Lipolysis triacylglycerol, adipose tissue

Correct answer = D. Clofibrate and gemfibrozil Increase the activity of lipoprotein lipase, thereby increasing the removal of VLDL from plasma. Niacin inhibits lipolysis in adipose tissue and thus eliminates the building blocks needed by the liver to produce triacylglycerol and there-... 

There is a continuous release of non-esterified fatty acids from adipose tissue. In the fed state most of the fatty acids are taken up by the liver, re-esterified to form triacylglycerol and exported in VLDL (section 5.6.2.2). This apparently futile (and ATP-expensive) cycling between lipolysis in adipose tissue and re-esterification in the liver permits increased utilization of fatty acids as fuel in muscle by increasing the rate of fatty acid uptake into muscle without the need to increase the rate of lipolysis. As discussed in section 10.6, the extent to which muscle utilizes fatty acids is determined to a considerable extent by the intensity of physical activity, rather than by their availability. 

Otfier fiormones accelerate tfie release of free fatty acids from adipose tissue and raise tfie plasma free fatty acid concentration by increasing the rate of lipolysis of the triacylglycerol stores (Figure 25—8). These include epinephrine, norepinephrine, glucagon, adrenocorticotropic hormone (ACTH), a- and P-melanocyte-stimulat-ing hormones (MSH), thyroid-stimulating hormone (TSH), growth hormone (GH), and vasopressin. Many of these activate the hormone-sensitive hpase. For an optimal effect, most of these lipolytic processes require the presence of glucocorticoids and thyroid hormones. These hormones act in a facilitatory or permissive capacity with respect to other lipolytic endocrine factors. 

Adipose tissue Storage and breakdown of triacylglyc-erol Esterification of fatty acids and lipolysis lipogenesis Glucose, lipoprotein triacylglycerol Free fatty acids, glycerol Lipoprotein lipase, hormone-sensitive lipase... 

The largest store of fuel in the body occurs in adipose tissue. Approximately 80% of adipose tissue is triacylglycerol (the remainder is connective tissue, water, proteins and DNA). Approximately 90% of an individual adipocyte is triacylglycerol (Figure 7.5). Despite this, triacylglycerol is not released from the adipose tissue. Instead hydrolysis (lipolysis) of the triacylglycerol within 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).

Mobilisation of triacylglycerol is due to the increased rate of lipolysis. Adipose tissue triacylglycerol contains some essential fatty acids (linoleic and linolenic acids) and these are mobilised along with the non-essential fatty acids. The... 

The initial event in the utilization of fat as an energy source is the hydrolysis of triacylglycerols by lipases, an event referred to as lipolysis. The lipase of adipose tissue are activated on treatment of these cells with the hormones epinephrine, norepinephrine, glucagon, and adrenocorticotropic hormone. In adipose cells, these hormones trigger 7TM receptors that activate adenylate cyclase (Section 15,1.3 ). The increased level of cyclic AMP then stimulates protein kinase A, -which activates the lipases by phosphorylating them. Thus, epinephrine, norepinephrine, glucagon, and adrenocorticotropic hormone induce lipolysis (Figure 22.6). In contrast, insulin inhibits lipolysis. The released fatty acids are not soluble in blood plasma, and so, on release, serum albumin binds the fatty acids and serves as a carrier. By these means, free fatty acids are made accessible as a fuel in other tissues. 

C. VLDL levels are elevated because the decreased insulin and increased glucagon cause lipolysis of adipose triacylglycerols. The fatty acids and glycerol are repackaged in VLDL, which are secreted by the liver. Therefore, both triacylglycerols and cholesterol are elevated in the blood. Lipoprotein lipase is decreased because its synthesis and secretion by adipose tissue are stimulated by insulin. 

Because Di Abietes produces very little insulin, she is prone to developing ketoacidosis. When insulin levels are low, HSL of adipose tissue is very active, resulting in increased lipolysis. The fatty acids that are released travel to the liver, where they are converted to the triacylglycerols of VLDL. They also undergo p-oxidation and conversion to ketone bodies. If Di does not take exogenous insulin or if her insulin levels decrease abruptly for some physiologic reason, she may develop a ketoacidosis (DKA). In fact, she has had repeated bouts of DKA. 

The availability of free fatty acids in the blood, which depends on their release from adipose tissue triacylglycerols by hormone-sensitive lipase. During prolonged exercise, the small decrease of insulin, and increases of glucagon, epinephrine and norepinephrine, cortisol, and possibly growth hormone all activate adipocyte tissue lipolysis. 

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