Approach to metabolic syndrome by analysing the energy metabolism homeostasis

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Administration of FXR agonist accentuated body weight gain and glucose intolerance induced by the high fat diet and led to a pronounced worsening of the changes in liver and adipose tissue. Mechanistically, treatment with FXR agonist decreased BA biosynthesis, BA pool size and energy expenditure. Our data hence suggest that activation of FXR with synthetic agonists is not useful for long term management of the metabolic syndrome, as it reduces the BA pool size and subsequently decreases energy expenditure, translating in weight gain and insulin resistance. In addition, it was suggested that bile acid participated in amino acid metabolism in energy homeostasis by DNA micro array and metabolome analysis.