https://wiki.tiffa.net/w/index.php?action=history&feed=atom&title=Translations%3AObesity%2F57%2FenTranslations:Obesity/57/en - Revision history2026-08-15T04:51:16ZRevision history for this page on the wikiMediaWiki 1.43.0https://wiki.tiffa.net/w/index.php?title=Translations:Obesity/57/en&diff=124610&oldid=prevFuzzyBot: Importing a new version from external source2024-03-05T05:18:27Z<p>Importing a new version from external source</p>
<p><b>New page</b></p><div>At a biological level, there are many possible [[pathophysiology|pathophysiological]] mechanisms involved in the development and maintenance of obesity. This field of research had been almost unapproached until the [[leptin]] gene was discovered in 1994 by J. M. Friedman's laboratory. While leptin and [[ghrelin]] are produced peripherally, they control appetite through their actions on the [[central nervous system]]. In particular, they and other appetite-related hormones act on the [[hypothalamus]], a region of the brain central to the regulation of food intake and energy expenditure. There are several circuits within the hypothalamus that contribute to its role in integrating appetite, the [[melanocortin]] pathway being the most well understood. The circuit begins with an area of the hypothalamus, the [[arcuate nucleus]], that has outputs to the [[lateral hypothalamus]] (LH) and [[ventromedial hypothalamus]] (VMH), the brain's feeding and satiety centers, respectively.</div>FuzzyBot