Larazotide acetate as a preventive and therapeutic pharmacotherapy in obesity and metabolic syndrome

Abstract

Obesity and associated metabolic diseases are on the rise due to many factors, including changing dietary patterns and physical inactivity. The complex multifactorial pathogenesis of obesity involves genetics, epigenetics, and microbiota, among others. Regarding the latter, multiple studies revealed compositional and functional alteration in the microbiota of metabolic syndrome patients when compared to healthy controls. In fact, a decrease in bacterial strains that promote intestinal homeostasis was established in obesity, type 2 diabetes, non-alcoholic fatty liver disease (NAFLD), and coronary arterial disease (CAD). This is accompanied by increased systemic lipopolysaccharide levels and inflammation, both of which are insulin-desensitizers and dyslipidemia-promoters. In accord, treatment with the anti-zonulin receptor pro-tight junction assembly peptide larazotide acetate may improve intestinal barrier function, reduce inflammatory by-products translocation, and improve insulin sensitivity and lipidomics in patients with metabolic syndrome.