|1.||Shimano, Hitoshi: 13 articles (01/2015 - 01/2002)|
|2.||Yamada, Nobuhiro: 7 articles (08/2011 - 06/2005)|
|3.||Matsuzaka, Takashi: 6 articles (08/2011 - 06/2005)|
|4.||Suzuki, Hiroaki: 5 articles (08/2011 - 06/2005)|
|5.||Nakagawa, Yoshimi: 5 articles (08/2011 - 06/2005)|
|6.||Takahashi, Akimitsu: 5 articles (08/2011 - 06/2005)|
|7.||Yahagi, Naoya: 5 articles (08/2011 - 06/2005)|
|8.||Deng, Xiong: 4 articles (01/2013 - 12/2004)|
|9.||Videla, Luis A: 4 articles (01/2012 - 11/2009)|
|10.||Sone, Hirohito: 4 articles (08/2011 - 06/2005)|
03/03/2015 - "The present study was conducted to explore the mechanism of SREBP-1c in the regulation of IRS-1 in skeletal muscle cells and elucidate the role of SREBP-1c in high fat-induced skeletal muscle insulin resistance. "
10/01/2008 - "The present study aimed to confirm the previously reported association in a Chinese population and to examine the two SREBP-1c SNPs for their associations with insulin resistance and blood lipid. "
03/01/2004 - "In summary, we have conducted the first study of the SREBP-1c gene as a candidate for human insulin resistance. "
03/01/2014 - "These findings imply that SREBP-1c could serve as an attractive therapeutic target for insulin resistance."
03/01/2014 - "Our data indicate for the first time that SREBP-1c activation participates in skeletal muscle insulin resistance through a direct effect of suppressing Irs-1 transcription. "
10/01/2006 - "However, putative elevation of SREBP-1c activity in these tissues did not cause hypertriglyceridemia. "
07/01/2005 - "Conversely, inhibition of SOCS-1 and -3 in obese diabetic mice improves insulin sensitivity, normalizes the increased expression of SREBP-1c, and dramatically ameliorates hepatic steatosis and hypertriglyceridemia. "
07/13/2004 - "Conversely, inhibition of SOCS-1 and -3 in obese diabetic mice improves insulin sensitivity, normalizes the increased expression of SREBP-1c, and dramatically ameliorates hepatic steatosis and hypertriglyceridemia. "
02/08/2012 - "Insulin resistance leads to hypertriglyceridemia and hepatic steatosis and is associated with increased SREBP-1c, a transcription factor that activates fatty acid synthesis. "
05/01/2007 - "Uncontrolled activation of nuclear SREBP-1c in the liver can cause hepatosteatosis, hypertriglyceridemia, and hepatic insulin resistance due to direct suppression of insulin signaling pathways, precipitating development of metabolic syndrome. "
12/01/2004 - "This study clearly demonstrates that substitution of dietary polyunsaturated fatty acid for carbohydrate in the corpulent JCR:LA-cp rat reduces de novo lipogenesis, at least in part, by reducing hepatic expression of SREBP-1c and that strategies directed toward reducing SREBP-1c expression in the liver may mitigate the adverse effects of hyperinsulinemia on hepatic lipid production."
01/01/2014 - "Hyperinsulinemia induces transcription of SREBP-1c via activation of liver X receptor (LXR) and specificity protein 1 (Sp1). "
05/01/2013 - "Hyperinsulinemia induces SREBP-1c transcription through liver X receptor (LXR), specificity protein 1, and SREBP-1c itself. "
11/01/2011 - "These changes may lead to hepatic steatosis by different mechanisms, namely, (i) IR-dependent higher peripheral lipolysis and FA flux to the liver, (ii) n-3 LCPUFA depletion-induced changes in DNA binding activity of sterol regulatory element-binding protein 1c (SREBP-1c) and peroxisome proliferator-activated receptor α (PPAR-α) favouring lipogenesis over FA oxidation, and (iii) hyperinsulinemia-induced activation of lipogenic factor PPAR-γ. "
05/01/2006 - "L-p85DKO mice failed to activate PI3K or generate PIP(3) upon insulin stimulation or activate its two major effectors, Akt and PKClambda/xi. Decreased Akt activation resulted in increased gluconeogenic gene expression, impaired glucose tolerance, and hyperinsulinemia, while the defective activation of PKClambda/xi by insulin was associated with hypolipidemia and decreased transcription of SREBP-1c. "
04/01/2015 - "In this article we reported a novel synthetic compound 2-(3-benzoylthioureido)-4,5,6,7-tetrahydrobenzo[b]thiophene-3-carboxylic acid (ZJ001) that inhibited the SREBP-1c pathway, and effectively reduced hepatic lipid accumulation in diet-induced obesity (DIO) mice. "
01/01/2015 - "[SREBP-1c and Elovl6 as Targets for Obesity-related Disorders]."
07/02/2013 - "LXRs are essential for obesity-driven SREBP-1c and ChREBP activity in liver, but not fat. "
04/01/2005 - "Interestingly, the inability of LXR-/- mice to induce SREBP-1c-dependent lipogenesis does not explain the LXR-/- phenotype, since SREBP-1c null mice are not obesity resistant. "
11/01/2001 - "Sterol regulatory element binding protein 1c (SREBP-1c) expression in human obesity."
|5.||Alcoholic Fatty Liver
12/01/2009 - "lanceolata root water extract appears to be protective against alcoholic fatty liver through the regulation of SREBP-1c, LXRalpha, HMGR, and LDLR genes and by the phosphorylation of AMPKalpha and ACC, which are implicated in lipid metabolism."
04/01/2008 - "In addition, activation of hepatocellular STAT3 ameliorates alcoholic fatty liver via inhibition of sterol regulatory element-binding protein 1c expression."
02/01/2010 - "Increased liver oxidative stress and altered PUFA metabolism precede development of non-alcoholic steatohepatitis in SREBP-1a transgenic spontaneously hypertensive rats with genetic predisposition to hepatic steatosis."
|3.||Messenger RNA (mRNA)
|4.||Fatty Acid Synthetase Complex (Fatty Acid Synthase)
|6.||Non-alcoholic Fatty Liver Disease
|1.||Heterologous Transplantation (Xenotransplantation)
|2.||Fat-Restricted Diet (Diet, Fat Restricted)
|3.||Nutrition Therapy (Medical Nutrition Therapy)