Author: Jung, Yoonji; Kwon, Sujeong; Ham, Seokjin; Lee, Dongyeop; Park, Hae-Eun H.; Yamaoka, Yasuyo; Jeong, Dae-Eun; Artan, Murat; Altintas, Ozlem; Park, Sangsoon; Hwang, Wooseon; Lee, Yujin; Son, Heehwa G.; An, Seon Woo A.; Kim, Eun Ji E.; Seo, Mihwa; Lee, Seung-Jae V.
Description: 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 w-6 polyunsaturated fatty acids (PUFAs), linoleic acid and arachidonic acid, were increased by knockdown of lpin-1 but decreased by glucose feeding. Importantly, these w-6 PUFAs attenuated the short lifespan of glucose-fed lpin-1-inhibited animals. Thus, the production of w-6 PUFAs is crucial for protecting animals from living very short under glucose-rich conditions.
Subject headings: Animals; Caenorhabditis elegans; Diet; Fatty Acids, Unsaturated; Glucose; Humans; Phosphatidate Phosphatase; C. elegans; LPIN-1; Aging; Metabolism; w-6 polyunsaturated fatty acids
Publication year: 2020
Journal or book title: Aging Cell
Volume: 19
Issue: 6
Pages: e13150
Find the full text: https://www.strategian.com/fulltext/Jung2020.pdf
Find more like this one (cited by): https://scholar.google.com/scholar?cites=12118012435706919178&as_sdt=1000005&sciodt=0,16&hl=en
Serial number: 3572