Muscle triglycerides

Manco, M., Mingrone, G., Greco, A. V., Capristo, E., Gniuli, D., De Gaetano, A., Gasbarrini, G. Metabolism 49, 2000, 220-224. Insulin resistance directly correlates with increased saturated fatty acids in skeletal muscle triglycerides. 

Nutrient homeostasis cell uptake of glucose (especially important in adipose and muscle), amino acids (all cells) and fatty acids stimulation of glycolysis but inhibition of gluconeogenesis (liver), synthesis of glycogen (liver and muscle), triglyceride (liver and adipose) and protein (all cells) ... 

During the early minutes of exercise, carbohydrate (plasma glucose and muscle glycogen) is the predominant fuel for the working muscles. When the exercise is prolonged and intensive, carbohydrate remains a predominant fuel with lipids (plasma free fatty acids and muscle triglycerides) being of lesser importance. When the exercise is of moderate intensity, lipids eventually become the primary fuel as carbohydrate stores are reduced. 

Endothelial anchored enzyme in muscle and adipose tissue primarily responsible for hydrolysis of chylomicron and VLDL triglycerides. 

Lipoprotein metabolism is the process by which hydrophobic lipids, namely triglycerides and cholesterol, are transported within the interstitial fluid and plasma. It includes the transport of energy in the form of triglycerides from intestine and liver to muscles and adipose, as well as the transport of cholesterol both from intestine and liver to peripheral tissues, as well as from peripheral tissues back to the liver. 

The steps in the subsequent utilization of muscle LCFAs may be summarized as follows. The free fatty acids, liberated from triglycerides by a neutral triglyceride lipase, are activated to form acyl CoAs by the mediation of LCFAcyl-CoA synthetase which is situated on the outer mitochondrial membrane. The next step involves carnitine palmitoyl transferase I (CPT I, see Figure 9) which is also located on the outer mitochondrial membrane and catalyzes the transfer of LCFAcyl residues from CoA to carnitine (y-trimethyl-amino-P-hydroxybutyrate). LCFAcyl... 

The lipid in muscle is composed primarily of triglycerides (depot fats) and of phospholipids (membrane components), and is a constituent which varies enormously not only in amount present, but also in properties such as degree of saturation (species dependent). The ash of lean meat is comprised of various minerals such as phosphorus, potassium, sodium, magnesium, calcium, iron and zinc Carbohydrate was not noted in the proximate composition because while some may be present, it is normally there in low concentration compared to the other constituents. Glycogen is the carbohydrate occurring in greatest concentration in muscle but is normally degraded soon after the animal is sacrificed. 

Isotretinoin Capsules 10, 20, 40 mg 0.5-1 mg/kg/per day in two divided doses Maximum dose 2 mg/kg per day Cumulative dose 120-150 mg/day Dry skin and mucous membranes, muscle and joint pain, elevated liver enzymes and triglycerides, depression, teratogenicity... 

Intravenous lipid emulsion particles are hydrolyzed in the bloodstream by the enzyme lipoprotein lipase to release free fatty acids and glycerol. Free fatty acids then are be taken up into adipose tissue for storage (triglycerides), oxidized to energy in various tissues (e.g., skeletal muscle), or recycled in the liver to make lipoproteins. 

Metformin is the only biguanide available in the United States. It enhances insulin sensitivity of both hepatic and peripheral (muscle) tissues. This allows for increased uptake of glucose into these insulin-sensitive tissues. Metformin consistently reduces A1C levels by 1.5% to 2%, FPG levels by 60 to 80 mg/dL, and retains the ability to reduce FPG levels when they are very high (>300 mg/dL). It reduces plasma triglycerides and low-density lipoprotein (LDL) cholesterol by 8% to 15% and modestly increases high-density lipoprotein (HDL) cholesterol (2%). It does not induce hypoglycemia when used alone. 

All muscle types require ATP to achieve contraction. Glucose, fatty acids and amino acids may all be used as oxidizable substrates to produce ATP and all three energy sources may be obtained from stored intracellular sources (glycogen, triglyceride and protein) or imported from the blood stream. In quantitative terms, skeletal muscle is... 

Fatty acid utilized by muscle may arise from storage triglycerides from either adipose tissue depot or from lipid stores within the muscle itself. Lipolysis of adipose triglyceride in response to hormonal stimulation liberates free fatty acids (see Section 9.6.2) which are transported through the bloodstream to the muscle bound to albumin. Because the enzymes of fatty acid oxidation are located within subcellular organelles (peroxisomes and mitochondria), there is also need for transport of the fatty acid within the muscle cell this is achieved by fatty acid binding proteins (FABPs). Finally, the fatty acid molecules must be translocated across the mitochondrial membranes into the matrix where their catabolism occurs. To achieve this transfer, the fatty acids must first be activated by formation of a coenzyme A derivative, fatty acyl CoA, in a reaction catalysed by acyl CoA synthetase. 

The primary fuel used to support muscle contraction depends on the magnitude and duration of exercise as well as the major fibers involved. Skeletal muscle has stores of both glycogen and some triglycerides. Blood glucose and free fatty acids also may be used. 

Chylomicrons and VLDL are primarily triglyceride particles, although they each have small quantities of cholesterol esters. Chylomicrons transport dietary trig lyceride to adipose tissue and muscle, whereas VLDL transport triglyceride synthesized in the liver to these same tissues. Both chylomicrons and VLDL have apoC-II, apoE, and apoB (apoB-48 on chylomicrons and apoB-IOO on VLDL). The metabolism of these particles is shown in Figure H5-5. 

In capillaries of adipose tissue (and muscle), apoC-II activates lipoprotein lipase, the fetty adds released enter the tissue for storage, and the glycerol is retrieved by the liver, which has glycerol kinase. The chylomicron remnant is picked up by hepatocytes through the apoE receptor thus, dietary cholesterol, as well as any remaining triglyceride, is released in the hepatocyte. 

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