Abstract
Cherries are fruits containing fiber and bioactive compounds (e.g., polyphenolics) with the potential of helping patients with diabetes and weight disorders, a phenomenon likely related to changes in the complex host-microbiota milieu. The objective of this study was to investigate the effect of cherry supplementation on the gut bacterial composition, concentrations of caecal short-chain fatty acids (SCFAs) and biomarkers of gut health using an in vivo model of obesity. Obese diabetic (db/db) mice received a supplemented diet with 10% cherry powder (supplemented mice, n = 12) for 12 weeks; obese (n = 10) and lean (n = 10) mice served as controls and received a standard diet without cherry. High-throughput sequencing of the 16S rRNA gene and quantitative real-time PCR (qPCR) were used to analyze the gut microbiota; SCFAs and biomarkers of gut health were also measured using standard techniques. According to 16S sequencing, supplemented mice harbored a distinct colonic microbiota characterized by a higher abundance of mucin-degraders (i.e., Akkermansia) and fiber-degraders (the S24-7 family) as well as lower abundances of Lactobacillus and Enterobacteriaceae. Overall this particular cherry-associated colonic microbiota did not resemble the microbiota in obese or lean controls based on the analysis of weighted and unweighted UniFrac distance metrics. qPCR confirmed some of the results observed in sequencing, thus supporting the notion that cherry supplementation can change the colonic microbiota. Moreover, the SCFAs detected in supplemented mice (caproate, methyl butyrate, propionate, acetate and valerate) exceeded those concentrations detected in obese and lean controls except for butyrate. Despite the changes in microbial composition and SCFAs, most of the assessed biomarkers of inflammation, oxidative stress, and intestinal health in colon tissues and mucosal cells were similar in all obese mice with and without supplementation. This paper shows that dietary supplementation with cherry powder for 12 weeks affects the microbiota and the concentrations of SCFAs in the lower intestinal tract of obese db/db diabetic mice. These effects occurred in absence of differences in most biomarkers of inflammation and other parameters of gut health. Our study prompts more research into the potential clinical implications of cherry consumption as a dietary supplement in diabetic and obese human patients.
Highlights
The digestive tract of humans and other animals has coevolved over millions of years with a complex assemblage of many different types of microorganisms
Cherry powder contributed with phenolics and dietary fiber as bioactive compounds that might reach the lower intestinal tract because of their low bioavailability and most likely modulate microbial populations in the large intestine
This study describes the effect of cherry consumption on the colonic microbiota, short-chain fatty acids, and biomarkers of intestinal health using an in vivo model of genetic obesity
Summary
The digestive tract of humans and other animals has coevolved over millions of years with a complex assemblage of many different types of microorganisms (gut microbiota). This coevolution has brought benefits to both forms of life, with the latter sustaining life in the former by helping regulate digestion of nutrients, behavior and the activity of the immune system (Conlon & Bird, 2014). The membership of the gut microbiota (both at the mucus layer and in the lumen) is relatively constant overtime and resilient to change This complex host-microbial ecosystem can experience extensive variability (both over time within an individual or among different individuals) depending on a variety of factors including the age of the host, dietary patterns, body weight and physical activity. There is still a lot of room for understanding and most studies have only analyzed the fecal microbiota, we know that dietary modifications can change the composition and activity of the gut microbiota which in turn may promote wellbeing in the host (Sheflin et al, 2016; Velly, Britton & Preidis, 2016)
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