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Compound C75
- Thread starter bigrand
- Start date
I researched C75 two years ago. It isn't the answer. The problem is that it kills the appetite while blocking fat synthesis. There is a biochemist at Baylor U working on a drug that blocks fat synthesis at the rate-determining step, which is the step before where C75 works. At the rate determining step, fat synthesis is blocked and appetite is not suppressed. There was an article in the Houston Chronicle about two years ago about this research. The researcher's name is Dr. Salih Wakil. If he is able to develop a drug that will block this step, look for a Nobel Prize. The theory is that if the body isn't storing fat, it is using it. Do a search and see if you can find the article in the Houston Chronicle.
From what ive read, it actually opens up the michtochondria to abundant fatty acid oxidation. The idea of something that curbs the appitite is not what strikes me, its that the high levels of malonyl-CoA makes the body think its well fed even if it isnt getting any food intake. So now, starvation diet=no starvation mode of the body. Metabolic rate is never compromised and fatty acid is never synthesised. This compound makes a calorie defficent diet much more effective and less catabolic. I have attatched an abstract explaining noted decrease in adipose stores. There was some more into how malonyl-CoA plays into keeping the michtochondria oxidizing fatty acids at a very high level, i will try to find it.
Proc Natl Acad Sci U S A 2002 Jul 9;99(14):9498-502 (ISSN: 0027-8424)
Thupari JN; Landree LE; Ronnett GV; Kuhajda FP
Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.
C75, a known inhibitor of fatty acid synthase is postulated to cause significant weight loss through decreased hypothalamic neuropeptide Y (NPY) production. Peripherally, C75, an alpha-methylene-gamma-butyrolactone, reduces adipose tissue and fatty liver, despite high levels of malonyl-CoA. To investigate this paradox, we studied the effect of C75 on fatty acid oxidation and energy production in diet-induced obese (DIO) mice and cellular models. Whole-animal calorimetry showed that C75-treated DIO mice had a 50% greater weight loss, and a 32.9% increased production of energy because of fatty acid oxidation, compared with paired-fed controls. Etomoxir, an inhibitor of carnitine O-palmitoyltransferase-1 (CPT-1), reversed the increased energy expenditure in DIO mice by inhibiting fatty acid oxidation. 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. Studies in human cancer cells showed that C75 competed with malonyl-CoA, as measured by CPT-1 activity assays. Thus, C75 acts both centrally to reduce food intake and peripherally to increase fatty acid oxidation, leading to rapid and profound weight loss, loss of adipose mass, and resolution of fatty liver. The pharmacological stimulation of CPT-1 activity is a novel finding. The dual action of the C75 class of compounds as fatty acid synthase inhibitors and CPT-1 agonists has therapeutic implications in the treatment of obesity and type II diabetes.
Comment In: Comment In: RefSource
roc Natl Acad Sci U S A. 2002 Jul 9; 99(14):9096-7/PMID:12093927
Proc Natl Acad Sci U S A 2002 Jul 9;99(14):9498-502 (ISSN: 0027-8424)
Thupari JN; Landree LE; Ronnett GV; Kuhajda FP
Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.
C75, a known inhibitor of fatty acid synthase is postulated to cause significant weight loss through decreased hypothalamic neuropeptide Y (NPY) production. Peripherally, C75, an alpha-methylene-gamma-butyrolactone, reduces adipose tissue and fatty liver, despite high levels of malonyl-CoA. To investigate this paradox, we studied the effect of C75 on fatty acid oxidation and energy production in diet-induced obese (DIO) mice and cellular models. Whole-animal calorimetry showed that C75-treated DIO mice had a 50% greater weight loss, and a 32.9% increased production of energy because of fatty acid oxidation, compared with paired-fed controls. Etomoxir, an inhibitor of carnitine O-palmitoyltransferase-1 (CPT-1), reversed the increased energy expenditure in DIO mice by inhibiting fatty acid oxidation. 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. Studies in human cancer cells showed that C75 competed with malonyl-CoA, as measured by CPT-1 activity assays. Thus, C75 acts both centrally to reduce food intake and peripherally to increase fatty acid oxidation, leading to rapid and profound weight loss, loss of adipose mass, and resolution of fatty liver. The pharmacological stimulation of CPT-1 activity is a novel finding. The dual action of the C75 class of compounds as fatty acid synthase inhibitors and CPT-1 agonists has therapeutic implications in the treatment of obesity and type II diabetes.
Comment In: Comment In: RefSource
roc Natl Acad Sci U S A. 2002 Jul 9; 99(14):9096-7/PMID:12093927Oh yeah, it also induces malignant cell specific apoptosis, which isnt a bad thing.......and is non toxic, and has no negative effects on proliferating cellular compartments like marrow, GI tract, skin, and lymphoid tissue.
Glad to be able to discuss this weird stuff with someone!
Glad to be able to discuss this weird stuff with someone!
