An Investigation of the Antagonistic Effects of Rapamycin and Fructose on the Longevity of Caenorhabitis Elegans

Overview

Obesity persists to be one of the most prevalent causes of premature death, killing over 2.8 million people a year. Diets high in fructose have been suggested to be a cause of obesity, by increasing fat deposits and thus decreasing lifespan. To model human lipid storage, scientists have used C. elegans, a nematode proven to be a great model organism for both lipid storage and longevity. In C. elegans, fructose has been proven to activate TORC1, a complex known to promote lipogenesis. To quantify the effect of different fructose concentrations and rapamycin on the lipid storage of C. elegans, various amounts of fructose were added to OP50, in concentrations of 0-10% with or without rapamycin. A lipophilic dye (Nile Red) was applied to measure the amount of fat deposits for each treatment. C.elegans treated with lower levels of fructose did not lead to a significant increase in intestinal fat deposits until a 7% concentration; exposure to rapamycin mitigated the effect of fructose on IFDs. In order to study lifespan, C. elegans were treated with 0%, 3%, 7%, and 10% fructose with and without rapamycin. After 31 days, rapamycin prevented the lifespan-decreasing properties of a high fructose diet, and added to the lifespan-increasing properties of a low fructose diet. Overall, these experiments suggest rapamycin as a treatment to both the fat-increasing and lifespan-decreasing effects of a high fructose diet. This treatment has the potential to reduce obesity on an international scale, and can serve to lengthen the human lifespan.

Competition history

• JSHS 2022 Category not listed

Resources

• National JSHS abstract book ↗

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