Triacylglycerol breakdown

The glycerol backbones from triacylglycerol breakdown are sent to the liver for use in gluconeogenesis. 

The glycerol hackhone derived from lipase-mediated triacylglycerol breakdown is released into the bloodstream and taken up by the liver. 

Pancreatic lipase is one of the mammalian key digestive enzymes. It completes the dietary triacylglycerol breakdown initiated by preduode-nal lipases, including lingual and gastric enzymes, (see below). The enzyme is inhibited in the intestine by bile salts, but the activity is restored in the presence of colipase (CLP), a relatively short (95 residues) heat-stable polypeptide secreted by the pancreas (Semeriva and Desnuelle, 1979 Borgstrbm and Erlanson-Albertsson, 1984). The structural details of the interaction of colipase with lipase are described in Section III,C. 

Triacylglycerols can be mobilized by the hydrolytic action of lipases that are under hormonal control. Glucagon and epinephrine stimulate triacylglycerol breakdown by activating the lipase. Insulin, in contrast, inhibits lipolysis. Fatty acids are activated to acyl CoAs, transported across the inner mitochondrial membrane by carnitine, and degraded... 

Which one of the following products of triacylglycerol breakdown and subsequent P oxidation may undergo gluconeogenesis ... 

Triacylglycerol breakdown in adipose tissue is also stimulated by epinephrine, providing fuel for the muscle tissue. In consequence, glucose uptake into muscle is diminished, contributing to an increase in blood glucose levels. 

Pregnant women often have increased rates of triacylglycerol breakdown and, as a result, have elevated levels of ketone bodies in their blood. Why do they also often exhibit an increase in plasma lipoprotein levels ... 

The lipolytic process in germinating oil seeds is still unclear. How seed oils, present in oil bodies, are converted to products which can then be handled by the fatty acid oxidation system of glyoxysomes, is not clear. It appears that membrane-bound lipases are involved in the process. A further area for clarification is the intracellular transport of insoluble triacylglycerols from oil bodies to the site of complete (or partial) hydrolysis and thence to the glyoxysomal enzymes of gluconeogenesis. Recent electron microscope studies with several oil seeds have provided evidence for a close association of ribosome-containing membranes with spherosomes these may be lipolytic membranes involved in triacylglycerol breakdown (Wanner and Theimer, 1978). 

Steffensen, C.H., Roepstorff, C, Madsen, M., and IGens, B., Myocellular triacylglycerol breakdown in females but not in males during exercise. Am. J. Physiol. Endocrinol. Metab. 282, E634—E642, 2002. 

The metabolic breakdown of triacylglycerols begins with their hydrolysis to yield glycerol plus fatty acids. The reaction is catalyzed by a lipase, whose mechanism of action is shown in Figure 29.2. The active site of the enzyme contains a catalytic triad of aspartic acid, histidine, and serine residues, which act cooperatively to provide the necessary acid and base catalysis for the individual steps. Hydrolysis is accomplished by two sequential nucleophilic acyl substitution reactions, one that covalently binds an acyl group to the side chain -OH of a serine residue on the enzyme and a second that frees the fatty acid from the enzyme. 

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... 

Catabolism The breakdown of complex molecules to simpler ones to yield energy (e.g., triacylglycerols to fatty acids) and the inactivation of physiologically active molecules (e.g., acetylcholine to choline and acetic acid). 

Fatty acids and other breakdown products are taken up by the intestinal mucosa and converted into triacylglycerols. 

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. 

Variability in hormonal response patterns does not stop at the level of second-messenger synthesis. Thus, cyclic AMP can activate the well-known cAMP-dependent protein kinase A, but the possibility of other cAMP-respon-sive enzymes or cAMP-activated regulatory proteins should not be ruled out. The protein kinase activated by cAMP can activate a number of other enzymes. For example, in the liver, phosphorylase kinase (see fig. 24.15) is activated and catalyzes the breakdown of glycogen. In adipocytes, triacyl-glycerol lipase is activated and catalyzes the breakdown of triacylglycerols. 

Related topics Membrane lipids (El) Triacylglycerols (K4) Fatty acid breakdown (K2) Cholesterol (K5) Fatty acid synthesis (K3)... 

The rate of fatty acid degradation is controlled by the availability of free fatty acids in the blood which arise from the breakdown of triacylglycerols. 

The major source of free fatty acids in the blood is from the breakdown of triacylglycerol stores in adipose tissue which is regulated by the action of hormone-sensitive triacylglycerol lipase (see Topic K4). Fatty acid breakdown and fatty acid synthesis are coordinately controlled so as to prevent a futile cycle (see Topic K3). 

Breakdown The fatty acids in triacylglycerols are released from the glycerol backbone by the action of lipases. The free fatty acids can then be degraded by (3-oxidation to produce energy. The glycerol is converted into dihydroxyacetone phosphate which enters glycolysis. 

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