@article{oai:tsukuba.repo.nii.ac.jp:00017614,
 author = {Matsumoto, Michihiro and Ogawa, Wataru and Akimoto, Kazunori and Inoue, Hiroshi and Miyake, Kazuaki and Furukawa, Kensuke and Hayashi, Yoshitake and Iguchi, Haruhisa and Matsuki, Yasushi and Hiramatsu, Ryuji and 島野, 仁 and SHIMANO, Hitoshi and 山田, 信博 and YAMADA, Nobuhiro and Ohno, Shigeo and Kasuga, Masato and Noda, Tetsuo},
 issue = {6},
 journal = {The journal of clinical investigation},
 month = {Sep},
 note = {PKCλ is implicated as a downstream effector of PI3K in insulin action. We show here that mice that lack PKCλ specifically in the liver (L-λKO mice), produced with the use of the Cre-loxP system, exhibit increased insulin sensitivity as well as a decreased triglyceride content and reduced expression of the sterol regulatory element?binding protein-1c (SREBP-1c) gene in the liver. Induction of the hepatic expression of Srebp1c and of its target genes involved in fatty acid/triglyceride synthesis by fasting and refeeding or by hepatic expression of an active form of PI3K was inhibited in L-λKO mice compared with that in control animals. Expression of Srebp1c induced by insulin or by active PI3K in primary cultured rat hepatocytes was inhibited by a dominant-negative form of PKCλ and was mimicked by overexpression of WT PKCλ. Restoration of PKCλ expression in the liver of L-λKO mice with the use of adenovirus-mediated gene transfer corrected the metabolic abnormalities of these animals. Hepatic PKCλ is thus a determinant of hepatic lipid content and whole-body insulin sensitivity.},
 pages = {935--944},
 title = {PKCλ in liver mediates insulin-induced SREBP-1c expression and determines both hepatic lipid content and overall insulin sensitivity},
 volume = {112},
 year = {2003},
 yomi = {シマノ, ヒトシ and ヤマダ, ノブヒロ}
}