Lipolysis products

This suggests that the above mentioned mechanism is unlikely to have caused lactic acidosis in this patient. Rather, it may have resulted from beta2-adrenoceptor activation, with subsequent excess glycogenolysis and lipolysis, production of pyruvate, and final conversion to lactate. 

Further applications involves the analysis of both free fatty acids and fatty acids as constituents of fats, oils, etc. Tallent and Kleiman [173] analysed products from the lipolysis of oils (in addition to acids also mono-, di- and triglycerides). BSA is more suitable than an HMDS-TMCS mixture for the silylation of these compounds as more uniform products are produced. The reaction is carried out in a reaction vial in which 2—3 mg of dry lipolysis products are placed and 0.2-0.3 ml of the silylation agent (BSA—pyridine,... 

Native HPL is a glycosylated 50 kDa protein which is synthesized by acinar ceUs of the pancreas (Fig. 10.2). In the cell, this hpase is located with many other enzymes into the zymogen granules, and is then secreted through the pancreatic duct into the intestinal lumen together with the bile. Secretion of HPL can be stimulated by intestinal hormones such as CCK-PZ and secretin (Zieve et al., 1966a,b). Lipolysis products (FFAs) are known to stimulate the HPL secretion indirectly through the CCK action (Hildebrand et al., 1998). HPL secretion is drasti-... 

Intragastric lipolysis of meal triglycerides was estimated from the cumulated pyloric outputs of lipolysis products (free fatty acids FFA diglycerides DG monoglycerides MG) and residual triglycerides (TG) and was expressed as the percentage... 

Panels A and C show the pyloric output of lipolysis products in the absence and in the presence of the lipase inhibitor orlistat, respectively. Panels B and D show the duodenal output at the Angle of Treitz of lipolysis products in the absence and in the presence of the lipase inhibitor orlistat, respectively. 

The overall lipolysis occurring in both the stomach and the duodenum was estimated from the cumulated outputs of lipolysis products and residual triglycerides... 

Lipophilic drugs, being either weak acids, weak bases or non-ionized compounds, are dissolved in the lipid fraction of the food when the macroscopic structure of the food is broken down into microscopic particles during the formation of chyme. Consequently, lipophilic molecules are predissolved in triglyceride droplets when they enter the small intestine. For these compounds, it is especially relevant to include lipolysis products in the biorelevant media simulating the intestinal fluids. Sunesen et al. (2005) could only obtain fVTVC in the fed state for a non-ionized compound (danazol), when including lipolysis products in the media. 

For non-ioniTxd compounds, the concentration of solubilizers in the medium seems to be the major determinant for dissolution rate. In the fasted state, the level of surfactants in the gastric fluids is fairly low and the gastric dissolution often only plays a minor role (Vertzoni et al., 2005) therefore the use of only fasted state intestinal media would be a proper choice in this case (Galia et al., 1998). Considering the fed state, the dissolution in the fed stomach may be important and should be considered. In any case, the use of afed state dissolution medium will be necessary. In the case of a lipophilic drug, lipolysis products should be included in the media. 

Literature describing simulated media for the fasted stomach and small intestine are available. In the fed state, the simulation of the fed stomach seems to be problematic because the composition is highly dependent on the associated meal. Therefore only a few publications of fed state gastric media are available. With regard to media simulating intestinal fluids in the fed state, several attempts have been made to develop suitable media, both with and without the addition of lipolysis product. 

It is important to remember that ordinarily the major component of dietary fat is always triglyceride, not cholesterol. For example, milk and butter have very little cholesterol but are very high in triglyceride. Triglyceride (and other glycerolipids, such as phospholipids) are hydrolyzed in the intestinal lumen to yield monoglycerides and free fatty acids. These lipolysis products are then absorbed by the intestinal epithelial cells and resynthesized as triglycerides, phospholipids, and cholesterol esters. Thus, the intestine mediates both lipolysis (in the lumen) and re-esterification (within the epithelial cells) of dietary lipids. 

Insulin resistance occurs when the normal response to a given amount of insulin is reduced. Resistance of liver to the effects of insulin results in inadequate suppression of hepatic glucose production insulin resistance of skeletal muscle reduces the amount of glucose taken out of the circulation into skeletal muscle for storage and insulin resistance of adipose tissue results in impaired suppression of lipolysis and increased levels of free fatty acids. Therefore, insulin resistance is associated with a cluster of metabolic abnormalities including elevated blood glucose levels, abnormal blood lipid profile (dyslipidemia), hypertension, and increased expression of inflammatory markers (inflammation). Insulin resistance and this cluster of metabolic abnormalities is strongly associated with obesity, predominantly abdominal (visceral) obesity, and physical inactivity and increased risk for type 2 diabetes, cardiovascular and renal disease, as well as some forms of cancer. In addition to obesity, other situations in which insulin resistance occurs includes... 

The rate of mitochondrial oxidations and ATP synthesis is continually adjusted to the needs of the cell (see reviews by Brand and Murphy 1987 Brown, 1992). Physical activity and the nutritional and endocrine states determine which substrates are oxidized by skeletal muscle. Insulin increases the utilization of glucose by promoting its uptake by muscle and by decreasing the availability of free long-chain fatty acids, and of acetoacetate and 3-hydroxybutyrate formed by fatty acid oxidation in the liver, secondary to decreased lipolysis in adipose tissue. Product inhibition of pyruvate dehydrogenase by NADH and acetyl-CoA formed by fatty acid oxidation decreases glucose oxidation in muscle. 

Acetyl-CoA carboxylase is an allosteric enzyme and is activated by citrate, which increases in concentration in the well-fed state and is an indicator of a plentiful supply of acetyl-CoA. Citrate converts the enzyme from an inactive dimer to an active polymeric form, having a molecular mass of several milhon. Inactivation is promoted by phosphorylation of the enzyme and by long-chain acyl-CoA molecules, an example of negative feedback inhibition by a product of a reaction. Thus, if acyl-CoA accumulates because it is not esterified quickly enough or because of increased lipolysis or an influx of free fatty acids into the tissue, it will automatically reduce the synthesis of new fatty acid. Acyl-CoA may also inhibit the mitochondrial tricarboxylate transporter, thus preventing activation of the enzyme by egress of citrate from the mitochondria into the cytosol. 

As biscuits are a long-life product any fat used in them has to be stable under the conditions of storage. Fats can deteriorate in two ways. Firstly, any fat can suffer lipolysis if the fatty acids are split from the glycerol. This is what happens in soap making, where the fatty acids are... 

Cakes are in principle subject to all the threats to a long shelf life that any other bakery product is subject to. The product can dry out, the starch can retrograde or mould can grow. These are in addition to the threats of oxidation, loss of flavour and lipolysis by any enzymes present. 

Figure 17.20 Cytokines produced by activated Th cells and some of their effects. The cytokines produced have several functions activation of B-cells, macrophages and cytotoxic T-cells. The cytokines, along with endocrine hormones, stimulate responses in the whole body (e.g. lipolysis in adipose tissue, protein degradation in muscle, acute phase protein production in liver. Chapter 18).

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