Hydrolysis of dietary lipids

The action of pancreatic lipase in the hydrolysis of dietary lipids. 

In 1955 Blomstrand [93] fed phospholipids labeled with [ " C]palmitic acid to rats with both the bile and thoracic duct cannulated. The results indicated that in this situation 68% of the fatty acids were absorbed and that bile was not obligatory for absorption of phospholipid fatty acid. The distribution of the labeled fatty acid in the thoracic duct lipids showed the same pattern as after feeding the free fatty acid, indicating that the phospholipids had been hydrolyzed before absorption. The mechanism responsible for the hydrolysis of phospholipid in bile fistula rats is not obvious. A novel enzyme with phospholipase Aj activity has been demonstrated in the rat intestine [94]. This enzyme has its highest specificity for phosphatidyl glycerol and its role for the hydrolysis of dietary PC is unclear. 

The biochemical stability of food colloids is now attracting considerable research interest because of its obvious relevance to the delivery and bioavailability of nutrients and nutraceuticals in vivo. In particular, the processes of enzymatic hydrolysis occurring at the triglyceride-water interface appear important because most dietary lipids are present in the human stomach at some stage in the form of emulsified droplets (size 20-40 pm) (Armand et al., 1994 McClements et al., 2008 Dickinson, 2008 Singh et cil, 2009 McClements and Decker, 2009). 

Chylomicrons transport dietary triacylglycerol and cholesteryl ester from the intestine to other tissues in the body. Very-low-density lipoprotein functions in a manner similar to the transport of endogenously made lipid from the liver to other tissues. These two types of triacylglycerol-rich particles are initially degraded by the action of lipoprotein lipase, an extracellular enzyme that is most active within the capillaries of adipose tissue, cardiac and skeletal muscle, and the lactating mammary gland. Lipoprotein lipase catalyzes the hydrolysis of triacylglycerols (see fig. 18.3). The enzyme is specifically activated by apoprotein C-II, which... 

Dietary lipids (triglycerides) are emulsified into tiny fat droplets in the intestine by the action of bile salts. Pancreatic lipase catalyzes the hydrolysis of triglycerides into monoglycerides and fatty acids. These are absorbed by intestinal epithelial cells, reassembled into triglycerides, and combined with protein to form chylomicrons. Chylomicrons are transported to the cells of the body through the bloodstream. Fatty acids are stored as triglycerides (triacylglyc-erols) in fat droplets in the cytoplasm of adipocytes. 

As mentioned earlier (see p. 36), it is possible in non-ruminants to vary the fatty acid composition of body fats by altering the composition of dietary fats. In ruminants, this is normally not the case, and the predominating fatty acid of ruminant depot fats is the stearic acid resulting from hydrogenation in the rumen, ffowever, it is possible to treat dietary lipids in such a way that they are protected from attack in the rumen but remain susceptible to enzymic hydrolysis and absorption in the small intestine. If such lipids contain unsaturated acids, they will modify the composition of body (and milk) fats (see Chapter 25). 

The most important and typical enzymes that function at lipid-water interfaces in micelles, liposomes, emulsions, etc., are lipases. Lipases are carboxylic ester hydrolases and have been termed glycerol ester hydrolases (EC3.1.1.3) in the international system of classification. They differ greatly as regards both their origins (bacterial, fungal, plant, mammalian, etc.) and their properties, and they can catalyze the synthesis as well as the hydrolysis of a wide range of different carboxylic esters. Numerous reports have appeared about the structure and function of pancreatic lipases, because they are ubiquitous in mammalian species and play important roles in dietary fat absorption [29,30]. In this part, I will describe a structural feature and its relation to catalytic mechanism at the interfaces of lipases, particularly pancreatic lipases. 

Dietary retinyl esters, retinol, and provitamin A carotenoids are dispersed and emulsified in the stomach during the gastric phase of lipid digestion. They then enter the lumen of the duodenum where extensive hydrolysis of retinyl esters takes place. In infants, the bile salt-stimulated lipase in human milk may play a role in retinyl ester hydrolysis in the duodenum (Fredrikzon et al., 1978). The major retinyl ester hydrolase activity that acts in the intestines is, however, derived from the pancreas. 

Furthermore, flavonoids inerease seram paraoxonase aetivity, resulting in hydrolysis of lipid peroxides either in oxidized LDL or in lipid peroxide-rich macrophages and hence further prevent the formation of oxidized LDL. All these effects of flavonoids were demonstrated in vitro, as well as in vivo in humans and in the atherosclerotic apolipoprotein E-deficient mice, after dietary supplementation of nutrients rich in diverse flavonoids or of purified flavonoids. Dietary supplementation of pomegranate juice rich in flavonoids to atherosclerotic mice indeed resulted in a significant inhibition in the development of atherosclerotic lesions, along with the protection of LDL against oxidation [197-200]. 

They can be synthesized by the gut, following the absorption of hydrolyzed dietary lipid. They are combined with small amounts of protein, cholesterol and phospholipid to form chylomicrons. These are removed from the blood, mainly by adipose tissue. An enzyme, lipoprotein lipase is responsible for this hydrolysis of the chylomicron triglycerides. The free fatty acids liberated by these processes are resynthesized into triglycerides by the adipose tissue and stored. 

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