Abstract
The adiponectin receptors, AdipoR1 and AdipoR2, are thought to transmit the insulin-sensitizing effects of adiponectin, an adipokine secreted by adipocytes. Modifications of their expression in insulin-sensitive tissues (skeletal muscle, liver, and adipose tissue) could therefore play a role in the control of insulin sensitivity and the development of insulin resistance. Recent data in mice supported this possibility. We examined whether the expression of adiponectin receptors (messenger RNA [mRNA] concentrations) is controlled in vivo in rats (Wistar) by nutritional factors (high-fat [HF] vs high-carbohydrate diet, fasting vs fed state) and whether this expression is decreased in an experimental model of insulin resistance, the obese Zucker rat. In Wistar rats, neither an HF diet nor fasting modified the mRNA concentrations of AdipoR1 in muscle, liver, or adipose tissue; the only modification observed was a decrease ( P < .05) in AdipoR2 mRNA level in the liver of rats fed with an HF diet. In obese Zucker rats compared with their lean controls, neither AdipoR1 nor AdipoR2 expression was modified in muscle. AdipoR2 expression was slightly decreased in adipose tissue, whereas the expression of both AdipoR1 and AdipoR2 was increased ( P < .05) in the liver of obese Zucker rats. In conclusion, contrary to what was reported in mice, the expression of adiponectin receptors in rats is poorly responsive to changes in nutritional conditions and is not decreased in a model of insulin resistance. These results do not support an important role for the expression of AdipoR1 and AdipoR2 in the modulation of sensitivity to insulin.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.