|1.||Shulman, Gerald I: 11 articles (04/2013 - 02/2002)|
|2.||Coleman, Rosalind A: 9 articles (06/2014 - 07/2005)|
|3.||Farese, Robert V: 9 articles (04/2013 - 08/2002)|
|4.||Cline, Gary W: 7 articles (03/2011 - 04/2003)|
|5.||Rapoport, Stanley I: 6 articles (12/2014 - 11/2005)|
|6.||Watkins, Paul A: 5 articles (01/2014 - 09/2004)|
|7.||Chang, Catherine C Y: 4 articles (07/2015 - 01/2002)|
|8.||Chang, Ta-Yuan: 4 articles (07/2015 - 01/2002)|
|9.||Ellis, Jessica M: 4 articles (01/2015 - 10/2009)|
|10.||Muoio, Deborah M: 4 articles (06/2014 - 03/2004)|
07/10/2010 - "In vivo efficacy of acyl CoA: diacylglycerol acyltransferase (DGAT) 1 inhibition in rodent models of postprandial hyperlipidemia."
07/10/2010 - "Firstly, to describe and characterize a standardized model of postprandial hyperlipidemia in multiple rodent species; and secondly, apply these rodent models to the evaluation of a novel class of pharmacologic agent; acyl CoA:diacylglycerol acyltransferase (DGAT) 1 inhibitors. "
01/01/2000 - "Postprandial hyperlipidemia in streptozotocin-induced diabetic rats is due to abnormal increase in intestinal acyl coenzyme A:cholesterol acyltransferase activity."
09/01/2002 - "Avasimibe (also known as CI-1011 or PD-148515) is a selective acyl-coenzyme A:cholesterol O-acyltransferase (ACAT) inhibitory lipid-regulating agent under development by Pfizer (formerly Parke-Davis) for the potential treatment of hyperlipidemia and atherosclerosis. "
10/01/2011 - "It is known that fibrates, used in hyperlipidemia, induce acyl CoA synthetase and increase CoA concentration. "
07/01/2010 - "Accumulation of toxic lipid metabolites (fatty acyl CoA, diacylglycerol, ceramide) in muscle, liver, adipocytes, beta cells and arterial tissues contributes to insulin resistance, beta cell dysfunction and accelerated atherosclerosis, respectively, in type 2 diabetes. "
03/01/2013 - "Acyl-coenzyme A:cholesterol acyltransferase-1 (ACAT1) promotes accumulation of cholesterol ester in macrophages, thereby resulting in the foam cell formation, a hallmark of early stage in atherosclerosis. "
03/20/2012 - "Diabetes promotes an inflammatory macrophage phenotype and atherosclerosis through acyl-CoA synthetase 1."
11/01/2010 - "Acyl-coenzyme A:cholesterol O-acyltransferase-1 (ACAT-1) plays an essential role in macrophage foam cell formation and progression of atherosclerosis. "
05/01/2007 - "Monounsaturated fatty acyl-coenzyme A is predictive of atherosclerosis in human apoB-100 transgenic, LDLr-/- mice."
|3.||Bipolar Disorder (Mania)
03/01/2011 - "Valproate uncompetitively inhibits arachidonic acid acylation by rat acyl-CoA synthetase 4: relevance to valproate's efficacy against bipolar disorder."
04/01/2013 - "Propylisopropylacetic acid (PIA), a constitutional isomer of valproic acid, uncompetitively inhibits arachidonic acid acylation by rat acyl-CoA synthetase 4: a potential drug for bipolar disorder."
12/01/2014 - "Valproic acid (VPA), a mood stabilizer used for treating bipolar disorder (BD), uncompetitively inhibits acylation of arachidonic acid (AA) by recombinant AA-selective acyl-CoA synthetase 4 (Acsl4) at an enzyme inhibition constant (Ki ) of 25 mM. Inhibition may account for VPA's ability to reduce AA turnover in brain phospholipids of unanesthetized rats and to be therapeutic in BD. "
01/01/2006 - "Valproic acid selectively inhibits conversion of arachidonic acid to arachidonoyl-CoA by brain microsomal long-chain fatty acyl-CoA synthetases: relevance to bipolar disorder."
12/01/2008 - "Thus, AA turnover in brain phospholipids was reduced, and AA-selective cytosolic cPLA(2) or acyl-CoA synthetase, as well as cyclooxygenase (COX)-2, were downregulated in brains of rats given drugs effective against bipolar disorder, whereas DHA turnover and expression of DHA-selective calcium-independent iPLA(2) were unchanged. "
09/01/2009 - "Therefore agents that ameliorate the accumulation of fatty acyl CoA derivatives and/or their metabolites would be beneficial in the treatment or prevention of insulin resistance and T2D. "
08/01/2015 - "Acylcarnitines are derived from mitochondrial acyl-CoA metabolism and have been associated with diet-induced insulin resistance. "
06/01/2011 - "Amelioration of lipid-induced insulin resistance in rat skeletal muscle by overexpression of Pgc-1β involves reductions in long-chain acyl-CoA levels and oxidative stress."
03/01/2009 - "Our data provide clear evidence that a physiological increase in the capacity of long-chain fatty acyl CoA entry into mitochondria is sufficient to ameliorate lipid-induced insulin resistance in muscle."
07/01/2005 - "In contrast, HSL-KO mice were protected from diet-induced insulin resistance in skeletal muscle and heart, and these effects were associated with reduced intramuscular triglyceride and fatty acyl-CoA levels in the fat-fed HSL-KO mice. "
08/01/2015 - "Acyl CoA:monoacylglycerol acyltransferase-2 (MGAT2) has emerged as a potential peripheral target for the treatment of obesity and metabolic disorders. "
08/29/2008 - "The acyl-CoA-binding site in mammalian DGAT1 could represent a potential target for therapeutic interventions for disorders such as type-2 diabetes and obesity."
11/15/2001 - "BFIT, a unique acyl-CoA thioesterase induced in thermogenic brown adipose tissue: cloning, organization of the human gene and assessment of a potential link to obesity."
08/01/1995 - "We review evidence that increased tissue levels of fatty acyl CoA cause the beta-cell abnormalities of nondiabetic obesity and ultimately result in obesity-dependent diabetes. "
05/14/2015 - "Acyl CoA:monoacylglycerol acyltransferase-2 (MGAT2) has attracted interest as a novel target for the treatment of obesity and metabolic diseases. "
|5.||Acyl Coenzyme A (Acyl CoA)
|6.||Apolipoproteins E (ApoE)
|10.||Arachidonic Acid (Vitamin F)
|1.||Highly Active Antiretroviral Therapy (HAART)
|3.||Cardiopulmonary Resuscitation (CPR)
|4.||Gastroplasty (Vertical-Banded Gastroplasty)