In the article, “A Lepin Analog Locally Produced in the Brain Acts via a Conserved Neural Circuit to Modulate Obesity-Linked Behaviors in Drosophila,” Beshel used Drosophila, a fruit fly, to investigate the neural mechanisms behind obesity. The team looked at leptin, which is an adipose/fat hormone, in adipose tissues and in neurons. Leptin upd1 was selected because it is thought to inhibit Drosophila neuropeptide F, which in turn would inhibit the neural circuit, causing increased food attraction. They “knocked down” or did not express the leptin upd1 in both adipose tissues and in neurons to look at the effects. Only in the neurons did they find that when they knocked down upd1, did it increase obesogenic behaviors (the flies had an increased attraction to food and increased in weight). In summary, the inhibition of leptin upd1 in Drosophila neurons led to obesogenic conditions, or increased food attraction and weight gain (3).
Other studies are also being done, similar to Beshel’s work with leptin. In the article, “The Complex Interactions Between Obesity, Metabolism, and the Brain,” by Romina Maria Uranga and Jeffrey Neil Keller, the authors cite that leptin is responsible for regulating body weight homeostasis. Leptin is also key in regulating immune and inflammatory processes, not just metabolic and homeostasis processes. Those with obesity often suffer from pain and inflammation, and increased leptin might be the key to relieving that pain. Lastly, those who suffer from obesity have been linked to mental health disorders, cognitive decline, and at risk for other disorders such as dementia. This article highlights the risk obesity poses in overall health and the lasting health effects. The decrease in leptin, as noted by Beshel, can lead to an increase in inflammation in those with obesity, and obese patients can also have other consequences such as cognitive impairment, diabetes, and other related diseases (4).
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