@article{oai:tsukuba.repo.nii.ac.jp:00039470,
 author = {武内, 謙憲 and TAKEUCHI, Yoshinori and 矢作, 直也 and YAHAGI, Naoya and 會田, 雄一 and AITA, Yuichi and Murayama, Yuki and Sawada, Yoshikazu and Piao, Xiaoying and Toya, Naoki and Oya, Yukari and Shikama, Akito and Takarada, Ayako and Masuda, Yukari and Nishi, Makiko and Kubota, Midori and Izumida, Yoshihiko and Yamamoto, Takashi and Sekiya, Motohiro and Matsuzaka, Takashi and Nakagawa, Yoshimi and Urayama, Osamu and Kawakami, Yasushi and Iizuka, Yoko and Gotoda, Takanari and Itaka, Keiji and Kataoka, Kazunori and Nagai, Ryozo and Kadowaki, Takashi and Yamada, Nobuhiro and Lu, Yuan and Jain, Mukesh?K. and Shimano, Hitoshi},
 issue = {9},
 journal = {Cell Reports},
 month = {Aug},
 note = {Hepatic lipogenesis is nutritionally regulated (i.e., downregulated during fasting and upregulated during the postprandial state) as an adaptation to the nutritional environment. While alterations in the expression level of the transcription factor SREBP-1c are known to be critical for nutritionally regulated lipogenesis, upstream mechanisms governing Srebf1 expression remain unclear. Here, we show that the fasting-induced transcription factor KLF15, a key regulator of gluconeogenesis, forms a complex with LXR/RXR, specifically on the Srebf1 promoter. This complex recruits the corepressor RIP140 instead of the coactivator SRC1, resulting in reduced Srebf1 and thus downstream lipogenic enzyme expression during the early and euglycemic period of fasting prior to hypoglycemia and PKA activation. Through this mechanism, KLF15 overexpression specifically ameliorates hypertriglyceridemia without affecting LXR-mediated cholesterol metabolism. These findings reveal a key molecular link between glucose and lipid metabolism and have therapeutic implications for the treatment of hyperlipidemia.},
 pages = {2373--2386},
 title = {KLF15 Enables Rapid Switching between Lipogenesis and Gluconeogenesis during Fasting},
 volume = {16},
 year = {2016},
 yomi = {タケウチ, ヨシノリ and ヤハギ, ナオヤ and アイタ, ユウイチ}
}