Unraveling America’s Gross Appetite

Unraveling America’s Gross Appetite

     Over the past decade, Americans have put on more weight. Research shows that “nearly 40 percent of [American adults] were obese in 2015 and 2016”, and that the numbers are on a “sharp increase” (Ritchel and Jacobs). Simply put, obesity is a condition of excess body fat. Medically speaking, an individual is considered to be obese when they weigh over 20 percent of their ideal body weight (given their BMI). Typically, Leptin --an “adipose-derived ‘satiety hormone”-- curbs our appetite, preventing us from overeating. However, recent data suggests that there has been a drastic change within our conserved system. With adult weight gain on the raise, a number of neurologists have set out to uncover the link between appetite and the neurological system.

     In her research, Dr. Jen Beshel and her colleagues at Loyola University Chicago, used Drosophila melanogaster (fruit flies) to investigate the brain’s feeding pathways. Within Beshel’s presentation, Using drosophila to Unravel the Neural Systems Controlling Food Intake and Appetite, she describes how the manipulation of fat tissue (specific for the GAL4 system) affected food intake, food odor attraction, and overall weight. In these experiments, Dr. Beshel utilized two different groups of fruit flies: starved and fed. The starved flies were found to be very attracted to food odor; whereas the fed flies were not. Seeing as how manipulation of fat tissue outside of the brain resulted in a knockdown of Upd2 protein -- causing a decrease in weight, with no effect on food intake or odor attraction-- Beshel and colleagues turned their study toward Upd1. They discovered that the unpaired 1 protein (Upd1) --a glycol-protein-- was expressed within the brain. Thus, by reducing the expression of neural Upd1 (knockdown), several hallmarks of obesity were exhibited; the most notable being an increase in food attraction. After suppressing the expression of Upd1 in the fed flies, Beshel was able to change their behavior to mirror that of the starved flies. In other words, the fed fruit flies (whom were originally non-reactive to the food odor) became very attracted to food odor. The same observation was noted in the food intake; thus, these fed flies were now eating more food.

In the second half of Beshel’s experiment, her lab examined the association between neuropeptides and weight gain. Utilizing a cohort of rodents, it was discovered that food deprivation resulted in an increase in neuropeptide Y (NPY) activity and foraging. Applying these results to her Drosophila experiment, Beshel’s lab surveyed the relationship between neuropeptide F (NPF) and weight gain. They discovered that not only was NPF necessary for food attraction, but that it was essential to accurately predict food behavior. When the food receptors were knocked out, the starved flies group did not react to the smell of their favorite food (foraging decreased). These result was attributed to the fact that NPF acts a novel processing stimuli. Therefore, those flies with the NPF domeless knockdown displayed the hallmarks of obesity (increased weight, food intake, etc.). Taking her analysis a step further, Beshel placed the flies on a high fat diet to mimic the diet of many Americans. It was discovered that the genetic perturbations in Upd1-NPF (a leptin analog) axis, lead to a “hypersensitivity to obesogenic conditions” (Beshel). In essence, the modifying and suppression of Upd1 resulted in a leptin resistance within the Drosophila. This leptin resistance in the neural pathway, caused the flies to eat more --in turn gaining more weight.  

In the Huffington Post article, Is Obesity a Self-Fulfilling Prophecy?, the authors discuss the results of a recent psychological study carried out by Florida State University. In the study, psychological scientists Angelina Sutin and Antonio Terracciano looked into the relationship between self-stigmatization and obesity. In other words, do teens who “embody the caricature of a fat person, literally grow into that caricature?” (Herbert). Utilizing data from the National Longitudinal Study of Adolescent Health, a cohort of 6,000 normal weight 16 year old participants (based on BMI) was analyzed. At the conclusion of the analysis, it was found that a majority of the teens who had “distorted perceptions of themselves actually became obese at age 28”. Likewise, “the fit teens who saw themselves as fat had a whopping 40 percent greater risk of being obese at 28, compared to fit teens with accurate perceptions”. The inability to perceive their bodies accurately, caused these teens to become “prone to extreme dieting practices”; as well as “internalized weight biases” which can lead to a decrease in self-control (Herbert). Although Sutin and Terracciano’s study looks at obesity from a psychological perspective, the data from their research is connected with that of Beshel’s.

The research outlined in Beshel’s talk, as well as the research conducted by the scientists at Florida State, demonstrate the important interplay between the brain and environment. Likewise, both studies suggest that obesity and weight gain can be the result of an undiscovered predisposition (whether genetic or psychological). There are several consequences associated with obesity, the most notable being an increased risk of heart attacks and heart disease. Though we now know the role of upd and Leptin in appetite, hopefully future studies can break the cycle of weight gain and uncover the direct link to obesity.

Works Cited:

Herbert, Wray. “Is Obesity a Self-Fulfilling Prophecy?” The Huffington Post, TheHuffingtonPost.com, 8 Mar. 2015, www.huffingtonpost.com/wray-herbert/is-obesity-a-self-fulfill_b_6424336.html.

Richtel, Matt, and Andrew Jacobs. “American Adults Just Keep Getting Fatter.” The New York Times, The New York Times, 23 Mar. 2018, www.nytimes.com/2018/03/23/health/obesity-us-adults.html.

Link to Beshel’s paper: https://reader.elsevier.com/reader/sd/pii/S1550413116306465?token=DB74262D5E3CFD28A4403F61DB1DC4BB1B165D0183BBF7C1D3F03F38DC81E108692FAE06A82EB0A47CC4A18C16B36D92