アイテム詳細

登録内容を編集

このアイテムは取り下げられました。詳細要約

取り下げ

学術論文

Activation of AMPK by the putative dietary restriction mimetic metformin is insufficient to extend lifespan in Drosophila

MPS-Authors

Slack, C.
Max Planck Society;

Foley, A.
Max Planck Society;

Partridge, L.
Max Planck Society;

External Resource

(アクセスなし)

Fulltext (restricted access)

There are currently no full texts shared for your IP range.

フルテキスト (公開)

公開されているフルテキストはありません

付随資料 (公開)

There is no public supplementary material available

引用

Slack, C., Foley, A., & Partridge, L. (2012). Activation of AMPK by the putative dietary restriction mimetic metformin is insufficient to extend lifespan in Drosophila. PLoS ONE, 7(10), e47699. doi:10.1371/journal.pone.0047699.

要旨

The biguanide drug, metformin, commonly used to treat type-2 diabetes, has been shown to extend lifespan and reduce fecundity in C. elegans through a dietary restriction-like mechanism via the AMP-activated protein kinase (AMPK) and the AMPK-activating kinase, LKB1. We have investigated whether the longevity-promoting effects of metformin are evolutionarily conserved using the fruit fly, Drosophila melanogaster. We show here that while feeding metformin to adult Drosophila resulted in a robust activation of AMPK and reduced lipid stores, it did not increase lifespan in either male or female flies. In fact, we found that when administered at high concentrations, metformin is toxic to flies. Furthermore, no decreases in female fecundity were observed except at the most toxic dose. Analysis of intestinal physiology after metformin treatment suggests that these deleterious effects may result from disruptions to intestinal fluid homeostasis. Thus, metformin appears to have evolutionarily conserved effects on metabolism but not on fecundity or lifespan.