Host genetics and diet composition interact to modulate gut microbiota and predisposition to metabolic syndrome in spontaneously hypertensive stroke-prone rats

What is it about?

The prevalence of obesity, diabetes, dyslipidemia, hypertension and stroke are rapidly increasing worldwide, and are together often referred to as the "metabolic syndrome" . To understand the mechanisms of these diseases it is essential to study them in animal models but there are very few animal models that can mimic all of these disease conditions. Here, we studied the effects of high-fat diet on food intake, body weight and composition, microbiota in the gut, and multiple other tissue markers in spontaneously hypertensive stroke-prone (SHRSP) and the normal Wistar-Kyoto (WKY) rats. We found that SHRSP rats have very high blood pressure, they consume more calories and their food consumption is not inhibited by satiety signals, and that they burn more energy. Notably, key markers that contribute to enhanced energy expenditure in brown adipose and skeletal muscle tissues were increased in SHRSP than WKY rats. A high fat diet promoted weight gain, body fat, increased blood levels fo glucose and lipid, increased fat in the liver, and increased plasma hormones in both SHRSP and WKY. Importantly, despite differences in gut microbiota composition between the strains, diet had a major impact on gut flora with some of them being strongly associated with metabolism in the host. Together, we provide evidence that interactions between host genetics and diet modulate gut microbiome and increase susceptibility of SHRSP rats to developing metabolic syndrome.

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