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.
journal_name
Fly (Austin)journal_title
Flyauthors
J Gray L,B Sokolowski M,J Simpson Sdoi
10.1080/19336934.2021.1896960subject
Has Abstractpub_date
2021-12-01 00:00:00pages
47-59issue
1eissn
1933-6934issn
1933-6942journal_volume
15pub_type
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