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Fatty acids from adipose tissue

Hormones Signal the Release of Fatty Acids from Adipose Tissue... [Pg.776]

Metabolism—increased use of glucose (sugar) and liberation of fatty acids from adipose tissue... [Pg.200]

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. [Pg.215]

Fatty acids are released from adipose tissue into the bloodstream, from where they can be taken up and used by aerobic tissues, with the exception of brain and the intestine. In addition, an increase in the plasma fatty acid concentration is one factor that increases the rate of fatty acid oxidation by tissues. Flence, an increase in the mobilisation of fatty acid from adipose tissue is an immediate signal for tissues such as muscle, heart and kidney cortex to increase... [Pg.143]

It increases the release of fatty acids from adipose tissue which raises the plasma level of long-chain fatty acids, to provide a fuel for muscle, if it becomes physically active (Chapter 13). It also increases the cycling between triacylglycerol and fatty acids in adipose tissue. [Pg.262]

Changes in the blood levels of these hormones all contribute to regulation of blood glncose level in several conditions. After a meal glucose utilisation is increased, since insulin stimulates glucose uptake by muscle and inhibits release of fatty acids from adipose tissue. Physical activity... [Pg.263]

Physical activity was running on a treadmill at 65% y02m - Blood was taken via an indwelling catheter. Data from Kiens et al. (1993). The concentration of glycerol is an indication of the rate of release of fatty acids from adipose tissue. [Pg.288]

Glycogen conversion to Blood glucose Blood fatty acids (from adipose tissue triacylglycerol)... [Pg.291]

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). [Pg.419]

Hydrolysis of triacylglycerol and release of the resultant fatty acids from adipose tissue is increased and accounts, in part, for loss of body weight. Despite this, the plasma fatty acid level is not always increased, which suggests... [Pg.497]

Because digestion of food in the intestinal tract is dispensable and only counterproductive, the propulsion of intestinal contents is slowed to the extent that peristalsis diminishes and sphinc-teric tonus increases. However, in order to increase nutrient supply to heart and musculature, glucose from the liver and free fatty acid from adipose tissue must be released into the blood. The bronchi are dilated, enabling tidal volume and alveolar oxygen uptake to be increased. [Pg.80]

The release of free fatty acids from adipose tissue (lipolysis) is mediated through (33-adrenoceptors. Isoproterenol is the most potent agonist, followed by epinephrine and norepinephrine. [Pg.103]

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. [Pg.806]

Skeletal muscle can use free fatty acids, ketone bodies, or glucose as fuel, depending on the degree of muscular activity (Fig. 23-17). In resting muscle, the primary fuels are free fatty acids from adipose tissue and... [Pg.898]

Release of fatty acids from adipose tissue... [Pg.121]

Which one of the following is characteristic of low insulin levels A. Increased glycogen synthesis B. Decreased gluconeogenesis from lactate C. Decreased glycogenolysis D. Increased formation of 3-hydroxybutyrate E. Decreased action of hormone-sensitive lipase Correct answer = D. 3-hydroxybutyrate—a ketone body—synthesis is enhanced in the liver by taw insulin levels, which favor activation of hormone-sensitive lipase and release of fatty acids from adipose tissue. Glycogen synthesis is decreased, whereas gluconeogenesis is increased. [Pg.318]

Fatty liver refers to the abnormal accumulation of fat in hepatocytes. At the same time there is a decrease in plasma lipids and lipoproteins. Although many toxicants may cause lipid accumulation in the liver (Table 14.1), the mechanisms may be different. Basically lipid accumulation is related to disturbances in either the synthesis or the secretion of lipoproteins. Excess lipid can result from an oversupply of free fatty acids from adipose tissues or, more commonly, from impaired release of triglycerides from the liver into the plasma. Triglycerides are secreted from the liver as lipoproteins (very low density lipoprotein, VLDL). As might be expected, there are a number of points at which this process can be disrupted. Some of the more important ones are as follows (Figure 14.1) ... [Pg.264]

Limited information was located regarding reducing body burden following exposure to CDDs in humans. A recent study examined the influence of short-term dietary measures on CDD and CDF concentrations in human milk (Pluim et al. 1994c). The authors hypothesized that mobilization of fatty acids from adipose tissue cause the concomitant release of CDDs and CDFs, which will then be eliminated in the breast milk. Two diets were tested for their ability to reduce the concentration of CDDs... [Pg.350]

The release of fatty acids from adipose tissue is regulated by the rate of hydrolysis of triacylglycerol and the rate of esterification of acyl-CoA with glycerol 3-phosphate. The rate of hydrolysis is stimulated by hormones that bind to cell-surface receptors and stimulate adenylate cyclase (which catalyzes the production of cAMP from ATP). Hormone-sensitive lipase (Sec. 13.4) can exist in two forms, one of which exhibits very low activity and a second which is phosphorylated and has high activity. Before hormonal stimulation of adenylate cyclase, the low-activity lipase predominates in the fat cell. Stimulation of protein kinase by an increase in cAMP concentration leads to phosphorylation of the low-activity lipase. An increase in the rate of hydrolysis of triacylglycerol and the release of fatty acids from the fat cell follows. This leads to a greater utilization of fatty acids by tissues such as heart, skeletal muscle, and liver. [Pg.392]


See other pages where Fatty acids from adipose tissue is mentioned: [Pg.122]    [Pg.161]    [Pg.215]    [Pg.479]    [Pg.227]    [Pg.159]    [Pg.257]    [Pg.264]    [Pg.368]    [Pg.418]    [Pg.527]    [Pg.808]    [Pg.906]    [Pg.308]    [Pg.327]    [Pg.331]    [Pg.337]    [Pg.35]    [Pg.427]    [Pg.432]    [Pg.112]    [Pg.516]    [Pg.158]    [Pg.394]    [Pg.229]    [Pg.229]    [Pg.1270]   
See also in sourсe #XX -- [ Pg.65 ]




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