Triacylglycerols in liver

B) stimulates the conversion of glucose to glycogen and triacylglycerol in liver... 

Figure 6-8. Synthesis of triacylglycerols in liver, adipose tissue, and intestinal cells. R = fatty acyl moiety. VLDL = very-low-density-lipoprotein.

Synthesis of phosphatidylcholine. The rate-limiting reaction is that catalyzed by cytidylyltransferase (reaction 2) which appears to be active only when attached to the endoplasmic reticulum, although it is also found free in the cytosol. Cytidylyltransferase is inactivated by a cAMP-dependent protein kinase and activated by a phosphatase. Translocation to the endoplasmic reticulum can be stimulated by substrates such as fatty acyl Coenzyme A (CoA). Choline deficiency can result in deposition of triacylglycerol in liver and reduced phospholipid synthesis. Enzymes (1) choline kinase ... 

Increased synthesis of fatty acids and triacylglycerols in liver and adipose tissue ... 

Fig. 33.20. Synthesis of triacylglycerol in liver and adipose tissue. Glycerol 3-phosphate is produced from glucose in both tissues. It is also produced from glycerol in liver, but not in adipose tissue, which lacks glycerol kinase. The steps from glycerol 3-phosphate are the same in the two tissues. FA = fatty acyl group.

Glutamine is found in all cells in a combined form in peptides or proteins, but also in a free form. The highest free concentration of glutamine is found in muscle, where it acts as a store for use by other tissues. In fact, the total amount in all the skeletal muscle in the body is about 80 g, which is synthesised in the muscle from glucose and branched-chain amino acids (see Chapter 8). As with glycogen in the liver and triacylglycerol in adipose tissue. 

Medium-chain acyl-CoA synthetase, which is present within the mitochondrial matrix of the liver, activates fatty acids containing from four to ten carbon atoms. Medium-chain length fatty acids are obtained mainly from triacylglycerols in dairy products. However, unlike long-chain fatty acids, they are not esterified in the epithelial cells of the intestine but enter the hepatic portal vein as fatty acids to be transported to the liver. Within the liver, they enter the mitochondria directly, where they are converted to acyl-CoA, which can be fully oxidised and/or converted into ketone bodies. The latter are released and can be taken up and oxidised by tissues. 

The physiological pathway for oxidation of ketone bodies starts with the hydrolysis of triacylglycerol in adipose tissue, which provides fatty acids that are taken up by the liver, oxidised to acetyl-CoAby P-oxidation and the acetyl-CoA is converted to ketone bodies, via the synthetic part of the pathway. Both hydroxybutyrate and acetoacetate are taken up by the tissues, which can oxidise them to generate ATP (Figure 7.19). 

Lipogenesis in liver and possibly adipose tissue, leading to increased synthesis of phospholipids and triacylglycerol. 

A variety of fuels are available to generate ATP for muscle activity phosphocreatine glycogen (which can be converted to lactic acid or completely oxidised to CO2) glucose (from liver glycogen, transported to the muscle via the blood and completely oxidised to CO2) triacylglycerol within the muscle (completely oxidised to CO2) and fatty acids from triacylglycerol in adipose tissue (completely oxidised to CO2). 

Fuels are stored within the muscle, liver and adipose tissue (Table 13.4) and amounts vary according to the nutritional status of the subject and the previous physical activity (see also Chapter 2). Triacylglycerol that is stored within the muscle can be used but the most significant fat fuel is long-chain fatty acids, derived from triacylglycerol in adipose tissue. 

In the ebb phase, there is increased activity of the sympathetic nervous system and increased plasma levels of adrenaline and glucocorticoids but a decreased level of insulin. This results in mobilisation of glycogen in the liver and triacylglycerol in adipose tissue, so that the levels of two major fuels in the blood, glucose and long-chain fatty acids, are increased. This is, effectively, the stress response to trauma. These changes continue and are extended into the flow phase as the immune cells are activated and secrete the proinflammatory cytokines that further stimulate the mobilisation of fuel stores (Table 18.2). Thus the sequence is trauma increased endocrine hormone levels increased immune response increased levels of cytokines metabolic responses. 

Figure 21.21 Diagram to illustrate the intertissue triacylglycerol/ fatty acid cycle, (i) Fatty acids released from adipose tissue are esterified in the liver, (ii) The triacylglyceral is released in the form of VLDL. (iii) The triacylglycerol in the latter is hydrolysed in the capillaries in the adipose tissue. Some fatty acids are taken up by adipose b ssue, but about 30% are release in the circulation that give life to the extracellular cycle. The intracellular cycle exists in the adipocytes.

Animals can synthesize and store large quantities of triacylglycerols, to be used later as fuel (see Box 17-1). Humans can store only a few hundred grams of glycogen in liver and muscle, barely enough to supply the body s energy needs for 12 hours. In contrast, the total amount of stored triacylglycerol in a 70-kg man of... 

Fig. 21-20 see also Fig. 17-1). Flux through this tri-acylglycerol cycle between adipose tissue and liver may be quite low when other fuels are available and the release of fatty acids from adipose tissue is limited, but as noted above, the proportion of released fatty acids that are reesterified remains roughly constant at 75% under all metabolic conditions. The level of free fatty acids in the blood thus reflects both the rate of release of fatty acids and the balance between the synthesis and breakdown of triacylglycerols in adipose tissue and liver. 

When the diet contains more fatty acids than are needed immediately as fuel, they are converted to triacylglycerols in the liver and packaged with specific apolipoproteins into very-low-density lipoprotein (VLDL). Excess carbohydrate in the diet can also be converted to triacylglycerols in the liver and exported as VLDLs (Fig. 21-40a). In addition to triacylglycerols, VLDLs contain some cholesterol and cholesteryl esters, as well as apoB-100, apoC-I, apoC-II, apoC-III, and apo-E (Table 21-3). These lipoproteins are transported in the blood from the liver to muscle and adipose tissue, where activation of lipoprotein lipase by apoC-II causes the release of free fatty acids from the VLDL triacylglycerols. Adipocytes take up these fatty acids, reconvert them to triacylglycerols, and store the products in intracellular lipid droplets myocytes, in contrast, primarily oxidize the fatty acids to supply energy. Most VLDL remnants are removed from the circulation by hepatocytes. The uptake, like that for chylomicrons, is... 

The fuel reserves of a healthy adult human are of three types glycogen stored in the liver and, in relatively small quantities, in muscles large quantities of triacylglycerols in adipose tissues and tissue proteins, which can be degraded when necessary to provide fuel (Table 23-5). 

PA is the precursor of many other phosphoglycerides. The steps in its synthesis from glycerol phosphate and two fatty acyl CoAs were illustrated in Figure 16.14, p. 187, in which PA is shown as a precursor of triacylglycerol. [Note Essentially all cells except mature ery-. throcytes can synthesize phospholipids, whereas triacylglycerol synthesis occurs essentially only in liver, adipose tissue, lactating mammary glands, and intestinal mucosal cells.]... 

Figure 21-1 Movement of triacylglycerols from liver and intestine to body cells and lipid carriers of blood. VLDL very low density lipoprotein which contains triacylglycerols, phospholipids, cholesterol, and apolipoproteins B, and C. IDL intermediate density lipoproteins found in human plasma. LDL low density lipoproteins which have lost most of their triacylglycerols. ApoB-100, etc., are apolipoproteins listed in Table 21-2. LCAT, lecithin cholesterol acyltransferase CETP, cholesteryl ester transfer protein (see Chapter 22).

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