Abstract
Dietary fibers are fermented by gut bacteria into the major short chain fatty acids (SCFAs) acetate, propionate, and butyrate. Generally, fiber-rich diets are believed to improve metabolic health. However, recent studies suggest that long-term supplementation with fibers causes changes in hepatic bile acid metabolism, hepatocyte damage, and hepatocellular cancer in dysbiotic mice. Alterations in hepatic bile acid metabolism have also been reported after cold-induced activation of brown adipose tissue. Here, we aim to investigate the effects of short-term dietary inulin supplementation on liver cholesterol and bile acid metabolism in control and cold housed specific pathogen free wild type (WT) mice. We found that short-term inulin feeding lowered plasma cholesterol levels and provoked cholestasis and mild liver damage in WT mice. Of note, inulin feeding caused marked perturbations in bile acid metabolism, which were aggravated by cold treatment. Our studies indicate that even relatively short periods of inulin consumption in mice with an intact gut microbiome have detrimental effects on liver metabolism and function.
Highlights
Obesity and associated disorders have become a major global health burden, and preventive measures as well as effective treatments are strongly required
We aim to investigate the effects of short-term inulin supplementation on hepatic cholesterol and bile acid metabolism in normobiotic wild type (WT) mice
While long-term inulin feeding has been shown to result in disturbed liver bile acid metabolism, cholestasis, liver damage, and even hepatocellular cancer [22], our present study aimed to investigate the impact of short-term (12 days) dietary inulin supplementation
Summary
Obesity and associated disorders have become a major global health burden, and preventive measures as well as effective treatments are strongly required. Obesity arises as a consequence of imbalanced energy intake and energy expenditure, and interventional approaches targeting one or the other have been introduced. One way to increase energy expenditure is activating the brown adipose tissue (BAT). Activation of BAT by its natural stimulus cold, promotes cholesterol elimination via triggering hepatic remnant lipoprotein uptake and increasing hepatic bile acid synthesis, as well as fecal bile acid excretion. Overall, these processes protect against the development of atherosclerosis [4,5]. Strategies to reduce energy intake, on the other hand, mainly involve dietary modifications. Fibers cannot be broken down by human digestive enzymes, but are fermented
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