Summary: | 博士 === 國防醫學院 === 生命科學研究所 === 101 === In general, the survival of an organism, such as human, is highly dependent on
its ability to respond to constant environmental and metabolic stresses such as drought
and famine. Metabolic adaptations include the ability to store excess energy as fat
during food abundance and to respond to food shortage by mobilizing these fat stores.
Embarking on the trail to understand lipid metabolism under stress, we have used
adult male Caenorhabditis elegans as our model organism. C. elegans, as living
organisms willing to survive, are also able to mount an adaptive response to food
deprivation by depleting their intestinal fat stores. These fat stores possibly provide
resources to launch the necessary adaptations to survive through the stress. Herein,
we provide evidences that starvation stress improves viability coupled with an
enhanced oxidative and thermal stress response and improved reproductive fitness.
This delay in reproductive aging is regulated by arresting spermatogenesis during the
starvation stress period and possibly mediated by GLP-1/Notch pathway.
Furthermore, this short-term starvation stress-induced viability and vitality is
mediated by DAF-16/FOXO transcription factor through the coordinated action of the
insulin/IGF-1 receptor and the GLP-1/Notch pathway acting independently but in
parallel. Facilitating strict molecular regulation during starvation period, it is
imaginable that transcription and translation of new proteins are occurring.
Previously, our laboratory had reported the increase in protein biosynthesis as well as
ribosome biogenesis during the initial phase of starvation in C. elegans before the
total depletion of their intestinal fat stores. We have further uncovered several
ribosomal protein genes that are likely candidate for regulation.
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