabolismo , Ejercicio Físico/fisiología , Microbioma Gastrointestinal/fisiología , Mucosa Intestinal/metabolismo , Neurotransmisores/metabolismo , Peso Corporal/fisiología , Motilidad Gastrointestinal/fisiología , Humanos , Mucosa Intestinal/microbiología , PermeabilidadRESUMEN
SCOPE: Gut peptides regulate appetite and adipogenesis. Early weaning (EW) leads to later development of obesity that can be prevented by calcium supplementation. We evaluated gut peptides that may have a role in the establishment of this dysfunction. METHODS AND RESULTS: At birth, lactating Wistar rats were separated in: EW, lactating rats involved with a bandage interrupting the lactation during the last 4 days of standard lactation, and C (control) dams whose pups had free access to milk during throughout lactation. At 120 days old, half of EW group received calcium supplementation (EWCa); EW and C received standard diet. At 21 days old, EW presented higher glucagon-like peptide 1 (GLP-1) in plasma and glucagon-like peptide 1 receptor (GLP1-R) in adipose tissue and hypothalamus, but lower GLP-1 and GLP1-R in the gut. At 180 days old, GLP-1 response to food intake was blunted in EW and restored by calcium. GLP-1 in the gut was lower in EW and its receptor was lower in adipose tissue, and GLP1-R was higher in the gut of calcium EW group. CONCLUSION: Thus, EW had short- and long-term effects upon GLP-1 profile, which may have contributed to obesity development, hyperphagia, and insulin resistance due to its adipogenic and appetite control roles. Calcium supplementation was able to prevent most of the changes in GLP-1 caused by EW.