|1.||Tsutsumi, Kazuhiko: 12 articles (10/2011 - 01/2002)|
|2.||Yin, Weidong: 8 articles (10/2011 - 01/2002)|
|3.||Nakaya, Yutaka: 6 articles (10/2011 - 06/2002)|
|4.||Kusunoki, Masataka: 5 articles (10/2011 - 06/2002)|
|5.||Nakamura, Takao: 5 articles (10/2011 - 06/2002)|
|6.||Tsutsumi, K: 5 articles (03/2004 - 02/2000)|
|7.||Miyata, Tetsuro: 4 articles (10/2011 - 06/2002)|
|8.||Wang, Zongbao: 4 articles (10/2011 - 01/2003)|
|9.||Liu, Yi: 4 articles (01/2011 - 07/2006)|
|10.||Zhang, Chi: 4 articles (01/2011 - 07/2006)|
07/01/1993 - "In summary, the results of our study indicate that compound NO-1886 increases LPL activity, causing an elevation in HDL levels, and that long-term administration of NO-1886 to rats with experimental atherosclerosis provides significant protection against the development of coronary artery lesions."
01/01/2002 - "Furthermore, NO-1886 provided protection against the development of atherosclerosis in the aorta. "
09/01/2006 - "These results demonstrate that the mechanism of atherosclerosis inhibition for NO-1886 is associated with its effect on ABCA1."
09/01/2006 - "However, the mechanism of atherosclerosis inhibition for NO-1886 is not fully understood. "
09/01/2006 - "NO-1886 has been proven to be highly effective at increasing HDL-C and reducing atherosclerosis. "
03/01/2004 - "Therefore, NO-1886 is potentially beneficial for the treatment of insulin-resistance syndrome."
01/01/2003 - "In the current study, we investigated the effects of NO-1886 on insulin resistance and beta-cell function in rabbits. "
03/01/2004 - "However, supplementing 1% NO-1886 (200 mg/kg per day) into the high-fat/high-sucrose diet decreased ectopic lipid deposition, improved insulin resistance, and alleviated the beta cell damage. "
06/01/2002 - "Administration of the LPL activator NO-1886 improved the insulin resistance, resulting in an improvement in the relationship between triglyceride and glycogen content in liver of high-fat-fed rats."
01/01/2010 - "These findings indicate that NO-1886 upregulates IGF1 secretion and CYP7A1 expression to improve insulin resistance and hepatic cholesterol accumulation, which may represent an alternative therapeutic avenue of NO-1886 for T2DM and metabolic syndrome."
02/22/2005 - "In this study, therefore, the effects of NO-1886 on hyperlipidemia and intestinal polyp formation were investigated in Min mice. "
05/01/2000 - "The aim of this study was to ascertain whether NO-1886 suppresses the renal injury by treatment of the hyperlipidemia in an Adriamycin (Kyowa Hakko Kogyo, Tokyo, Japan) induced nephrosis rat model fed a high-protein diet that induced renal dysfunction and tubulointerstitial injury. "
02/22/2005 - "Concurrent suppression of hyperlipidemia and intestinal polyp formation by NO-1886, increasing lipoprotein lipase activity in Min mice."
12/01/1996 - "Suppression of hyperlipidemia-associated cataracts in diabetic rats with the lipoprotein lipase activator NO-1886."
06/01/2002 - "When the lipoprotein lipase (LPL) activator NO-1886 was administered to the high-fat-fed rats at a daily dose of 50 mg/kg body weight for 10 weeks, GIR (9.87 +/- 3.76 mg/kg/min, P <.05 v high-fat-fed control group) improved, causing an improvement of the hyperlipidemia, hyperglycemia, and hyperinsulinemia. "
|4.||Body Weight (Weight, Body)
02/01/2006 - "However, the effect of NO-1886 on body weight, fat accumulation, and energy expenditure in ovariectomized (OVX) rats is not clear. "
12/01/2005 - "NO-1886 suppressed the body weight increase seen in the high-fat control group after the 8-week administration (585 +/- 39 vs 657 +/- 66 g, P < .05). "
02/01/2006 - "NO-1886 decreased accumulation of visceral fat and suppressed the increase in body weight resulting from the ovariectomy. "
10/15/2011 - "In summary, the combined administration of pioglitazone and NO-1886 prevented the pioglitazone-induced body weight gains and ameliorated insulin resistance observed in high-fat fed rats. "
09/01/2006 - "Administration of NO-1886 (0.1 g/kg body weight/day) in the diet for 5 months significantly reduced atherosclerosis lesions and significantly increased plasma HDL-C and apolipoprotein A-I levels. "
02/01/2006 - "Our study indicates that the LPL-promoting agent NO-1886 may be potentially beneficial in the treatment of obesity and obesity-linked health problems in postmenopausal women."
02/01/2008 - "Administration of NO-1886 attenuated the obesity-induced hypercontractility of the colonic rings of OLETF rats. "
12/01/2003 - "However, the anti-obesity mechanism of NO-1886 has not been clearly understood. "
02/01/2006 - "The primary aim of this study was to ascertain whether NO-1886 ameliorated obesity in OVX rats and to examine the effects on fatty acid oxidation-related enzymes. "
02/01/2006 - "Therefore, amelioration of obesity by NO-1886 in OVX rats is possibly because of an the increased expression of fatty acid oxidation-related enzymes and UCP3, both of which are related to fatty acid transfer and fat use. "
|1.||Lipoprotein Lipase (Diacylglycerol Lipase)
|2.||4- diethoxyphosphorylmethyl- N- (4- bromo- 2- cyanophenyl)benzamide
|6.||Messenger RNA (mRNA)