Adipose tissue stores release

Adipose Tissue stores fats as triacylglycerol and releases fatty acids as needed for energy. 

Release of Lipid from Adipose Tissue Stores... 

The source of the fatty acids can be dietary fat, fatty acids synthesized in the liver, or fatty acids released from adipose tissue stores. Adipose tissue lipolysis increases after ethanol consumption, possibly because of a release of epinephrine. 

Rashef and Shapiro (1960) reported that pretreatment of adrenalecto-mizc d rats with either epinephrine or eortisone inereased the depressed rate of free fatty acid release by their mesenteric adipose tissue in vitro however, maximal effects were, obtained only when both were given. It was further pointed out that epinephrine alone was highly effective in restorii the depressed rate of free fatty acid release by tissue from adrenal demedul-lated rats. Reshef and Shapiro (1960) also observed that pretreatment of starved intact rats with cortisone had little effect on the release of free fatty acid by mesenteric adipose tissue. Such treatment, however, inereased and prolonged the response of tissue removed from rats injected with epinephrine (sec Section VI, A). These results may reflect in part the effects of glucocorticoid administration on the adipose tissue stores of the intact animal, but the interesting relation between the effects of epinephrine and adrenocortical steroids on the release of free fatty acids deserves further study. 

Chylomicrons are assembled from TAG in the intestine. Their apoprotein components are synthesized and modified in the rough endoplasmic reticulum but the chylomicron itself is assembled in the Golgi. Chylomicrons are synthesized with a unique apoB48 on their surface, but also acquire apoE and apoCII once they are in the circulation. The apoCII allows the chylomicrons to interact with lipoprotein in the capillaries of the adipose tissue to release most of the triglyceride. Lipoprotein lipase hydrolyses chylomicron TAG to monoacylglycerol, FA and glycerol so that they can enter the adipocyte where TAG is re-synthesized and stored. Chylomicron remnants containing cholesterol and fat soluble vitamins are removed from the circulation by the liver. 

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. 

The major types of adipose tissue are (1) white adipose tissue, which manufactures, stores, and releases lipid and (2) brown adipose tissue, which dissipates energy via uncoupled mitochondrial respiration. Obesity research includes evaluation of the activity of adrenergic receptors and their effect on adipose tissue with respect to energy storage and expenditure or thermogenesis. 

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... 

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). 

The liver is the most important site for the formation of fatty acids, fats (triacylglycewls), ketone bodies, and cholesterol. Most of these products are released into the blood, in contrast, the triacylglycerols synthesized in adipose tissue are also stored there. 

Chylomicrons deliver tiiacylglycerols to tissues, where lipoprotein lipase releases free fatty acids for entry into cells. Triacylglycerols stored in adipose tissue are mobilized by a hormone-sensitive triacylglycerol lipase. The released fatty acids bind to serum albumin and are carried in the blood to the heart, skeletal muscle, and other tissues that use fatty acids for fuel. 

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... 

A. the stored fatty acids are released from adipose tissue into the plasma as components of the serum lipoprotein particle, VLDL. 

Increased degradation of triacylglycerols The activation of hormone-sensitive lipase (see p. 187) and subsequent hydrolysis of stored triacylglycerol are enhanced by the elevated catecholamines epinephrine and, particularly, norepinephrine. These compounds, which are released from the sympathetic nerve endings in adipose tissue, are physiologically important activators of hormone-sensitive lipase (Figure 24.13, ) ... 

Vitamins are chemically unrelated organic compounds that cannot be synthesized by humans and, therefore, must must be supplied by the diet. Nine vitamins (folic acid, cobalamin, ascorbic acid, pyridoxine, thiamine, niacin, riboflavin, biotin, and pantothenic acid) are classified as water-soluble, whereas four vitamins (vitamins A, D, K, and E) are termed fat-soluble (Figure 28.1). Vitamins are required to perform specific cellular functions, for example, many of the water-soluble vitamins are precursors of coenzymes for the enzymes of intermediary metabolism. In contrast to the water-soluble vitamins, only one fat soluble vitamin (vitamin K) has a coenzyme function. These vitamins are released, absorbed, and transported with the fat of the diet. They are not readily excreted in the urine, and significant quantities are stored in Die liver and adipose tissue. In fact, consumption of vitamins A and D in exoess of the recommended dietary allowances can lead to accumulation of toxic quantities of these compounds. 

Regulation The concentration of free fatty acids in the blood is controlled by the rate at which hormone-sensitive triacylglycerol lipase hydrolyzes the triacylglycerols stored in adipose tissue. Glucagon, epinephrine and norepinephrine cause an increase in the intracellular level of cAMP which allosterically activates cAMP-dependent protein kinase. The kinase in turn phosphorylates hormone-sensitive lipase, activating it, and leading to the release of fatty acids into the blood. Insulin has the opposite effect it decreases the level of cAMP which leads to the dephosphorylation and inactivation of hormone-sensitive lipase. 

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