4.7 Article

Pediococcus acidilactici (pA1c®) alleviates obesity-related dyslipidemia and inflammation in Wistar rats by activating beta-oxidation and modulating the gut microbiota

Journal

FOOD & FUNCTION
Volume 14, Issue 24, Pages 10855-10867

Publisher

ROYAL SOC CHEMISTRY
DOI: 10.1039/d3fo01651j

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This study evaluated the effects of the probiotic strain Pediococcus acidilactici (pA1c (R)) on diet-induced obesity in rats. The results showed that supplementation with pA1c (R) improved adiposity, cholesterol and lipid metabolism, inflammation, and gut microbiota composition. Additionally, pA1c (R) activation of fatty acid beta-oxidation was observed in adipose tissue and the liver.
Due to the importance of the gut microbiota in the regulation of energy homeostasis, probiotics have emerged as an alternative therapy to ameliorate obesity-related disturbances, including cholesterol metabolism dysregulation, dyslipidemia and inflammation. Therefore, the objectives of this study were to evaluate the effect of the probiotic strain Pediococcus acidilactici (pA1c (R)) on the regulation of adiposity, cholesterol and lipid metabolism, inflammatory markers and gut microbiota composition in diet-induced obese rats. Twenty-nine four-week-old male Wistar rats were divided into three groups: rats fed a control diet (CNT group, n = 8), rats fed a high fat/high sucrose diet (HFS group, n = 11), and rats fed a HFS diet supplemented with pA1c (R) (pA1c (R) group, n = 10). Organs and fat depots were weighed, and different biochemical parameters were analysed in serum. Gene expression analyses in the adipose tissue were conducted using real-time quantitative-PCR. Faecal microbiota composition was evaluated using 16S metagenomics. Animals supplemented with pA1c (R) exhibited a lower proportion of visceral adiposity, a higher proportion of muscle, an improvement in the total-cholesterol/HDL-cholesterol ratio and a decrease in the total cholesterol, triglyceride and aspartate aminotransaminase (AST) serum levels, together with a decrease in several inflammation-related molecules. The expression of key genes related to adipose (Adipoq, Cebpa and Pparg) and glucose (Slc2a1 and Slc2a4) metabolism in the adipose tissue was normalized by pA1c (R). Moreover, it was demonstrated that pA1c (R) supplementation activated fatty acid beta-oxidation in the adipose tissue and the liver. Metagenomics demonstrated the presence of pA1c (R) in the faecal samples, an increase in alpha diversity, an increase in the abundance of beneficial bacteria, and a decrease in the abundance of harmful micro-organisms, including the Streptococcus genus. Thus, our data suggest the potential of pA1c (R) in the prevention of obesity-related disturbances including hypercholesterolemia, hypertriglyceridemia, inflammation and gut microbiota dysbiosis.

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