ABSTRACT Evolved metabolic thriftiness in humans is a proposed contributor to the obesity epidemic. Insect models have been shown to evolve both ‘metabolic thrift’ in response to rearing on high-protein diets that promote leanness, and ‘obesity resistance’ when reared on fattening high-carbohydrate, low-protein foods. Despite the hypothesis that human obesity is caused by evolved metabolic thrift, genetic contributions to this physiological trait remain elusive. Here we conducted a pilot study to determine whether thrift and obesity resistance can arise under laboratory based ‘quasi-natural selection’ in the genetic model organism Drosophila melanogaster. We found that both these traits can evolve within 16 generations. Contrary to predictions from the ‘thrifty genotype/phenotype’ hypothesis, we found that when animals from a metabolic thrift inducing high-protein environment are mismatched to fattening high-carbohydrate foods, they did not become ‘obese’. Rather, they accumulate less triglyceride than control animals, not more. We speculate that this may arise through as yet un-quantified parental effects – potentially epigenetic. This study establishes that D. melanogaster could be a useful model for elucidating the role of the trans- and inter-generational effects of diet on the genetics of metabolic traits in higher animals.
Drosophila as a useful model for understanding the evolutionary physiology of obesity resistance and metabolic thrift
Lindsey J Gray,Marla B Sokolowski,Stephen J Simpson
Published 2021 in Fly
ABSTRACT
PUBLICATION RECORD
- Publication year
2021
- Venue
Fly
- Publication date
2021-01-02
- Fields of study
Biology, Medicine, Environmental Science
- Identifiers
- External record
- Source metadata
Semantic Scholar, PubMed
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