In A Leptin Analog Locally Produced in the Brain Acts via a Conserved Neural Circuit to Modulate Obesity-Linked Behaviors in Drosophila, Beshel et al. explain how in obese species, leptin is upregulated, causing increased food intake and thefore more adipose tissue. She found that manipulation of upd1 (the fly leptin analog) amplified responsiveness to food cues, eventually leading to weight gain. Upd1 acts to inhibit the NPF neuron (similar to the neuropeptide NPY in humans) as a function of satiety, so when flies lack upd1, they become obese because this pathway is no longer inhibited. In other words, once someone eats and is satisfactorily full, the leptin pathway will act as a negative feedback loop to let the brain know they are no longer hungry. In obese mammals, this pathway does not work as well, leading to increased eating habits and weight gain.
While obesity can be caused by both genetic or environmental factors, Freidman and Beshel would both conclude it’s a dangerous, slippery slope. The more overweight one is, the more likely they are to have upregulated levels of leptin leading to uncontrollable eating, and eventually extra pounds added on. Some often look at the obese people in our society and wonder how they could possibly let themselves get that large. Well, as with many things regarding the body, the answer is on a cellular and molecular level. If we can learn anything from this research on the obesity epidemic, it’s that we should constantly be reminding ourselves to ignore the unhealthy marketing campaigns and eat everything in moderation to avoid potential, unmanageable weight gain, because once we reach that level, it’s hard to turn back.
Kolata, G. (2004, June 8). The Fat Epidemic: He Says It's an Illusion. Retrieved from https://www.nytimes.com/2004/06/08/health/i-beg-to-differ-the-fat-epidemic-he-says-it-s-an-illusion.html.
Beshel, J., Dubnau, J. (2017). A Leptin Analog Locally Produced in the Brain Acts
via a Conserved Neural Circuit to Modulate ObesityLinked Behaviors in Drosophila.
Cell Metabolism 25, 208–217.
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