{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,5]],"date-time":"2026-10-05T10:54:36Z","timestamp":1791197676799,"version":"4.1.0"},"reference-count":169,"publisher":"Portland Press Ltd.","issue":"3","content-domain":{"domain":["portlandpress.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2020,2,14]]},"abstract":"<jats:p>Obesity results from energy imbalance, when energy intake exceeds energy expenditure. Brown adipose tissue (BAT) drives non-shivering thermogenesis which represents a powerful mechanism of enhancing the energy expenditure side of the energy balance equation. The best understood thermogenic system in BAT that evolved to protect the body from hypothermia is based on the uncoupling of protonmotive force from oxidative phosphorylation through the actions of uncoupling protein 1 (UCP1), a key regulator of cold-mediated thermogenesis. Similarly, energy expenditure is triggered in response to caloric excess, and animals with reduced thermogenic fat function can succumb to diet-induced obesity. Thus, it was surprising when inactivation of Ucp1 did not potentiate diet-induced obesity. In recent years, it has become clear that multiple thermogenic mechanisms exist, based on ATP sinks centered on creatine, lipid, or calcium cycling, along with Fatty acid-mediated UCP1-independent leak pathways driven by the ADP\/ATP carrier (AAC). With a key difference between cold- and diet-induced thermogenesis being the dynamic changes in purine nucleotide (primarily ATP) levels, ATP-dependent thermogenic pathways may play a key role in diet-induced thermogenesis. Additionally, the ubiquitous expression of AAC may facilitate increased energy expenditure in many cell types, in the face of over feeding. Interest in UCP1-independent energy expenditure has begun to showcase the therapeutic potential that lies in refining our understanding of the diversity of biochemical pathways controlling thermogenic respiration.<\/jats:p>","DOI":"10.1042\/bcj20190463","type":"journal-article","created":{"date-parts":[[2020,2,14]],"date-time":"2020-02-14T16:48:43Z","timestamp":1581698923000},"page":"709-725","update-policy":"https:\/\/doi.org\/10.1042\/crossmark_policy","source":"Crossref","is-referenced-by-count":155,"title":["UCP1-independent thermogenesis"],"prefix":"10.1042","volume":"477","author":[{"given":"Anna","family":"Roesler","sequence":"first","affiliation":[{"name":"Goodman Cancer Research Centre, McGill University, Montreal, QC H3A 1A3, Canada"},{"name":"Department of Biochemistry, McGill University, Montreal, QC H3G 1Y6, Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-7591-2544","authenticated-orcid":false,"given":"Lawrence","family":"Kazak","sequence":"additional","affiliation":[{"name":"Goodman Cancer Research Centre, McGill University, Montreal, QC H3A 1A3, Canada"},{"name":"Department of Biochemistry, McGill University, Montreal, QC H3G 1Y6, Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"288","published-online":{"date-parts":[[2020,2,14]]},"reference":[{"key":"2021112218063103900_BCJ-2019-0463CC1","doi-asserted-by":"publisher","first-page":"5","DOI":"10.1016\/j.cmet.2007.06.004","article-title":"A nonadaptive scenario explaining the genetic predisposition to obesity: the \u201cpredation release\u201d hypothesis","volume":"6","year":"2007","journal-title":"Cell Metab."},{"key":"2021112218063103900_BCJ-2019-0463CC2","doi-asserted-by":"publisher","first-page":"425","DOI":"10.1038\/372425a0","article-title":"Positional cloning of the mouse obese gene and its human homologue","volume":"372","year":"1994","journal-title":"Nature"},{"key":"2021112218063103900_BCJ-2019-0463CC3","doi-asserted-by":"publisher","first-page":"632","DOI":"10.1038\/379632a0","article-title":"Abnormal splicing of the leptin receptor in diabetic mice","volume":"379","year":"1996","journal-title":"Nature"},{"key":"2021112218063103900_BCJ-2019-0463CC4","doi-asserted-by":"publisher","first-page":"491","DOI":"10.1016\/S0092-8674(00)81294-5","article-title":"Evidence that the diabetes gene encodes the leptin receptor: identification of a mutation in the leptin receptor gene in db\/db mice","volume":"84","year":"1996","journal-title":"Cell"},{"key":"2021112218063103900_BCJ-2019-0463CC5","doi-asserted-by":"publisher","first-page":"843","DOI":"10.1126\/science.1073160","article-title":"betaAR signaling required for diet-induced thermogenesis and obesity resistance","volume":"297","year":"2002","journal-title":"Science"},{"key":"2021112218063103900_BCJ-2019-0463CC6","doi-asserted-by":"publisher","first-page":"155","DOI":"10.1038\/509","article-title":"Severe early-onset obesity, adrenal insufficiency and red hair pigmentation caused by POMC mutations in humans","volume":"19","year":"1998","journal-title":"Nat. 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