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A new AMPK isoform mediates glucose-restriction induced longevity non-cell autonomously by promoting membrane fluidity
- Title
- A new AMPK isoform mediates glucose-restriction induced longevity non-cell autonomously by promoting membrane fluidity
- Authors
- Jeong; Jin-Hyuck; Han; Jun-Seok; Jung; Youngae; Lee; Seung-Min; Park; So-Hyun; Mooncheol; Shin; Min-Gi; Kim; Nami; Kang; Mi Sun; Seokho; Kwang-Pyo; Kwon; Ki-Sun; Chun-A.; Yang; Yong Ryoul; Hwang; Geum-Sook; Eun-Soo
- Ewha Authors
- 황금숙
- SCOPUS Author ID
- 황금숙
- Issue Date
- 2023
- Journal Title
- Nature Communications
- ISSN
- 2041-1723
- Citation
- Nature Communications vol. 14, no. 1
- Publisher
- Nature Research
- Indexed
- SCIE; SCOPUS
- Document Type
- Article
- Abstract
- Dietary restriction (DR) delays aging and the onset of age-associated diseases. However, it is yet to be determined whether and how restriction of specific nutrients promote longevity. Previous genome-wide screens isolated several Escherichia coli mutants that extended lifespan of Caenorhabditis elegans. Here, using 1H-NMR metabolite analyses and inter-species genetics, we demonstrate that E. coli mutants depleted of intracellular glucose extend C. elegans lifespans, serving as bona fide glucose-restricted (GR) diets. Unlike general DR, GR diets don’t reduce the fecundity of animals, while still improving stress resistance and ameliorating neuro-degenerative pathologies of Aβ42. Interestingly, AAK-2a, a new AMPK isoform, is necessary and sufficient for GR-induced longevity. AAK-2a functions exclusively in neurons to modulate GR-mediated longevity via neuropeptide signaling. Last, we find that GR/AAK-2a prolongs longevity through PAQR-2/NHR-49/Δ9 desaturases by promoting membrane fluidity in peripheral tissues. Together, our studies identify the molecular mechanisms underlying prolonged longevity by glucose specific restriction in the context of whole animals. © 2023, The Author(s).
- DOI
- 10.1038/s41467-023-35952-z
- Appears in Collections:
- 자연과학대학 > 화학·나노과학전공 > Journal papers
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