Fatty acids in blood

There are limitations in the use of FDG for viability assessment. Normal myocardium (normal perfusion and normal metabolism) in diabetics may not take up FDG due to insulin resistance associated with elevated free fatty acids in blood. Consequently, there is no FDG uptake anywhere in the heart and the study is uninterpretable. Flowever, giving insulin intravenously at the time of glucose loading enhances myocardial uptake, reduces free fatty acids in blood, and provides diagnostic images. 

Bile salts secreted into the intestine are efficiently reabsorbed (greater than 95 percent) and reused. The mixture of primary and secondary bile acids and bile salts is absorbed primarily in the ileum. They are actively transported from the intestinal mucosal cells into the portal blood, and are efficiently removed by the liver parenchymal cells. [Note Bile acids are hydrophobic and require a carrier in the portal blood. Albumin carries them in a noncovalent complex, just as it transports fatty acids in blood (see p. 179).] The liver converts both primary and secondary bile acids into bile salts by conjugation with glycine or taurine, and secretes them into the bile. The continuous process of secretion of bile salts into the bile, their passage through the duodenum where some are converted to bile acids, and their subsequent return to the liver as a mixture of bile acids and salts is termed the enterohepatic circulation (see Figure 18.11). Between 15 and 30 g of bile salts are secreted from the liver into the duodenum each day, yet only about 0.5 g is lost daily in the feces. Approximately 0.5 g per day is synthesized from cholesterol in the liver to replace the lost bile acids. Bile acid sequestrants, such as cholestyramine,2 bind bile acids in the gut, prevent their reabsorption, and so promote their excretion. They are used in the treatment of hypercholesterolemia because the removal of bile acids relieves the inhibition on bile acid synthesis in the liver, thereby diverting additional cholesterol into that pathway. [Note Dietary fiber also binds bile acids and increases their excretion.]... 

Milk fat contains several compounds that have demonstrated anticancer activity in animal models. The more important ones are rumenic acid, a potent inhibitor of mammary tumorigenesis, sphingomyelin and other sphingolipids that prevent the development of intestinal tumors and butyric acid, which prevents colon and mammary tumor development. Emerging evidence suggests that milk fat can prevent intestinal infections, particularly in children, prevent allergic disorders, such as asthma and improve the level of long-chain co-3 polyunsaturated fatty acids in blood. 

Although the effects of insulin on postprandial metabolism are profound, other factors (e.g., substrate supply and allosteric effectors) also affect the rate and degree to which these processes occur. For example, elevated levels of fatty acids in blood promote lipogenesis in adipose tissue. Regulation by several allosteric effectors further ensures that competing pathways do not occur simultaneously for example, in many cell types fatty acid synthesis is promoted by citrate (an activator of acetyl-CoA carboxylase), whereas fatty acid oxidation is depressed by malonyl-CoA (an inhibitor of carnitine acyltransferase I activity). The control of fatty acid metabolism is described in Section 12.1. 

Egan, B. M., Greene, E. L., Goodfriend, T. L. (2001) Nonesterified fatty acids in blood pressure control and cardiovascular complications. Curr. Hypertens. Rep. 3 107-116. 

It is well known that ethanol may be both produced and metabolized by microbial action in biological specimens. Small amounts of hexanal may arise from degradation of fatty acids in blood on long-term storage even at — 5 to — 20°C. Hex-anal is resolved from toluene on the SPB-1 capillary GC system discussed above, but resolution may be lost if an isothermal quantitative analysis is performed. Interference from hexanal is only likely to be important, however, if very low concentrations of toluene (0.1mgl or less) are to be measured. 

Gas Phase Study of Fatty Acids in Blood Liquids. I. Technical Note Biochim, Biol. Sper. 3(4) 343-356 (1964) CA 64 2500e... 

Long-Chain Fatty Acids in Blood Fresenius Z. Anal. Chem. 267(5) 342-346 (1973) CA 80 79740z... 

Determination of Higher Fatty Acids in Blood Serum by Gas-Li quid Chromatography Using Diazomethane for Their Methylation Lab. Delo 1975(2) 90-92 CA 82 ... 

Two effects of niacin—interruption of fat cell lipolysis resulting in greatly reduced levels of non-esterified fatty acids in blood, and skin flushing are mediated by a G protein-coupled receptor, GPR109A, discovered in 2003. 

Hibino, H., Fukuda, N., Kudo, K., Kawamura, M. and Naito, C. (1984) A rapid quantitative analysis of polyunsaturated fatty acid in blood lipids by a short capillary column gas chromatography. Yukagaku 33, 625-627. 

Tsuchiya, H. Hayashi, T. Sato, M. Tatsumi, M. Takagi, N. Simultaneous separation and sensitive determination of free fatty acids in blood plasma by high-performance liquid chromatography, J.Chromatogr., 1984,309, 43-52. 

In compensation for this abnormal situation, fat is preferentially used as a sole energy source in the body. The metabolic shift to lipid utilization leads to hypertriglyceridemia accompanied by elevation of free fatty acid in blood and, in very advanced stages by elevation of ketone bodies including acetoacetate and 3-hydroxy-butyrate in blood. Increased level of CoA and acyl CoA in the diabetic rat liver was reported by Smith et al. [1]. This seems to be a metabolic response to increased utilization of fatty acid in diabetic state and suggests increased requirement for CoA in diabetic tissues. It is, therefore, interesting to study the effect of some precursors of CoA on diabetic hyperlipidemia. The present paper deals with a favorable effect of pantethine on lipid metabolism in streptozotocin diabetic rats. Pantethine treatment has been found to reduce increased levels of serum triglycerides,... 

Animal cells can modify arachidonic acid and other polyunsaturated fatty acids, in processes often involving cyclization and oxygenation, to produce so-called local hormones that (1) exert their effects at very low concentrations and (2) usually act near their sites of synthesis. These substances include the prostaglandins (PG) (Figure 25.27) as well as thromboxanes (Tx), leukotrienes, and other hydroxyeicosanoic acids. Thromboxanes, discovered in blood platelets (thrombocytes), are cyclic ethers (TxBg is actually a hemiacetal see Figure 25.27) with a hydroxyl group at C-15. 

The clearance of labeled chylomicrons from the blood is rapid, the half-time of disappearance being under 1 hour in humans. Larger particles are catabolized more quickly than smaller ones. Fatty acids originating from chylomicron triacylglycerol are delivered mainly to adipose tissue, heart, and muscle (80%), while about 20% goes to the liver. However, the liver does not metabolize native chylomicrons or VLDL significantly thus, the fatty acids in the liver must be secondary to their metabolism in extrahepatic tissues. 

Cortisol-induced lipolysis not only provides substrates for gluconeogenesis (formation of glucose from noncarbohydrate sources) but it also increases the amount of free fatty acids in the blood. As a result, the fatty acids are used by muscle as a source of energy and glucose is spared for the brain to use to form energy. 

In the fasting state, resting muscle uses fatty acids derived from free fatty acids in the blood. Ketones maybe used if the fasting state is prolonged. 

Acetoacetate and 3-hydroxybutyrate are known as ketone bodies. They are classified as fat fuels since they arise from the partial oxidation of fatty acids in the liver, from where they are released into the circulation and can be used by most if not all aerobic tissues (e.g. muscle, brain, kidney, mammary gland, small intestine) (Figure 7.7, Table 7.1). There are two important points (i) ketone bodies are used as fuel by the brain and small intestine, neither of which can use fatty acids (ii) ketone bodies are soluble in plasma so that they do not require albumin for transport in the blood. 

The packaging of triacylglycerol into chylomicrons or VLDL provides an effective mass-transport system for fat. On a normal Western diet, approximately 400 g of triacylglycerol is transported through the blood each day. Since these two particles cannot cross the capillaries, their triacylglycerol is hydrolysed by lipoprotein lipase on the luminal surface of the capillaries (see above). Most of the fatty acids released by the lipase are taken up by the cells in which the lipase is catalytically active. Thus the fate of the fatty acid in the triacylglycerol in the blood depends upon which tissue possesses a catalytically active lipoprotein lipase. Three conditions are described (Figure 7.23) ... 

Fatty acids require about 7% more oxygen than does carbohydrate to generate the same amount of ATP. Under circumstances where oxygen supply is limiting, for example in parts of the myocardium after an occlusion in one of the arteries, glucose is the preferred fuel and attempts are made to increase blood glucose levels and decrease mobilisation of fatty acids in this condition (see Chapter 22). 

The plasma level of fatty acids in a fed subject is between 0.3 and 0.5 mmol/L. As discussed above, the maximal safe level is about 2 mmol/L. This is not usually exceeded in any physiological condition since, above this concentration, that of the free (not complexed with albumin) fatty acids in the blood increases markedly. This can then lead to the formation of fatty acid micelles which can damage cell membranes the damage can cause aggregation of platelets and interfere with electrical conduction in heart muscle (Chapter 22). The cells particularly at risk are the endothelial cells of arteries and arterioles, since they are directly exposed to the micelles, possibly for long periods of time. Two important roles of endothelial cells are control of the diameter of arterioles of the vascular system and control of blood clotting (Chapter 22). Damage to endothelial cells could be sufficiently severe to interfere with these functions i.e. the arterioles could constrict, and the risk of thrombosis increases. Both of these could contribute to the development of a heart attack (Chapter 22) (Box 7.4). 

Figure 16.2 Redprocal relationship between the changes in the concentrations of glucose and fatty adds in blood during starvation in adult humans. As the glucose concentration decreases, fatty acids are released from adipose tissue (for mechanisms see Figure 16.4). The dotted line is an estimate of what would occur if fatty acid oxidation did not inhibit glucose utilisation. Such a decrease occurs if fatty acid oxidation in muscle is decreased by specific inhibitors.

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