Abstract
Male Tsumura Suzuki obese diabetes (TSOD) mice spontaneously develop obesity and obesity-related metabolic syndrome. Gut dysbiosis, an imbalance of gut microbiota, has been implicated in the pathogenesis of metabolic syndrome, but its mechanisms are unknown. Short-chain fatty acids (SCFAs) are the main fermentation products of gut microbiota and a link between the gut microbiota and the host’s physiology. Here, we investigated a correlation among gut dysbiosis, SCFAs, and metabolic syndrome in TSOD mice. We detected enriched levels of Gram-positive bacteria and corresponding decreases in Gram-negative bacteria in 24-wk-old metabolic syndrome-affected TSOD mice compared with age-matched controls. The abundance of Bacteroidetes species decreased, the abundance of Firmicutes species increased, and nine genera of bacteria were altered in 24-wk-old TSOD mice. The total plasma SCFA level was significantly lower in the TSOD mice than in controls. The major plasma SCFA—acetate—decreased in TSOD mice, whereas propionate and butyrate increased. TSOD mice had no minor SCFAs (valerate and hexanoate) but normal mice did. We thus concluded that gut dysbiosis and consequent disruptions in plasma SCFA profiles occurred in metabolic syndrome-affected TSOD mice. We also propose that the TSOD mouse is a useful model to study gut dysbiosis, SCFAs, and metabolic syndrome.
Highlights
Metabolic syndrome comprises a combination of obesity-related metabolic alterations that increases the risk of type 2 diabetes mellitus and cardiovascular disease[1,2]
Because microbiota in fecal samples is widely accepted as a surrogate for gut microbiota, we collected feces from 24-wk-old Tsumura Suzuki obese diabetes (TSOD) male mice and Tsumura Suzuki non-obesity (TSNO) mice, and we analyzed the taxonomic compositions of the microbiota by using 16S ribosomal RNA gene sequencing of DNA extracted from the fecal samples
To investigate the hypothesis that alterations in the gut microbial community may contribute to the spontaneous development of metabolic syndrome in TSOD mice, we analyzed the gut microbiota and plasma Short-chain fatty acids (SCFAs) profiles in 24-wk-old TSOD mice
Summary
Metabolic syndrome comprises a combination of obesity-related metabolic alterations that increases the risk of type 2 diabetes mellitus and cardiovascular disease[1,2]. Tsumura Suzuki obese diabetes (TSOD) mice were originally established as a spontaneous model of type 2 diabetes mellitus[31,32] and were shown to spontaneously develop NASH33, a progressive phenotype of NAFLD34. Given that these pathological manifestations in TSOD mice are closely related to low-grade inflammation, we hypothesized that alterations in gut microbiota and plasma SCFA profiles in TSOD mice may affect a host’s immune system and induce inflammation, which would underlie the development of metabolic syndrome in TSOD mice. We analyzed the gut microbiome and plasma SCFA profiles in 24-wk-old TSOD mice that had already developed insulin resistance and NASH33
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