Adiponectin signaling modulates fat taste responsiveness in mice

Abstract

AbstractWe previously reported that the adiponectin receptor agonist AdipoRon selectively enhances cellular responses to fatty acids in a human taste cell line. The enhancement role of AdipoRon on fatty acid-induced cell responses is mediated by the activation of AMPK and translocation of CD36 on human taste cells. It has also been shown that adiponectin selectively increases taste behavioral responses to intralipid in mice. However, the molecular mechanism underlying the physiological effects of adiponectin on fat taste in mice remains unclear. Here we define AdipoR1 as the mediator responsible for the enhancement role of adiponectin/AdipoRon on fatty acid-induced responses in mouse taste bud cells. Calcium imaging data demonstrate that AdipoRon enhances linoleic acid-induced calcium responses in a dose-dependent fashion in mouse taste cells isolated from circumvallate and fungiform papillae. Similar to the human taste cells, the enhancement role of AdipoRon on fatty acid-induced responses was impaired by the co-administration of an AMPK inhibitor (Compound C) or a CD36 inhibitor (SSO). Utilizing Adipor1-deficient animals we determined the enhancement role of AdipoRon/adiponectin is dependent on AdipoR1 since AdipoRon/adiponectin failed to increase fatty acid-induced calcium responses in taste bud cells isolated from these mice. Brief-access taste tests were performed to determine whether AdipoRon’s enhancement role was correlated with any differences in taste behavioral responses to fat. Although AdipoRon enhances the cellular responses of taste bud cells to fatty acids, it does not appear to alter fat taste behavior in mice. However, fat naïveAdipor1−/−animals were indifferent to increasing concentrations of intralipid, suggesting that adiponectin signaling may have profound effects on the ability of mice to detect fatty acids in the absence of previous exposure to fatty acids and fat-containing diets.