Obesity is a widespread issue that impacts many people and may contribute to the severity of symptoms caused by comorbid conditions or even underlying conditions. As obesity’s impact on the human population increases, the need to study obesity, as well as its impacts on long-term health, becomes more and more important and prevalent. One of the biological relationships studied in this condition is the linkage between obesity and leptin concentration in the body.
In the article “A Leptin Analog Locally Produced in the Brain Acts via a conserved Neural Circuit to Modulate Obesity-Linked Behaviors in Drosophila”, Beshel and colleagues investigate the role of leptin and analog unpaired 1 (upd1) in Drosophila. Firstly, leptin is a hormone secreted by adipose tissue, and levels of leptin are correlated with body fat. If an organism has excess body fat, more leptin is released into the bloodstream, resulting in satiation, and the organism is not hungry anymore. However, in obesity, this pathway is unbalanced, which leads to high leptin levels in the bloodstream, which eventually leads to hunger signals not turning off properly. According to this study, deletion of upd1 led to increased attraction to eating, which led to that, in addition to genetic factors, obesity may be influenced by the type of food that is available.
In another article titled “Interplay of circulating leptin and obesity in cognition and cerebral volumes in older adults”, Zonneveld and colleagues investigated the independent relationships of leptin and body mass index (BMI) with cognitive decline and brain volume by use of magnetic resonance imaging (MRI) in older subjects that are at risk for cardiovascular disease. According to the results, obese participants with a BMI above 30 had larger volumes of the hippocampus and amygdala than reference individuals, independent of leptin levels in the bloodstream. Individuals with a high BMI level also performed worse on a cognitive function task than the reference subjects. In addition, individuals with high leptin levels also displayed a larger volume of the amygdala, independent of BMI status. However, individuals with high leptin levels performed the same as reference individuals on the cognitive task with no statistically significant differences. Although there is no direct link between leptin and obesity that causes or contributes to cognitive decline, these results indicate that leptin and obesity may both independently have an impact on brain volume levels, which may possibly contribute to other cognitive impairments or conditions that were not measured by the task used in this experiment.
The results of both Beshel et al. and Zonneveld et al. demonstrate the need for research on the relationship between leptin and obesity. Although this biological relationship has been studied in some contexts, there may be further research that needs to be done to be able to show the results of this relationship and how it may impact other parts and functions in the body. According to Zonneveld et al., the link between leptin and obesity may be significant when determining brain volume and according to Beshel et al., external food sources and choice may potentially influence obesity and the eventual release of leptin. Further research is necessary to solidify this relationship to be able to influence it positively to potentially reverse the negative impacts of obesity. With a condition that negatively impacts so many people, any kind of new research finding might be able to help alleviate symptoms.
CITATIONS:
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
Zonneveld, M.H., Noordam, R., van der Grond, J., van Heemst, D., Mooijaart, S.P., Sabayan, B., Jukema, J.W., Trompet, S. (2021). Interplay of circulating leptin and obesity in cognition and cerebral volumes in older adults. Peptides, 135, 170424. https://doi.org/10.1016/j.peptides.2020.170424
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