Big Chemical Encyclopedia

Chemical substances, components, reactions, process design ...

Articles Figures Tables About

Adipose tissue lipolysis

Figure 25-8. Control of adipose tissue lipolysis. (TSH, thyroid-stimulating hormone FFA, free fatty acids.) Note the cascade sequence of reactions affording amplification at each step. The lipolytic stimulus is "switched off" by removal of the stimulating hormone the action of lipase phosphatase the inhibition of the lipase and adenylyl cyclase by high concentrations of FFA the inhibition of adenylyl cyclase by adenosine and the removal of cAMP by the action of phosphodiesterase. ACTFI,TSFI, and glucagon may not activate adenylyl cyclase in vivo, since the concentration of each hormone required in vitro is much higher than is found in the circulation. Positive ( ) and negative ( ) regulatory effects are represented by broken lines and substrate flow by solid lines. Figure 25-8. Control of adipose tissue lipolysis. (TSH, thyroid-stimulating hormone FFA, free fatty acids.) Note the cascade sequence of reactions affording amplification at each step. The lipolytic stimulus is "switched off" by removal of the stimulating hormone the action of lipase phosphatase the inhibition of the lipase and adenylyl cyclase by high concentrations of FFA the inhibition of adenylyl cyclase by adenosine and the removal of cAMP by the action of phosphodiesterase. ACTFI,TSFI, and glucagon may not activate adenylyl cyclase in vivo, since the concentration of each hormone required in vitro is much higher than is found in the circulation. Positive ( ) and negative ( ) regulatory effects are represented by broken lines and substrate flow by solid lines.
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]

N. Gaudiot, A.M. Jaubert, and E. Charbonnier, et al.. Modulation of white adipose tissue lipolysis by nitric oxide, J. Biol. Chem., 1998, 273, 13475-13481. [Pg.322]

Langin, D Amer, P. 2006. Importance of TNFalpha and neutral lipases in human adipose tissue lipolysis. Trends Endocrinol. Metab. 17 314—320. [Pg.304]

The rate of fatty acid oxidation is linked to the rate of NADH, FAD(2H), and acetyl CoA oxidation, and, thus, to the rate of oxidative phosphorylation and ATP utilization. Additional regulation occurs through malonyl CoA, which inhibits formation of the fatty acyl carnitine derivatives. Fatty acids and ketone bodies are used as a fuel when their level increases in the blood, which is determined by hormonal regulation of adipose tissue lipolysis. [Pg.419]

During Otto s distance running (a moderate-intensity exercise), decreases in insulin and increases in insulin counterregulatory hormones, such as epinephrine and norepinephrine, increase adipose tissue lipolysis. Thus, his muscles are being provided with a supply of fatty acids in the blood that they can use as a fuel. [Pg.420]

Lofata Burne developed symptoms during fasting, when adipose tissue lipolysis was elevated. Under these circumstances, muscle tissue, liver, and many other tissues are oxidizing fatty acids as a fuel. After overnight fasting, approximately 60 to 70% of our energy supply is derived from the oxidation of fatty acids. [Pg.420]

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. [Pg.464]

Now that the use of aspirin has been curtailed, the few residual cases of Reye s syndrome that still occur are mainly in children with another potentiating factor, in particular a previously latent genetic defect in mitochondrial 6-oxidation enzymes (Rowe et al. 1988). In these children, the deficit is suddenly revealed because the fever increases energy demands, while the viral infection further damages the mitochOTidria. Furthermore, the anorexia may result in insufficient nutrition, which triggers adipose tissue lipolysis, thus flooding the liver with free fatty acids that are not oxidized by deficient mitochondria. [Pg.349]

In some cases it has been proposed that the tumor elaborates substances that block hepatic glucose release and adipose tissue lipolysis. Although this type of tumor is usually incurable, excision of the tumor usually eliminates the hypoglycemia. [Pg.527]

It is well established that many animal tissues can oxidize ketone bodies (Snapper and Grunbaum, 1927 Wick and Drury, 1941 Williamson and Krebs, 1961), and this has led to the concept that it is a physiological function of ketone bodies to serve as a fuel of respiration when carbohydrate is in short supply (Krebs, 1961). Experiments have shown that increased production of ketone bodies is closely matched by increased utilization (Bates et al., 1968). These authors suggest the sequence of events leading to "physiological ketosis" as a consequence of hormonal interrelationships a low blood sugar concentration causes an increase in adipose tissue lipolysis and a rise in the concentration of free fatty acids in the plasma. This in turn results in an increased rate of ketogenesis in the liver, which is followed by a rise in blood ketone-body concentrations, and an increased rate of peripheral utilization. [Pg.57]

COMPARATIVE ASPECTS OF HORMONAL REGULATION OF ADIPOSE TISSUE LIPOLYSIS... [Pg.207]

In this essay I intend to review briefly the results of these experiments, in order to illustrate the differences in the patterns of hormonal control of adipose tissue lipolysis noted... [Pg.208]

The results of our in vivo and in vitro experiments, together with other observations in the literature, strongly suggest the existence of different patterns of hormonal control of adipose tissue lipolysis among the species studied. [Pg.211]

In presenting this essay to honor Severe Ochoa, I am well aware of the fact that our data pose many questions and give only few answers. Perhaps the main value of the data is that they give some more proof for the existence of a variety of patterns of hormonal control of adipose tissue lipolysis, and the number of questions they pose regarding the biochemical mechanisms of hormone action and the physiological significance of the diversity of patterns of control. [Pg.213]

Llpotroplc Hormone. LPH - The involvement of pituitary hormones in releasing free fatty acids from adipose tissue (lipolysis) has been discussed at a symposiuml39. The amino acid sequence (58 amino acids) of porcine a-lipotropic hormone (or-LPH) is closely homologous to that previously reported for ovine y-LPH. The porcine y-LPH sequence appears to be identical to the N-terminal 1-58 sequence of porcine p-LPH in a relationship similar to that previously observed for p- and a-LPH of bovine origin. Also, as has been the case with the ovine hormone, the C-terminal sequence of porcine y-LPH is identical to the entire 18 amino acid sequence of p-MSH from the same species. Partial characterization of human lipotropins was described. ... [Pg.201]

FIGURE 5 Sources of fatty acid for hepatic triglyceride synthesis. (1) Adipose tissue lipolysis, catalyzed by hormone-sensitive lipase, provides fatty acids that travel through the bloodstream to the liver. (2) Chylomiaon remnants still carry some triglyceride and are cleared from the circulation by the liver. (3) Carbohydrate is converted to fatty acids when glycogen stores are maintained. [Pg.81]

In Type I diabetes mellitus, there is a severe deficiency (or total absence) of insulin due to an autoimmune attack on the cells that produce insulin, pancreatic j8-cells. The absence of insulin produces a deficiency in adipose tissue lipoprotein lipase. This causes sluggish catabolism of VLDL and leads to hypertriglyceridemia. Another mechanism by which insulin deficiency promotes increased VLDL levels is the failure to inhibit the activity of adipose tissue hormone-sensitive lipase. This enzyme hydrolyzes cytoplasmic triglyceride droplets. The fatty acids then go to the liver, where they are re-esterified to form triglycerides. These triglycerides are exported on VLDL particles. Since adipose tissue-derived fatty acids are an important substrate for hepatic VLDL triglycerides, the failure to suppress adipose tissue lipolysis is an important contributor to the enhanced rate of VLDL triglyceride secretion. [Pg.91]

Irigaray, P Ogier, V Jacquenet, S Notet, V Sibille, P Mejean, L et al. (2006). benzo[a]pyrene impairs beta-adrenergic stimulation of adipose tissue lipolysis and causes weight gain in mice a novel molecular mechanism of toxicity for a common food pollutant. FEBSJ, 273,1362-1372. [Pg.461]


See other pages where Adipose tissue lipolysis is mentioned: [Pg.104]    [Pg.239]    [Pg.56]    [Pg.1268]    [Pg.1022]    [Pg.334]    [Pg.107]    [Pg.110]    [Pg.434]    [Pg.468]    [Pg.859]    [Pg.321]    [Pg.246]    [Pg.203]    [Pg.351]    [Pg.209]    [Pg.211]    [Pg.211]    [Pg.213]    [Pg.303]    [Pg.547]   


SEARCH



Adipose

Adipose tissue

Adipose tissue lipolysis, glucagon-induced

Lipolysis

Lipolysis triacylglycerol, adipose tissue

© 2024 chempedia.info