Obesity is a widespread condition that affects millions of people across the world. Obesity is a health concern and puts a person at higher risk for complications when exposed to diseases such as COVID-19. There is a need to understand the effects on the brain and the human body of an obese person. This will help to treat and combat this important issue that affects a large portion of the world’s population. The brain has been found to regulate eating habits through the leptin pathway, which can be affected by sugar intake.
In the article “A Leptin Analog Locally Produced in the Brain Acts via a conserved Neural Circuit to Modulate Obesity-Linked Behaviors in Drosophila” Dr. Beshel and colleagues analyzed the role of leptin and analog unpaired 1 (upd1) in Drosophila. This study found that when upd 1 in flies was deleted, flies had more attraction to eating, which resulted in weight gain. In more general terms, leptin is a hormone that is secreted by adipose cells. The levels of leptin in a person are directly correlated with their body fat. When a person has extra body fat, they release more leptin into the bloodstream that signals to the person’s brain that they are no longer hungry. However, in obesity, there is a constant high level of leptin in the bloodstream, which prevents receptors from being as sensitive to leptin and result in hunger signals not being turned off. Dr. Beshel’s findings point to triggers not only genetically based but also on the food availability that a fly consumed. Therefore, understanding the homeostasis of the leptin pathway is essential, but what types of food a fly or person consumes can also play a significant role in weight gain and affect leptin levels.
Another article that talks about obesity include, “Sugar consumption, metabolic disease and obesity: The state of controversy” by Kimber Stanhope, mentions the critical impact of sugar consumption on metabolism levels and obesity. This study has shown that added sugars in food can interrupt metabolic behavior in the body. Fructose consumption can interrupt the metabolic regulation of lipids and carbohydrates. This interference can lead to weight gain in a person. This study’s findings suggest that when there is increased fructose intake, the leptin levels are reduced. The reduction in leptin could be because fructose increases energy and reduces spent energy, resulting in stored fat. Many of the foods we eat have added sugars. These added sugars could be what is disrupting the homeostasis of our body weight. Therefore, this study argues that more research needs to be done, but limiting the number of additive sugars in our diets could prevent dysfunction in the leptin pathway and body fat produced within the body.
In conclusion, both of these articles are making strides towards preventing and finding a cause for obesity. The world needs a treatment or advice on how to prevent obesity. This would greatly help improve the life spans of those affected by obesity. Obesity is a complicated disorder because it is thought to be a human responsibility to eat the right food. However, this is not the case. There is a dysfunction in the leptin pathway that causes a person to eat more in many cases. Like many other diseases when homeostasis within the body cannot be reached, there is an issue. Due to the production or the lack of leptin production, a person’s diet and eating patterns vary. This leptin pathway can be impacted by consuming certain sugars like fructose. Overall, it is important to take information from both of these studies to better understand the cause of obesity and ways to treat or combat the disorder.
Works Cited:
Beshel, J., Dubnau, J., & Zhong, Y. (2017). A Leptin Analog Locally Produced in the Brain Acts via a Conserved Neural Circuit to Modulate Obesity-Linked Behaviors in Drosophila. Cell metabolism, 25(1), 208–217. https://doi.org/10.1016/j.cmet.2016.12.013
Stanhope K. L. (2016). Sugar consumption, metabolic disease and obesity: The state of the controversy. Critical reviews in clinical laboratory sciences, 53(1), 52–67. https://doi.org/10.3109/10408363.2015.1084990
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