Abstract
Intestinal permeability (IP) is essential in maintaining gut-metabolic functions in health. An unequivocal evaluation of IP, as marker of intestinal barrier integrity, however, is missing in health and in several diseases. We aimed to assess IP in the whole gastrointestinal tract according to body mass index (BMI) and liver steatosis. In 120 patients (61F:59M; mean age 45 ± SEM 1.2 years, range: 18–75), IP was distinctively studied by urine recovery of orally administered sucrose (SO, stomach), lactulose/mannitol ratio (LA/MA, small intestine), and sucralose (SA, colon). By triple quadrupole mass-spectrometry and high-performance liquid chromatography, we measured urinary recovery of saccharide probes. Subjects were stratified according to BMI as normal weight, overweight, and obesity, and answered questionnaires regarding dietary habits and adherence to the Mediterranean Diet. Liver steatosis was assessed by ultrasonography. IP at every gastrointestinal tract was similar in both sexes and decreased with age. Stomach and small intestinal permeability did not differ according to BMI. Colonic permeability increased with BMI, waist, neck, and hip circumferences and was significantly higher in obese than in lean subjects. As determined by logistic regression, the odds ratio (OR) of BMI increment was significantly higher in subjects in the highest tertile of sucralose excretion, also after adjusting for age and consumption of junk food. The presence of liver steatosis was associated with increased colonic permeability. Patients with lower score of adherence to Mediterranean diet had a higher score of ‘junk food’. Intestinal permeability tended to increase in subjects with a lower adherence to Mediterranean diet. In conclusion, colonic (but not stomach and small intestinal) permeability seems to be linked to obesity and liver steatosis independently from dietary habits, age, and physical activity. The exact role of these last factors, however, requires specific studies focusing on intestinal permeability. Results should pave the way to both primary prevention measures and new therapeutic strategies in metabolic and liver diseases.
Highlights
IntroductionNutrients 2020, 12, 564 the mucus, the enterocytes, the gut immune system, and the gut–vascular barrier
Intestinal permeability (IP) is dependent on the structure and function of the intestinal barrier [1,2].The gut barrier integrity is the result of ongoing equilibrium and crosstalk involving the microbiome, Nutrients 2020, 12, 564; doi:10.3390/nu12020564 www.mdpi.com/journal/nutrientsNutrients 2020, 12, 564 the mucus, the enterocytes, the gut immune system, and the gut–vascular barrier
The derangement of IP can originate from conditions involving chronic local and systemic inflammation, intestinal dysbiosis, and metabolic changes occurring during onset and development of metabolic syndrome, obesity, and liver steatosis [7]
Summary
Nutrients 2020, 12, 564 the mucus, the enterocytes, the gut immune system, and the gut–vascular barrier In this context, a link exists between antigenic/toxic molecules in the gut lumen and the systemic status in health and disease [3,4,5,6]. The derangement of IP can originate from conditions involving chronic local and systemic inflammation, intestinal dysbiosis, and metabolic changes occurring during onset and development of metabolic syndrome, obesity, and liver steatosis [7]. Increased IP occurs in obese women with metabolic syndrome [9], and abnormal IP may develop in association with changes of gut microbiota, a source of endotoxins whose increase in plasma is related to obesity and insulin resistance [10]. Further evidences point to a link between increased IP and pathogenic aspects of non-alcoholic fatty liver disease (NAFLD) [11,12]
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