Obesity and polycystic ovary syndrome influence on intestinal permeability at fasting, and modify the effect of diverse macronutrients on the gut barrier

• Published in: Food research international 2024-06, Vol.186, p.114338-114338, Article 114338
• Main Authors: Martínez-García, M.Ángeles, Quintero-Tobar, Alejandra, de Lope Quiñones, Sara, Insenser, María, Fernández-Durán, Elena, Escobar-Morreale, Héctor Francisco, Luque-Ramírez, Manuel
• Format: Article
• Language: English
• Subjects: Acute-Phase Proteins - metabolism; Adult; Biomarkers - blood; Carrier Proteins; Dietary Fats; Endotoxemia; Fasting - blood; Female; Gastrointestinal Microbiome; Glucagon-Like Peptide 2 - blood; Glucose - metabolism; Haptoglobins - metabolism; Humans; Hyperandrogenism; Intestinal Barrier Function; Intestinal Mucosa - metabolism; Intestinal permeability; Lipopolysaccharide Receptors - blood; Macronutrients; Male; Membrane Glycoproteins - blood; Membrane Glycoproteins - metabolism; Nutrients; Obesity; Permeability; Polycystic Ovary Syndrome - metabolism; Postprandial response; Protein Precursors; Young Adult
• ISSN: 0963-9969; 1873-7145
• DOI: 10.1016/j.foodres.2024.114338

[Display omitted] •Postprandial intestinal permeability (IP) is distinctly influenced by macronutrients.•Lipids and proteins exert the most unfavorable and favorable effects, respectively.•Obesity markedly disturbs fasting and postprandial IP biomarkers.•Sex and polycystic ovary syndrome (PCOS) exert a mild influence on IP.•Interactions between sex hormones and obesity may lead to impaired IP in PCOS women. Women with the extremely prevalent polycystic ovary syndromegather multiple cardiovascular risk factors and chronic subclinical inflammation. Interactions between diet, adiposity, and gut microbiota modulate intestinal permeabilityand bacterial product translocation, and may contribute to the chronic inflammation process associated with the polycystic ovary syndrome. In the present study, we aimed to address the effects of obesity, functional hyperandrogenism, and diverse oral macronutrients on intestinal permeabilityby measuring circulating markers of gut barrier dysfunction and endotoxemia. Participants included 17 non-hyperandrogenic control women, 17 women with polycystic ovary syndrome, and 19 men that were submitted to glucose, lipid, and protein oral loads. Lipopolysaccharide-binding protein, plasma soluble CD14, succinate, zonulin family peptide, and glucagon-like peptide-2 were determined at fasting and after oral challenges. Macronutrient challenges induced diverse changes on circulating intestinal permeabilitybiomarkers in the acute postprancial period, with lipids and proteins showing the most unfavorable and favorable effects, respectively. Particularly, lipopolysaccharide-binding protein, zonulin family peptide, and glucagon-like peptide-2 responses were deregulated by the presence of obesity after glucose and lipid challenges. Obese subjects showed higher fasting intestinal permeabilitybiomarkers levels than non-obese individuals, except for plasma soluble CD14. The polycystic ovary syndromeexacerbated the effect of obesity further increasing fasting glucagon-like peptide-2, lipopolysaccharide-binding protein, and succinate concentrations. We observed specific interactions of the polycystic ovary syndromewith obesity in the postprandial response of succinate, zonulin family peptide, and glucagon-like peptide-2. In summary, obesity and polycystic ovary syndromemodify the effect of diverse macronutrients on the gut barrier, and alsoinfluence intestinal permeabilityat fasting,contributing to the morbidity of functional hyperandrogenism by in