Within the United States, many medical crises have emerged from the habits that we have developed over the past few decades. As foods that are unhealthy become cheaper while healthier foods increase in price, obesity has become a staple problem that our society has had to face. Obesity occurs when an individual’s energy intake is greater than the energy expended, and to be considered obese, one must be greater than 20% his or her ideal weight. This may be caused by genetic or environmental factors, but nevertheless, obesity has debilitating effects for both the individual and society, decreasing life expectancy and earnings while increasing health care costs. Not only does obesity have social and economic consequences, but it also produces joint issues, liver issues, and different kinds of cancer. As a result, obesity is being heavily investigated to find causes and potential solutions to ease the recovery from obesity, and this has become a multi-disciplinary investigation, spanning a number of subjects including biology, psychology, chemistry, neuroscience, and many more.
As new and innovative experiments further explore how the body interacts with various chemicals using many unique and innovative procedures, hormones have become a very relevant topic, especially leptin, ghrelin, and adiponectin. Leptin in particular has been heavily scrutinized as a possible regulator of weight and appetite. Researchers like Dr. Jen Beshel from the Department of Biology at Loyola University Chicago have studied and manipulated particular leptin receptors in flies to further understand leptin’s role in weight. Using the Gal4/UAS system to biochemically manipulate the cytokine unpaired 1 and 2 genes (upd1 and upd2), the fly’s equivalent to human leptin, Beshel sought to investigate how flies’ leptin levels affect their obesity. Along with this, Beshel studied Neuropeptide F (NPF) neurons in flies, and how the manipulation of these neurons affected appetite. Specifically affecting the olfactory system within flies, NPF promotes feeding and is regulated by the upd1 gene. She discovered that the lack of this gene instigated overindulgence in feeding. Overall, Beshel concluded that changes to locally produced leptin led to inevitable obesity, and genetic differences can be magnified when tested in obesogenic environments.
Jen Beshel wants to further her study by investigating various characteristics of leptin, including its origin, sequencing, and the phenomenon of leptin resistance, or excess weight maintenance in the face of a higher leptin baseline. As evidence suggests, most obese people have high circulating levels of leptin, and as a result, experimenters attempted to inject excess leptin within obese humans to potentially decrease food intake and, ultimately, weight. As a result, this procedure caused the potential phenomenon to be coined as leptin resistance due to its similarity to insulin resistance, or the addition of insulin in type 2 diabetics to lower blood sugar within the patient’s body. Drs. Jeffrey and Eleftheria Flier from the Department of Neurobiology and the Department of Medicine, respectively, at Harvard Medical School discussed in their 2017 journal article that leptin level increases are not a solution of obesity, producing very limited or no reductions in food intake and body weight. This discovery led these two researchers to instead investigate leptin’s role in starvation, and after gathering evidence from several previous studies, they concluded that falling leptin levels are physiologically essential starvation signs. Along with this, the Fliers point out that many of these studies state leptin’s role as a starvation signal while also stating that increased levels of leptin cause fat storages to rise, signaling the central nervous system to inhibit weight gain by diminishing food intake and increasing energy used. Although they do see decreased leptin levels as a starvation state, the Fliers do not see sufficient evidence to conclude that decreased appetite and increased activity are due to an increase in leptin levels.
Instead of leptin being the sole contributor to the inhibition of overfeeding to mediate weight gain, the Fliers suggest that another regulatory hormone may be responsible, and that leptin resistance is impossible to define due to the lack of research and the potential complexity that such a phenomenon may withhold when compared to the dozens of metabolic pathways that make up insulin resistance. Many questions still remain, however. Some of these questions include why the occurrence of leptin resistance does not work while insulin resistance in type 2 diabetics functions efficiently, what the physiology of leptin is, and if there are any secrets in the translation of the leptin hormone that may help us further understand obesity and many other disorders that may be associated with it. Beshel also inquires if obesogenic conditions may alter leptin receptor activity, which may help support the correlation between leptin and obesity. Whether leptin regulation plays an important role in obesity or as a starvation signal, one must acknowledge that leptin, although dwindling in popularity, is a hormone that needs to be extensively researched. In the world that we live in today, consisting of foods that are extremely rich in fats and sugars, hormones such as leptin must be fully understood to further promote healthy weight maintenance and reduce obesity within our society.
Works Cited
Beshel, J, et al. “A Leptin Analog Locally Produced in the Brain Acts via a Conserved Neural Circuit to Modulate Obesity-Linked Behaviors in Drosophila.” Cell Metabolism., U.S. National Library of Medicine, 10 Jan. 2017, www.ncbi.nlm.nih.gov/pubmed/28076762
Flier, J. S., & Maratos-Flier, E. (2017, July 5). Leptin's Physiologic Role: Does the Emperor of Energy Balance Have No Clothes. Retrieved from ScienceDirect: https://www.sciencedirect.com/science/article/pii/S1550413117303029?via%3Dihub
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