Triacylglycerols in adipose tissue

FIGURE 24.2 Liberation of fatty acids from triacylglycerols in adipose tissue is hormone-dependent. 

The free fatty acids (FFA, nonesterified fatty acids, im-esterified fatty acids) arise in the plasma from hpolysis of triacylglycerol in adipose tissue or as a result of the action of hpoprotein hpase during uptake of plasma tri-acylglycerols into tissues. They are found in combination with albumin, a very effective solubilizer, in concentrations varying between 0.1 and 2.0 ieq/mL of plasma. Levels are low in the ftiUy fed condition and rise to 0.7-0.8 leq/mL in the starved state. In uncontrolled diabetes mellitus, the level may rise to as much as 2 Ieq/mL. 

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. 

Figure 7.6 Release of fatty acids from the triacylglycerol in adipose tissue and their utilisation by other tissues. Fatty acids are long-chain fatty acids, abbreviated to FFA (see below). Hydrolysis (lipolysis) of triacylglycerol in adipose tissue produces the long-chain fatty acids that are released from the adipocytes into the blood for oxidation by various tissues by P-oxidation (see below).

Most of the long-chain fatty acids that are oxidised in the body are released from triacylglycerol in adipose tissue. The first step is hydrolysis of triacylglycerol within the... 

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). 

Figure 7.19 The physiological pathway for ketone body oxidation from triacylglycerol in adipose tissue to their oxidation in a variety of tissues/organs. The pathway spans three tissues/ organs. The flux-generating step is the triacylglycerol lipase and ends with CO2 in one or more of the tissues/organs.

The hormone leptin, which is secreted by adipose tissue, is considered to play a role in the control of the amount of triacylglycerol in adipose tissue by decreasing appetite and by increasing energy expenditure. Leptin increases the rate of the triacylglycerol fatty acid cycle (Chapter 15). 

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. 

The increased mobilisation of fatty acids from adipose tissue raises the plasma concentration, which increases the rate of fat oxidation by muscle. It also releases some essential fatty acids from the store in the triacylglycerol in adipose tissue. These are required for formation of new membranes in proliferating cells and those involved in repairing the wound (e.g. fibroblasts) (Chapters 11 and 21 Figure 21.22). 

One obvious symptom of a patient suffering from trauma is loss of body weight. This is due to increased mobilisation of both triacylglycerol in adipose tissue and degradation of protein in skeletal muscle. 

Several processes contribute to the loss of weight loss of triacylglycerol in adipose tissue loss of protein in muscle hypermetabolism (increased energy expenditure, due to the... 

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. 

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). 

Fatty acids are stored as components of triacylglycerol in adipose tissue. 

Synthesis and degradation of triacylglycerols in adipose tissue. Fatty acids are delivered to adipose tissue. In times of energy excess these are converted to triacylglycerols and stored until needed, at which point the triacylglycerols are converted back to fatty acids. 

The breakdown of fatty acids in (3-oxidation (see Topic K2) is controlled mainly by the concentration of free fatty acids in the blood, which is, in turn, controlled by the hydrolysis rate of triacylglycerols in adipose tissue by hormone-sensitive triacylglycerol lipase. This enzyme is regulated by phosphorylation and dephosphorylation (Fig. 5) in response to hormonally controlled levels of the intracellular second messenger cAMP (see Topic E5). The catabolic hormones glucagon, epinephrine and norepinephrine bind to receptor proteins on the cell surface and increase the levels of cAMP in adipose cells through activation of adenylate cyclase (see Topic E5). The cAMP allosterically activates... 

If it were possible to provide a person with a diet free of cholesterol and triacylglycerol. how would this affect the deposition of triacylglycerol in adipose tissue ... 

Figure 22.6. Mobilization of Triacylglycerols. Triacylglycerols in adipose tissue are converted into free fatty acids and glycerol for release into the bloodstream in response to hormonal signals. A hormone-sensitive lipase initiates the process.

It is more advantageous for the human body to store fuel as triacylglycerol in adipose tissue than as protein in muscle because adipose triacylglycerol stores contain... 

The storage of triacylglycerols in adipose tissue is mediated by insulin, which stimulates adipose cells to secrete lipoprotein lipase and to take up glucose, the source of glycerol for triacylglycerol synthesis. 

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