Malonyl Coenzyme A (Malonyl CoA)

05/01/2006 - "The concomitant increase in IMCL with the fall of malonyl-CoA support the concept that, as a reaction to starvation-induced FFA availability, muscle will activate lipid oxidation more the lower its oxidative capacity and then store the rest as IMCL."
05/01/2006 - "The decreases of malonyl-CoA in wTA and EDL during starvation were more pronounced in lean than in obese rats, although there were no changes in soleus muscles for both groups. "
06/01/1999 - "In contrast, during refeeding after starvation, the increase in malonyl-CoA in muscle is probably due to another mechanism."
09/15/1995 - "Peroxisomal and microsomal CPT also had decreased sensitivity to inhibition by malonyl-CoA during starvation. "
09/15/1995 - "Regulation of malonyl-CoA sensitivity of CPT-I in isolated mitochondrial outer membranes was indicated by an 8-fold increase in Ki during starvation and by a 50-fold increase in Ki in the diabetic state. "

12/01/2011 - "SWOP induced a shift towards LCFA oxidation during stenosis, despite increased malonyl-CoA, and marked protection of contractile function with a significant improvement in systolic wall thickening. "

01/01/2005 - "Paradoxically, high-dose GLA treatments of FAS-overexpressing breast cancer cells will promote malonyl-CoA-induced inhibition of CPT-I and FA oxidation, thus precipitating an energy crisis that triggers decreased proliferation or apoptotic cell death. "
11/01/2003 - "Recent data has shown that C75 directly stimulates CPT-1 increasing fatty acid oxidation in MCF-7 human breast cancer cells despite inhibitory concentrations of malonyl-CoA. "
08/20/2009 - "Similar to MCD siRNA, MPA inhibits MCD activity in MCF7 cells, increases cellular malonyl-CoA levels and is cytotoxic to a number of human breast cancer cell lines in vitro. "
06/01/2006 - "Collectively, our results indicate that inhibition of FAS in breast cancer cells causes accumulation of malonyl-CoA, which leads to inhibition of CPT-1 and up-regulation of ceramide and induction of the proapoptotic genes BNIP3, TRAIL, and DAPK2, resulting in apoptosis."
07/09/2002 - "C75 treatment of rodent adipocytes and hepatocytes and human breast cancer cells increased fatty acid oxidation and ATP levels by increasing CPT-1 activity, even in the presence of elevated concentrations of malonyl-CoA. "

07/09/2002 - "Studies in human cancer cells showed that C75 competed with malonyl-CoA, as measured by CPT-1 activity assays. "
08/01/2005 - "These findings indicate that accumulation of malonyl-CoA is not a prerequisite for cytotoxicity induced by inhibition of tumor-associated lipogenesis and suggest that in addition to FAS, ACC-alpha is a potential target for cancer intervention."
01/15/2000 - "The data suggest that differences in intermediary metabolism render tumor cells susceptible to toxic fluxes in malonyl-CoA, both in vitro and in vivo."
04/01/2009 - "Decrease in malonyl-CoA and its background metabolic alterations in murine model of cancer cachexia."
08/20/2009 - "Fatty acid synthase (FAS) inhibition initiates selective apoptosis of cancer cells both in vivo and in vitro, which may involve malonyl-CoA metabolism. "

02/01/2011 - "Hypothalamic malonyl-CoA and CPT1c in the treatment of obesity."
01/15/2007 - "This review will focus on the emerging role of malonyl-CoA as a key "metabolic effector" of both obesity and cardiac fatty acid oxidation. "
10/15/2006 - "In muscle, increased malonyl-CoA, decreased muscle CPT1 activity, and increased IML have all been reported in obesity. "
02/01/2006 - "These findings indicate that nutritional modulation of the hypothalamic abundance of malonyl-coenzyme A is required to restrain food intake and that a primary impairment in this central nutrient-sensing pathway is sufficient to disrupt energy homeostasis and induce obesity."
01/15/2007 - "Both hypothalamic and cardiac studies have demonstrated that control of malonyl-CoA levels has an important impact on obesity and heart disease. "