Objective: Besides their role in lipid absorption, bile acids (BAs) can act as signalling molecules. Cholic acid was shown to counteract obesity and associated metabolic disorders in high-fat-diet (cHF)-fed mice while enhancing energy expenditure through induction of mitochondrial uncoupling protein 1 (UCP1) and activation of non-shivering thermogenesis in brown adipose tissue (BAT). In this study, the effects of another natural BA, Chenodeoxycholic Acid (CDCA), on dietary obesity, UCP1 in both interscapular BAT and in white adipose tissue (brite cells in WAT), were characterized in dietary-obese mice.
Research design: To induce obesity and associated metabolic disorders, male 2-month-old C57BL/6J mice were fed cHF (35% lipid wt?wt?1, mainly corn oil) for 4 months. Mice were then fed either (i) for 8 weeks with cHF or with cHF with two different doses (0.5%, 1%; wt?wt?1) of CDCA (8-week reversion); or (ii) for 3 weeks with cHF or with cHF with 1% CDCA, or pair-fed (PF) to match calorie intake of the Chenodeoxycholic Acid mice fed ad libitum; mice on standard chow diet were also used (3-week reversion).
Objective: we study the effects on the respiratory system of Chenodeoxycholic Acid (CDCA). Methods: using concentrated ammonia induced cough method, sulfur dioxide induced cough method, volumetric method trachea, tracheal spiral strip method and phenol red excretion method. Results: The high and low dose of CDCA could significantly inhibit the concentrated aqueous ammonia and sulfur dioxide in mice induced cough cough frequency and latency; CDCA can significantly inhibit histamine-induced phosphorylation in vitro and in vivo guinea pig tracheal smooth muscle contraction; CDCA but also significantly increased in mice respiratory secretion amount of phenol red. Conclusion: CDCA has antitussive, expectorant and antiasthmatic effect.