{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,22]],"date-time":"2026-09-22T13:56:02Z","timestamp":1790085362078,"version":"4.0.1"},"reference-count":32,"publisher":"Public Library of Science (PLoS)","issue":"10","license":[{"start":{"date-parts":[[2023,10,9]],"date-time":"2023-10-09T00:00:00Z","timestamp":1696809600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/publicdomain\/zero\/1.0\/"}],"funder":[{"DOI":"10.13039\/100000062","name":"National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"publisher","award":["ZIA DK075062"],"award-info":[{"award-number":["ZIA DK075062"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000062","name":"National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"publisher","award":["ZIA DK075064"],"award-info":[{"award-number":["ZIA DK075064"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000062","name":"National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"publisher","award":["ZIA DK070002"],"award-info":[{"award-number":["ZIA DK070002"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["www.plosone.org"],"crossmark-restriction":false},"short-container-title":["PLoS ONE"],"abstract":"<jats:sec id=\"sec001\">\n<jats:title>Objective<\/jats:title>\n<jats:p>Otopetrin 1 (OTOP1) is a proton channel that is highly expressed in brown adipose tissue. We examined the physiology of <jats:italic>Otop1<\/jats:italic><jats:sup><jats:italic>-\/-<\/jats:italic><\/jats:sup> mice, which lack functional OTOP1.<\/jats:p>\n<\/jats:sec>\n<jats:sec id=\"sec002\">\n<jats:title>Methods<\/jats:title>\n<jats:p>Mice were studied by indirect calorimetry and telemetric ambulatory body temperature monitoring. Mitochondrial function was measured as oxygen consumption and extracellular acidification.<\/jats:p>\n<\/jats:sec>\n<jats:sec id=\"sec003\">\n<jats:title>Results<\/jats:title>\n<jats:p><jats:italic>Otop1<\/jats:italic><jats:sup><jats:italic>-\/-<\/jats:italic><\/jats:sup> mice had similar body temperatures as control mice at baseline and in response to cold and hot ambient temperatures. However, in response to fasting the <jats:italic>Otop1<\/jats:italic><jats:sup><jats:italic>-\/-<\/jats:italic><\/jats:sup> mice exhibited an exaggerated hypothermia and hypometabolism. Similarly, in ex vivo tests of <jats:italic>Otop1<\/jats:italic><jats:sup><jats:italic>-\/-<\/jats:italic><\/jats:sup> brown adipose tissue mitochondrial function, there was no change in baseline oxygen consumption, but the oxygen consumption was reduced after maximal uncoupling with FCCP and increased upon stimulation with the \u03b2<jats:sub>3<\/jats:sub>-adrenergic agonist CL316243. Mast cells also express <jats:italic>Otop1<\/jats:italic>, and <jats:italic>Otop1<\/jats:italic><jats:sup><jats:italic>-\/-<\/jats:italic><\/jats:sup> mice had intact, possibly greater hypothermia in response to mast cell activation by the adenosine A<jats:sub>3<\/jats:sub> receptor agonist MRS5698. No increase in insulin resistance was observed in the <jats:italic>Otop1<\/jats:italic><jats:sup><jats:italic>-\/-<\/jats:italic><\/jats:sup> mice.<\/jats:p>\n<\/jats:sec>\n<jats:sec id=\"sec004\">\n<jats:title>Conclusions<\/jats:title>\n<jats:p>Loss of OTOP1 does not change basal function of brown adipose tissue but affects stimulated responses.<\/jats:p>\n<\/jats:sec>","DOI":"10.1371\/journal.pone.0292610","type":"journal-article","created":{"date-parts":[[2023,10,9]],"date-time":"2023-10-09T17:42:51Z","timestamp":1696873371000},"page":"e0292610","update-policy":"https:\/\/doi.org\/10.1371\/journal.pone.corrections_policy","source":"Crossref","is-referenced-by-count":8,"title":["Loss of Otopetrin 1 affects thermoregulation during fasting in 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