{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,15]],"date-time":"2026-05-15T02:58:04Z","timestamp":1778813884845,"version":"3.51.4"},"reference-count":123,"publisher":"Oxford University Press (OUP)","issue":"8","license":[{"start":{"date-parts":[[2022,2,12]],"date-time":"2022-02-12T00:00:00Z","timestamp":1644624000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/journals\/pages\/open_access\/funder_policies\/chorus\/standard_publication_model"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2022,7,7]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>Obesity is characterized by chronic low-grade inflammation that could lead to other health complications, such as cardiovascular disease, diabetes, and various forms of cancer. Emerging evidence has shown that taste perception is altered during the development of obesity. Moreover, suppression of taste receptor or taste signaling molecules potentiate the inflammatory response, and the progression of inflammation attenuates the expression of taste receptors in vivo. Together, these findings suggest a possible interplay between taste signaling and inflammation. This review summarizes the interactions between type 1 (T1Rs) and type 2 taste receptors (T2Rs) and inflammation, as well as the impact of obesity on T1R- and T2R-mediated signaling. Furthermore, we evaluate the possible role that taste receptors play in regulating the inflammatory response during obesity as a therapeutic target to prevent the progression of comorbidities associated with obesity.<\/jats:p>","DOI":"10.1093\/nutrit\/nuac007","type":"journal-article","created":{"date-parts":[[2022,1,14]],"date-time":"2022-01-14T20:11:37Z","timestamp":1642191097000},"page":"1919-1926","source":"Crossref","is-referenced-by-count":8,"title":["Possible role of type 1 and type 2 taste receptors on obesity-induced inflammation"],"prefix":"10.1093","volume":"80","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-2783-1723","authenticated-orcid":false,"given":"Gar Yee","family":"Koh","sequence":"first","affiliation":[{"name":"School of Family and Consumer Sciences, Texas State University , San Marcos, Texas, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Matthew J","family":"Rowling","sequence":"additional","affiliation":[{"name":"Department of Food Science and Human Nutrition, Iowa State University , Ames, Iowa, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Samantha K","family":"Pritchard","sequence":"additional","affiliation":[{"name":"Clinical Nutrition, Rush University Medical Center , Chicago, Illinois, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"286","published-online":{"date-parts":[[2022,2,12]]},"reference":[{"key":"2022070807570422300_nuac007-B1","doi-asserted-by":"crossref","first-page":"77","DOI":"10.1016\/j.coph.2016.07.005","article-title":"Obesity and cancer: inflammation bridges the two","volume":"29","author":"Kolb","year":"2016","journal-title":"Curr Opin Pharmacol."},{"key":"2022070807570422300_nuac007-B2","doi-asserted-by":"crossref","first-page":"2422","DOI":"10.1210\/jc.2003-030178","article-title":"The potential influence of inflammation and insulin resistance on the pathogenesis and treatment of atherosclerosis-related complications in type 2 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