Abstract
The NIH Summit, Advances in Geroscience: Impact on Health Span and Chronic Disease, discusses several aspects of cellular degeneration that underlie susceptibility to chronic aging-associated diseases, morbidity, and mortality. In particular, the session on Metabolism focuses on the interrelationship between signal transduction, intermediary metabolism, and metabolic products and byproducts that contribute to pathophysiologic phenotypes and detrimental effects that occur during the aging process, thus leading to susceptibility to disease. Although it is well established that many metabolic pathways (ie, oxidative phosphorylation, insulin-stimulated glucose uptake) decline with age, it often remains uncertain if these are a cause or consequence of the aging process. Moreover, the mechanisms accounting for the decline in metabolic function remain enigmatic. Several novel and unexpected concepts are emerging that will help to define the roles of altered metabolic control in the degenerative mechanisms of aging. This brief review summarizes several of the topics to be discussed in the metabolism of aging session (http://www.geron.org/About%20Us/nih-geroscience-summit).
Highlights
Are the metabolic dysfunctions that occur during aging a result of cell autonomous defects or are they due to a CNS-mediated integrated response? Is there a relationship between hypothalamic degeneration and dysregulation of circadian control of metabolism?
Funding This article was funded by National Institutes of Health
Summary
The NIH Summit, Advances in Geroscience: Impact on Health Span and Chronic Disease, discusses several aspects of cellular degeneration that underlie susceptibility to chronic aging-associated diseases, morbidity, and mortality. Macroautophagy is characterized by de novo formation of double membrane phagophore structures that sequester organelles and long-lived proteins and subsequently generate large limited membrane vesicles termed autophagosomes that fuse with lysosomes, resulting in the degradation of the autophagosome contents It is well established in multiple systems that macroautophagy declines with aging, whereas its restoration prevents several age-related pathologies. AMPK activates macroautophagy, through inhibition of mTORC1 and by activating the ULK1 kinase [9,10,11,12,13] These findings provide an intriguing link between nutrient sensing and signaling pathways that may potentially account for the ability of rapamycin and metformin to promote longevity. Further studies are needed to determine whether enhanced nutrient catabolism modulates longevity by reducing death-inducing pathologies (eg, cardiovascular disease, cancer, etc.) and/or reduces aging-dependent phenotypes associated with extension of healthy life span
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callMore From: The Journals of Gerontology Series A: Biological Sciences and Medical Sciences
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
