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Challenges and frequently occurring misleading assumptions with this strategy are discussed. However, the recently reported peripherally restricted hepatotropic cannabinoid 1 receptor inverse agonist TM38837 is noteworthy due to the substantial weight loss efficacy in DIO rodents coupled with minimal CNS exposure, which suggests that such a chemotype may have clinical utility. Furthermore, hepatic cannabinoid 1 receptor upregulation is implicated as a major driver of the obese phenotype in rodents, which opposes current theories based upon experiments with genetically modified mice. Accordingly, a novel hypothesis is proposed, which implicates cannabinoid 1 receptor upregulation as a mediator of cell cycle progression, which drives lipid synthesis during the mitosis phase. The upregulation is initiated by increasing redox state and amplified by a feed\u2010forward effect whereby cannabinoid 1 receptor activation induces cannabinoid 1 receptor upregulation by increasing expression of pro\u2010oxidant enzymes. This mechanism is activated prematurely in the cell cycle by lifestyle factors, which are known to cause oxidative stress in hepatocytes and are associated with the development of obesity. The consequence of such aberrant cannabinoid 1 receptor upregulation is sustained lipogenesis, leading to reduced cellular ATP levels, which drive increased food intake and contribute to other pathologies.<\/jats:p>","DOI":"10.1111\/obr.70166","type":"journal-article","created":{"date-parts":[[2026,5,15]],"date-time":"2026-05-15T04:58:56Z","timestamp":1778821136000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Is Hepatic Cannabinoid 1 Receptor a Key Driver of Obesity? 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