Creatine metabolic role

Little is known about the role of inositol in nutrition. Inositol exhibits lipotropic activity in animals only when added to a hypolipotropic diet devoid of fat, and it exerts either no or slight activity when fat is added to the diet. Inositol has been suggested as an adjuvant in the prevention and treatment of chronic liver disease in man. It has been reported that inositol administration leads to a decrease in the level of cholesterol and lipid phosphorus in the serum of patients with diabetes mellitus. It has been postulated that inositol plays a role in creatine metabolism and therefore may be beneficial in the therapy of muscular dystrophy in conjunction with tocopherol. The value of inositol in any of the above situations remains unproved. 

After comparing the protein profiles of myocardial mitochondria between a chronic restraint stress group and a control group, 11 protein spots were found to change, of which seven were identified. Five of these proteins, carnitine palmitoyltransferase 2, mitochondrial acyl-CoA thioesterase 1, isocitrate dehydrogenase 3 (NAD ) alpha, fumarate hydratase 1, and pyruvate dehydrogenase beta, were foimd to decrease in abimdance following chronic restraint stress with fimctional roles in the Krebs cycle and lipid metabolism in mitochondria. The other two proteins, creatine kinase and prohibitin, increased after chronic restraint stress (liu et ak, 2004). 

Casey A and Greenhaff PL (2000) Does dietary creatine supplementation play a role in skeletal muscle metabolism and performance Amencaw Journal of Clinical Nutrition 72, 607S-17S. 

Skeletal muscles use many fuels to generate ATP. The most abundant immediate source of ATP is creatine phosphate. ATP also can be generated from glycogen stores either anaerobically (generating lactate) or aerobically, in which case pyruvate is converted to acetyl CoA for oxidation via the TCA cycle. All human skeletal muscles have some mitochondria and thus are capable of fatty acid and ketone body oxidation. Skeletal muscles are also capable of completely oxidizing the carbon skeletons of alanine, aspartate, glutamate, valine, leucine, and isoleucine, but not other amino acids. Each of these fuel oxidation pathways plays a somewhat unique role in skeletal muscle metabolism. 

Contact sites were first described by Hacken-BROCK (1968) in thin sections of liver mitochondria as places where the inner and outer mitochondrial membranes were in very close apposition. Van Ve-NETiE and Verkleij (1982) and Knoll and Brdiczka (1983) characterized them in freeze-fractured mitochondria. Knoll and Brdiczka (1983) and Brdiczka et al. (1986) postulated that contact sites play an important role in the regulation of the mirochondrial metabolism. Under nor-moxic conditions, the ATP formed in the mitochondria is converted into creatine phosphate by the activity of the translocase, and the mitochondrial isoenzyme of creatine kinase (Wallimann et al. 1992). So, if the cardiac metabolism is stimulated the mitochondrial ATP formation increases, as does the mitochondrial creatine kinase. Since mitochondrial creatine kinase is active in mitochondrial contact sites (Biermans et al. 1990, Nicolay et al. 1990, Jacob et al. 1992), and can even induce contact site formation (Rojo et al. 1991), the surface density of mitochondrial contact sites in this situation will be high. Mitochondria lose the ability to form contact sites after more than 15 min of ischaemia and this might be a first indication of irreversible injury (Barker et al. 1995). 

Creatine is quantitatively the main component of the NPN fraction. This molecule plays an important role in fish muscle metabolism in its phosphorylated form it is absent in crustaceans and molluscs. 

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