Scientists have actually found that metformin, a frequently prescribed drug for type 2 diabetes, can extend life expectancy in C. Elegans, a model organism. The drug achieves this by stimulating the production of ether lipids, a component of cell membranes. Research studies on C. elegans exposed that boosting the production of these lipids, whether through drug interventions or by changing genes, results in a longer life expectancy. While these findings are promising, further research studies on mammalian models are needed to identify their implications for human health.
Metformin, a widely recommended drug for type 2 diabetes, not only lowers blood sugar level levels however has also been shown to increase the life-span of C. Elegans– an animal model that shares comparable metabolic systems with humans and are frequently used to model human illness.
Research Study Findings and Ether Lipids
New research led by detectives at Massachusetts General Hospital (MGH), an establishing member of the Mass General Brigham health care system, exposes that metformin promotes durability by stimulating the bodys production of molecules called ether lipids, a significant structural part of cell membranes.
The findings, which are released in eLife, recommend that improving the production of ether lipids in human beings might support healthy aging and decrease the effect of aging-related illness.
Experimental Methodology and Outcomes
To determine the genes required to make it possible for lifespan extension in reaction to metformin and its sibling drug phenformin (drugs called biguanides), the scientists silenced specific genes in the roundworm Caenorhabditis elegans ( which shares over 80% of its proteins with people and has a typical life-span of about 2 weeks) and analyzed what takes place to the transformed worms after exposure to the medications.
The experiments reveal that genes that increase the production of ether lipids are required to extend lifespan in response to the biguanides.
Inactivation of the genes that encode for these enzymes totally avoided the longevity-promoting effects of biguanides.
Significantly, the inactivation of these genes prevented life expectancy extension in a variety of scenarios that are likewise understood to promote longevity, consisting of dietary limitation.
Ether Lipid Synthesis and Longevity
The team likewise discovered that increasing ether lipid synthesis alone (by overexpressing a single, crucial ether lipid biosynthetic enzyme called fard-1) sufficed to extend C. elegans lifespan, managing a metabolic tension defense response through a factor called SKN-1, which is the worm counterpart to the mammalian protein Nrf. This action modified metabolism to promote a longer lifespan.
” Our study links the promo of ether lipid biosynthesis as a novel restorative target to promote healthy aging. This suggests that dietary or pharmacologic intervention to promote ether lipid synthesis might one day represent a method to deal with aging and aging-related diseases,” says senior author Alexander A. Soukas, MD, PhD, Associate Director of the MGH Center for Genomic Medicine, an Associate Professor at Harvard Medical School and Weissman Family MGH Research Scholar 2018-2023.
” Because our research studies focused exclusively on interventions in C. elegans, additional studies in mammalian models (such as human cells and mice), epidemiological observation, and strenuous medical trials are required to identify the practicality of promoting ether lipid synthesis to promote human health-span and lifespan.”
Referral: “Ether lipid biosynthesis promotes lifespan extension and enables diverse pro-longevity paradigms in Caenorhabditis elegans” by Lucydalila Cedillo, Fasih M Ahsan, Sainan Li, Nicole L Stuhr, Yifei Zhou, Yuyao Zhang, Adebanjo Adedoja, Luke M Murphy, Armen Yerevanian, Sinclair Emans, Khoi Dao, Zhaozhi Li, Nicholas D Peterson, Jeramie Watrous, Mohit Jain, Sudeshna Das, Read Pukkila-Worley, Sean P Curran and Alexander A Soukas, 22 August 2023, eLife.DOI: doi:10.7554/ eLife.82210.
This work was moneyed by NIH/NIA Grants R01AG058259 and R01AG69677 (to A.A.S.) and R01AG058610 (to S.P.C.), by the Weissman Family MGH Research Scholar Award (to A.A.S.), by a NSF GRFP Award 1000253984 (to L.C.), and by NIH/NIAID R01AI130289 (to R.P.W.), and by IRACDA NIH Grant K12GM106996 (to L.C.).
Researchers have actually found that metformin, a commonly prescribed drug for type 2 diabetes, can extend life-span in C. Elegans, a design organism. The drug accomplishes this by stimulating the production of ether lipids, an element of cell membranes. Research studies on C. elegans exposed that boosting the production of these lipids, whether through drug interventions or by modifying genes, results in a longer lifespan. While these findings are promising, more studies on mammalian models are required to identify their implications for human health.
