question...this is prob a stupid question but how exactly does DCP work, because it rids of fatty acids in the bloodstream? but ingesting a 40-40-20 diet of pro-fat-carbs, would potentially have a lot of fat ingested..or is that a different fat? kind of a noob question i know, and what about fish oils, aren't those contradictory to ridding of the fat. because i mean if you take it 30min(dcp) before a meal what a purpose is it serving? to clean up that meal of fatty acids, but then i thought good fats helped you burn fat? ahhh IM CONFUSED!! some thorough explanation would really help my dosing schedule and overall understanding of DCP thanks
The center ingredient in which DCP is based off of is of TetradecylThioacetic Acid (TTA). TTA is a 3-thia fatty acid which increases mitochondrial activity, which in itself provides numerous benefits. Insulin resistance is strongly linked to the reduction of glucose oxidation in mitochondria and a subsequent build up of glycolysis byproducts. Adipocytes also contribute hormones when fat is stored in them, so, the more fat you are carrying, the more inhibition of mitochondrial function you have (1). Mitochondria proteins function mainly to produce ATP, enhancing their function will, in short, burn more fuel. TTA enhances mitochondrial oxidative capacity and reduces free fatty acid and triglyceride levels as described below.
The peroxisome proliferator-activated receptors (PPARs) are transcription factors regulated by fatty acid derivatives, among others. These receptors are intimately involved in glucose regulation, cellular proliferation and differentiation, and most important to us, fat metabolism. There are at present three types of PPARs: alpha, gamma, and delta. The liver is the main site where fatty acids are stored or burned for energy, depending on calorie intake. When fasting, fuel sources switch from carbohydrates and fats to mainly fats, and fatty acids are released from adipocytes. In the liver, they are either reesterified to triglycerides and form very low-density lipoproteins (VLDL), which then go on to restore in adipocytes or go to cardiac and skeletal muscle for energy. They can also be broken down through beta-oxidation to form ketones. PPAR-alpha mediates the genes controlling fatty acid uptake, beta-oxidation, and gamma-oxidation, which are upregulated when in a fasted state. TTA is a PPARalpha agonist, meaning it activates these receptors. Thus, you experience the same benefits even if you are in a fed state (9,15-18). PPAR-alpha also down-regulates apolipoprotein C-III which inhibits triglyceride hydrolysis, further enhancing lipid oxidation (2).
TTA also increases the activity of enzymes of the carnitine palmitoyltransferase (CPT) sytem (9), which shuttles the newly freed up fatty acids into mitochondria to be burned for fuel (10). This system is highly underestimated in a fat loss quest, and it's activity is depressed with increased fat. Propionyl-LCarnitine (PLCAR) was added to further stimulate the CPT system (11), and is converted into propionylcoenzyme A and free carnitine (12). PLCAR has also been suspected to scavenge free radicals, as well as protect DNA from UV damage (12).
