Taste Receptor Cells in Mice Express Receptors for the Hormone Adiponectin

Abstract

<jats:title>Abstract</jats:title> <jats:p>The metabolic hormone adiponectin is secreted into the circulation by adipocytes and mediates key biological functions, including insulin sensitivity, adipocyte development, and fatty acid oxidation. Adiponectin is also abundant in saliva, where its functions are poorly understood. Here we report that murine taste receptor cells (TRCs) express specific adiponectin receptors and may be a target for salivary adiponectin. This is supported by the presence of all three known adiponectin receptors in transcriptomic data obtained by RNA-seq analysis of purified circumvallate (CV) taste buds. As well, immunohistochemical analysis of murine CV papillae showed that two adiponectin receptors, ADIPOR1 and T-cadherin, are localized to subsets of TRCs. Immunofluorescence for T-cadherin was primarily co-localized with the Type 2 TRC marker phospholipase C β2, suggesting that adiponectin signaling could impact sweet, bitter, or umami taste signaling. However, adiponectin null mice showed no differences in behavioral lick responsiveness compared with wild-type controls in brief-access lick testing. AAV-mediated overexpression of adiponectin in the salivary glands of adiponectin null mice did result in a small but significant increase in behavioral lick responsiveness to the fat emulsion Intralipid. Together, these results suggest that salivary adiponectin can affect TRC function, although its impact on taste responsiveness and peripheral taste coding remains unclear.</jats:p>

Effect of physiological factors, pathologies, and acquired habits on the sweet taste threshold: A systematic review and meta‐analysis

“…This suggests that post‐ingestion hormone release is capable of regulating the peripheral gustatory apparatus by modulating the responsiveness of sweet stimuli (Depoortere, 2014). Receptors of adiponectin, a metabolic hormone that mediates insulin sensitivity, adipocyte development, and fatty acid oxidation, have also been found to be expressed in T1Rs, suggesting that adiponectin signaling could also impact sweet signaling (Crosson et al., 2019).…”

Systems genetic analysis of binge‐like eating in a C57BL/6J x DBA/2J‐F2 cross

“…Therefore, could Adipor2 dysfunction contribute to earlier physiological processes that initiate progression to BLE? Adipor1 , Adipor2 , and T‐cadherin transcripts (third adiponectin receptor) can be detected in taste receptor cells, 48 suggesting that saliva‐derived adiponectin could impact taste processing to influence eating. Also, adiponectin‐induced activation of Adipor1 expressed on dopamine neurons in the ventral tegmental area decreased spontaneous neuronal activity and firing and reversed stress‐induced increase in dopamine neuron firing and anxiety‐like behavior and Adipor1 haploinsufficiency increased dopamine neuron firing and anxiety‐like behavior 49 .…”

The Controversial Role of Adiponectin in Appetite Regulation of Animals

“…In addition, T-cadherin is expressed by projection neurons within the main and accessory OBs in mice [62]. Immunofluorescence analysis showed that T-cadherin was co-localized with Type 2 TRC marker phospholipase C β2 in mice [63]. Additionally, T-cadherin is expressed in the brain of adult human, including cerebral cortex, medulla, thalamus as well as midbrain, by northern blot analysis.…”