Fat taste responsiveness, but not dietary fat intake, is affected in Adipor1 null mice

Taste is a major driving force that influences food choices and dietary intake. Adiponectin has been shown to selectively enhance cellular responses to fatty acids by mediating the activation of AMPK and translocation of CD36 in taste cells via its receptor AdipoR1. Whether Adipor1 gene knockout affects fat taste responsiveness and dietary fat intake in animals remains unclear. In the present study, we evaluated cellular, neural, and behavioral responses to fat, as well as the dietary fat intake in global Adipor1 knockout mice and their WT controls. Sex-specific changes in cellular and behavioral responses to fatty acid were observed in Adipor1 knockout mice. Linoleic acid (LA)-induced calcium responsiveness appears to be reduced in taste cells from Adipor1-deficient males and increased in taste cells from Adipor1-deficient females. Brief-access taste testing revealed a loss of fat taste behavioral responsiveness in naïve Adipor1 ^-/- animals. Fat taste loss found in Adipor1 ^-/- males was restored after fat exposure and showed no significant differences in taste behavioral responses to fatty acids with WT controls in two-bottle preference and conditioned taste aversion tests. Adipor1 ^-/- females were found to have diminished preference for LA in two-bottle preference tests, lower intralipid/water lick ratio in a brief-access assay, and reduced avoidance for LA in conditioned taste aversion assay. Furthermore, the taste nerve responses to intralipid and the dietary fat intakes appeared to be the same between Adipor1 ^-/- and WT mice. In the high-fat diet feeding study, Adipor1 ^-/- females gained more weight, while no differences in body weight gain were found in males. Together, we show that adiponectin/AdipoR1 signaling plays crucial sex-specific roles in the modulation of fat taste and the maintenance of healthy body weight primarily by regulating energy expenditure rather than dietary fat intake in mice.