Beneficial effects of carotenoid-producing cells of Bacillus indicus HU16 in a rat model of diet-induced metabolic syndrome

• Published in: Beneficial microbes Vol. 8; no. 5; p. 823
• Main Authors: Crescenzo, R, Mazzoli, A, Cancelliere, R, Bucci, A, Naclerio, G, Baccigalupi, L, Cutting, S M, Ricca, E, Iossa, S
• Format: Journal Article
• Language: English
• Published: Netherlands 13.10.2017
• Subjects: Administration, Oral; Animals; Antioxidants - metabolism; Bacillus - growth & development; Bacillus - metabolism; Carotenoids - metabolism; Diet, High-Fat - adverse effects; Disease Models, Animal; Inflammation - pathology; Male; Metabolic Syndrome - pathology; Metabolic Syndrome - therapy; Oxidative Stress; Plasma - chemistry; Probiotics - administration & dosage; Rats, Sprague-Dawley; Treatment Outcome; insulin resistance; metabolic inflammation; Bacillus indicus HU16
• ISSN: 1876-2891
• DOI: 10.3920/BM2017.0025

A well-established rat model of diet-induced metabolic syndrome was used to evaluate the effects of the oral administration of spores or cells of HU16, a carotenoid-producing strain of Bacillus indicus. Symptoms of metabolic syndrome were induced in 90-days old, male Sprague-Dawley rats maintained for eight weeks on a high-fat diet, as previously reported. Parallel groups of animals under the same diet regimen also received a daily dose of 1×10 cells or spores of B. indicus HU16. Cells of strain HU16 were able to reduce symptoms of metabolic syndrome, plasma markers of inflammation and oxidative markers in plasma and liver to levels similar to those observed in rats under a standard diet. HU16 cells did not affect obesity markers or the accumulation of triglycerides in the liver of treated animals. Denaturing gradient gel electrophoresis analysis showed that the oral administration of HU16 cells did not significantly affect the gut microbiota of high fat-fed rats, suggesting that the observed beneficial effects are not due to a reshaping of the gut microbiota but rather to metabolites produced by HU16 cells.