Scientists and news
outlets discussed the obesity epidemic frequently over the past thirty years
without finding much regarding a solution. Diet fads have come and gone; it
feels like every week the food that was supposed to help one lose weight is now
the main cause of heart disease. One thing scientists do know is just how dangerous
obesity is to one’s health. Obesity can increase one’s risk for many types of
cancers—especially colon cancer. The mechanism behind why obesity has such a
strong link to cancer, and what puts certain individuals at higher risk for obesity
in the first place is still a mystery waiting to be solved.
Beshel’s lab hopes to discover a neural component to
obesity that would eventually lead to a drug therapy solution for individuals
who cannot lose weight through dieting alone. She studied the way the Drosophila
brain encodes different food odors during varying stages of satiation in
the paper she published with Zhong in 2013. Beshel presented hungry and
satiated fruit flies with different odors to study how and where in the brain
odors derive meaning and value. The researchers found that food odors evoked
activity in neurons expressing Drosophila neuropeptide F (dNPF) and the neuropeptide
Y homolog, both strongly correlating with food-odor attractiveness. They also
discovered that hunger enhances neural and behavioral responses to strictly food
odors when compared to non-food odors. Inactivation dNPF-expressing neurons or
receptors had the opposite effect: removing food-odor attractiveness.
Genetically enhancing dNPF activity increased attraction to food odors and
aversive odors. These results demonstrate a possible neural signal that encodes
values of odors in the brain that can be varied by hunger state.
The connection between Beshel’s work and obesity is only
in its beginning stages, but appears promising nonetheless. Her research could
possibly lead to further studies examining the effects of dNPF neuron
inactivation on feeding behavior. If the fruit flies consume less food after inhibiting
food odor attraction, these results could set Beshel up nicely for examining
dNPF inactivation as a possible therapeutic solution to obesity. Clearly there
are many steps that have to fall into place before any of these conclusions can
be made, but her work sets her in the right direction. Looking at what neural
components can possibly cause obesity may contain the way to treat it or even
prevent it in the future.
Lots of research has been performed looking into not what
causes obesity (like Beshel’s work), but instead what obesity can cause. Yilmaz
and Sabatini are two researchers who wanted to learn more about the link
between cancer in obesity. Their researchers fed mice high-fat and high-calorie
food for a year, then tested the effects of this diet on the number and
function of stem cells in their intestines. They found that the diet causes
mice to overeat and become overweight, and it also activated PPAR-gamma and
stimulated proliferation of intestinal stem cells. To test the association
between PPAR-gamma activation and intestinal stem cell proliferation, they
treated the mice with a drug that activates PPAR-gamma and found similar
results. Researchers believe the regeneration of these stem cells are more
likely to create tumors than other cells. The exact cause of this change in
intestinal stem cell behavior is unclear now. It could be the weight gain or
the fatty food. Unfortunately, it is possible that this mechanism may not even
exist in humans. The link between diet and cancer is also very difficult to research
in humans because of the multitude of possible confounding variables.
Nonetheless, Yilmaz’s team hopes to examine the relationship between a fatty
diet, obesity, and cancer risk further in follow-up studies.
Yilmaz’s research is accompanied by many other studies
that attempt to link diet, obesity, and cancer, but Yilmaz’s genetic component
sets the work apart. Finding out that PPAR-gamma activation can lead to stem
cell proliferation that increases cancer risk is a huge finding. It needs much
more research to confirm that this is not the result of some confounding variable,
but it is still promising. The obese mice in Yilmaz’s study provide a key piece
in the obesity and colon cancer puzzle.
Both Beshel and Yilmaz’s work demonstrate the
significance of biological research prior to the more well-known clinical and
translation research done on humans. Their work is crucial because these kinds
of experiments would be unethical to perform on humans. It also allows for
easier control of confounding variables and ease of implementation. They both
provide important information about the progression of obesity in the body. Research
like theirs have placed steppingstones on the road to understanding the mechanism
behind what causes obesity and how it can affect cancer risk.
Important Links
-
Yilmaz: https://www.scientificamerican.com/article/fat-mice-provide-clue-to-obesity-colon-cancer-puzzle/
Works
Cited
Beshel, J. & Zhong,
Y. (2013). Graded Encoding of Food Odor Value in the
Drosophila Brain. Journal
of Neuroscience, 33(40), 15693-15704.
Yilmaz et al. (2016). High-fat
diet enhances stemness and tumorigenicity of
intestinal progenitors.
Nature, 531, 53-58.
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