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Ting Xiao, Xiuci Liang, Hailan Liu, Feng Zhang, Wen Meng and Fang Hu

SREBP (p-SREBP) to functional mature SREBP (m-SREBP) ( Han & Wang 2018 ). However, the mechanisms underlying ER stress-induced hepatic lipogenesis and steatosis via the mTORC1- SREBP1 signaling pathway are yet to be completely elucidated. Similar to

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Yuumi Ishizuka, Kazuhiro Nakayama, Ayumi Ogawa, Saho Makishima, Supichaya Boonvisut, Atsushi Hirao, Yusaku Iwasaki, Toshihiko Yada, Yoshiko Yanagisawa, Hiroshi Miyashita, Masafumi Takahashi, Sadahiko Iwamoto and Jichi Medical University Promotion Team of a Large-Scale Human Genome Bank for All over Japan

hepatic lipogenesis, which affects very low density lipoprotein (VLDL) production ( Burkhardt et al . 2010 ). However, the molecular mechanisms remain unknown. Therefore, we explored the molecular pathways using a mouse model and functional variations in

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Horng-Yih Ou, Hung-Tsung Wu, Feng-Hwa Lu, Yu-Chu Su, Hao-Chang Hung, Jin-Shang Wu, Yi-Ching Yang, Chao-Liang Wu and Chih-Jen Chang

cells were used to clarify the possible mechanisms of FFAR1-regulated hepatic lipogenesis. Materials and methods Materials Chelethyrine and U73343 were purchased from Sigma–Aldrich. GW9805 and U73122 were purchased from Tocris Bioscience (Ellisville, MO

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Carolina Gustavsson, Tomoyoshi Soga, Erik Wahlström, Mattias Vesterlund, Alireza Azimi, Gunnar Norstedt and Petra Tollet-Egnell

, we hypothesise that high-fat feeding in female ZDF rats would lead to a more male-like hepatic phenotype, including increased FA oxidation and ROS production, reduced lipogenesis and/or increased gluconeogenesis. By identifying the genes and

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Young Ho Suh, Younyoung Kim, Jeong Hyun Bang, Kyoung Suk Choi, June Woo Lee, Won-Ho Kim, Tae Jeong Oh, Sungwhan An and Myeong Ho Jung

lipogenic genes, deteriorates with prolonged obesity ( Nadler et al. 2000 ) and reduced lipogenic adipocytes are associated with increased hepatic lipogenesis, which may be a shift in the lipogenic burden from adipocytes to other organs such as the liver

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Yajie Guo, Junjie Yu, Chunxia Wang, Kai Li, Bin Liu, Ying Du, Fei Xiao, Shanghai Chen and Feifan Guo

NAFLD is essential. The largest contributor to liver steatosis is dysregulated hepatic de novo lipogenesis (DNL) ( Fabbrini et al . 2010 ). DNL is a process in which the cell makes fatty acids from nonfat materials and liver is the most important

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Sachie Nakamichi, Yoko Senga, Hiroshi Inoue, Aki Emi, Yasushi Matsuki, Eijiro Watanabe, Ryuji Hiramatsu, Wataru Ogawa and Masato Kasuga

by PCR. For assay of hepatic gene expression during refeeding, C57BL/6 mice were deprived of food for 24 h and then fed with a high-carbohydrate chow containing 70% sucrose. Statistical analysis Unless indicated otherwise, quantitative data are

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W Becker, R Kluge, T Kantner, K Linnartz, M Korn, G Tschank, L Plum, K Giesen and HG Joost

New Zealand obese (NZO) mice exhibit severe insulin resistance of hepatic glucose metabolism. In order to define its biochemical basis, we studied the differential expression of genes involved in hepatic glucose and lipid metabolism by microarray analysis. NZOxF1 (SJLxNZO) backcross mice were generated in order to obtain populations with heterogeneous metabolism but comparable genetic background. In these backcross mice, groups of controls (normoglycemic/normoinsulinemic), insulin-resistant (normoglycemic/hyperinsulinemic) and diabetic (hyperglycemic/hypoinsulinemic) mice were identified. At 22 weeks, mRNA was isolated from liver, converted to cDNA, and used for screening of two types of cDNA arrays (high-density filter arrays and Affymetrix oligonucleotide microarrays). Differential gene expression was ascertained and assessed by Northern blotting. The data indicate that hyperinsulinemia in the NZO mouse is associated with: (i) increased mRNA levels of enzymes involved in lipid synthesis (fatty acid synthase, malic enzyme, stearoyl-CoA desaturase) or fatty acid oxidation (cytochrome P450 4A14, ketoacyl-CoA thiolase, acyl-CoA oxidase), (ii) induction of the key glycolytic enzyme pyruvate kinase, and (iii) increased mRNA levels of the gluconeogenic enzyme phosphoenolpyruvate carboxykinase. These effects were enhanced by a high-fat diet. In conclusion, the pattern of gene expression in insulin-resistant NZO mice appears to reflect a dissociation of the effects of insulin on genes involved in glucose and lipid metabolism. The data are consistent with a hypothetical scenario in which an insulin-resistant hepatic glucose production produces hyperinsulinemia, and an enhanced insulin- and substrate-driven lipogenesis further aggravates the deleterious insulin resistance of glucose metabolism.

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Yueting Dong, Zhiye Xu, Ziyi Zhang, Xueyao Yin, Xihua Lin, Hong Li and Fenping Zheng

. 2003 , Laffitte et al . 2003 ). It is generally believed that LXR-induced hepatic steatosis results from increased de novo lipogenesis (DNL) ( Chisholm et al . 2003 ). However, recent study using analysis of dynamic adaptations in parameter

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Haoyong Yu, Mingliang Zhang, Yunqin Ma, Junxi Lu, Jiemin Pan, Pan Pan, Haibing Chen and Weiping Jia

lipogenesis-related genes ACC, SREBP-1C and FAS, though no differences between the two groups were observed (data not shown). These findings implied that 5-ALA may alleviate hepatic steatosis through the AMPK signaling to increase fatty acid oxidation