Abstract
We previously reported that dietary supplementation with cholic acid (CA), the primary 12α-hydroxylated (12αOH) bile acid (BA), reduces plasma adiponectin concentration in rats. The aim of this study was to examine the distribution of adiponectin in the body of CA-fed rats and its influence on mucosal immunoglobulin A concentration in the intestine. Rats were fed a diet supplemented with or without CA (0.5 g CA/kg diet) for 13 weeks. A reduction in plasma adiponectin level was observed from week 3. At the end of the experiment, the CA diet reduced plasma adiponectin concentration both in the portal and aortic plasma. Accumulation of adiponectin was accompanied by an increase in cadherin-13 mRNA expression in the ileal mucosa of CA-fed rats. No increase was observed in adiponectin mRNA expression in the ileal and adipose tissues of the CA-fed rats. Immunoglobulin A concentration in the ileal mucosa was elevated in the CA-fed rats and was correlated with the ileal adiponectin concentration. 12αOH BAs may modulate mucosal immune response that are involved in the accumulation of adiponectin in the ileum.
Highlights
We previously reported that dietary supplementation with cholic acid (CA), the primary 12α-hydroxylated (12αOH) bile acid (BA), reduces plasma adiponectin concentration in rats
High levels of total BAs and 12αOH BAs were observed in the feces of CA-fed rats during the experimental period (Fig. 1a)
We observed a reduction in plasma adiponectin concentration in CA-fed rats in our previous studies[7,13], and confirmed the reduction in aortic plasma and in portal plasma (Fig. 2a) in the present study
Summary
We previously reported that dietary supplementation with cholic acid (CA), the primary 12α-hydroxylated (12αOH) bile acid (BA), reduces plasma adiponectin concentration in rats. No increase was observed in adiponectin mRNA expression in the ileal and adipose tissues of the CA-fed rats. A high-energy supply from diet enhances the production of 12αOH BA in the body Such an increase in 12αOH BAs is frequently observed in mice3, rats[4,5], and humans[6]. We simulated a high 12αOH BA environment via CA-supplementation in the diet of rats and observed alterations in the gut microbiota[7], hepatic steatosis without obesity, leaky gut, increased plasma transaminase activity, and reduced plasma adiponectin c oncentration[8]. Accumulation of adiponectin has been reported in several organs and tissues, and is associated with the adiponectin receptor, cadherin-13/T-cadherin (CAD13)[10]
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