Open AccessCaenorhabditis elegans Lipin 1 moderates the lifespan‐shortening effects of dietary glucose by maintaining ω‐6 polyunsaturated fatty acids
Author(s) -
Jung Yoonji,
Kwon Sujeong,
Ham Seokjin,
Lee Dongyeop,
Park HaeEun H.,
Yamaoka Yasuyo,
Jeong DaeEun,
Artan Murat,
Altintas Ozlem,
Park Sangsoon,
Hwang Wooseon,
Lee Yujin,
Son Heehwa G.,
An Seon Woo A.,
Kim Eun Ji E.,
Seo Mihwa,
Lee SeungJae V.
Publication year - 2020
Publication title -
aging cell
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.103
H-Index - 140
eISSN - 1474-9726
pISSN - 1474-9718
DOI - 10.1111/acel.13150
Subject(s) - biology , polyunsaturated fatty acid , caenorhabditis elegans , gene knockdown , arachidonic acid , lipolysis , linoleic acid , endocrinology , medicine , downregulation and upregulation , phosphatidic acid , biochemistry , fatty acid , adipose tissue , enzyme , phospholipid , gene , membrane
Excessive glucose causes various diseases and decreases lifespan by altering metabolic processes, but underlying mechanisms remain incompletely understood. Here, we show that Lipin 1/LPIN‐1, a phosphatidic acid phosphatase and a putative transcriptional coregulator, prevents life‐shortening effects of dietary glucose on Caenorhabditis elegans . We found that depletion of lpin‐1 decreased overall lipid levels, despite increasing the expression of genes that promote fat synthesis and desaturation, and downregulation of lipolysis. We then showed that knockdown of lpin‐1 altered the composition of various fatty acids in the opposite direction of dietary glucose. In particular, the levels of two ω‐6 polyunsaturated fatty acids (PUFAs), linoleic acid and arachidonic acid, were increased by knockdown of lpin‐1 but decreased by glucose feeding. Importantly, these ω‐6 PUFAs attenuated the short lifespan of glucose‐fed lpin‐1 ‐inhibited animals. Thus, the production of ω‐6 PUFAs is crucial for protecting animals from living very short under glucose‐rich conditions.