Triglyceride emulsion

FIGURE 9.4 Schematic showing the hydrolytic degradation of components of a phospho-lipids-stabilized triglyceride emulsion. (From Klegerman and Groves, 1992.)... 

Herman, C.J. and Groves, M.J. (1993) The in uence of free fatty acid formation on the pH of phospholipid-stabilized triglyceride emulsionS .harm. Res., 10 774-776. 

Lipids have an adverse effect on carbohydrate metabolism under basal conditions. The infusion of 20% triglyceride emulsion with heparin during basal insulin and glucose turnover conditions resulted in a rise of plasma free fatty acids from 0.4 to 0.8 mmol/1 at a low rate of infusion (0.5 ml/minute for 2 hours) to between 1.6 and... 

The influence of a shear field on emulsion crystallization is of great interest as it relates to behavior during product processing and distribution. Emulsions can be destabilized under shear in a controlled manner to deliver desirable properties uncontrolled or unintentional destabilization may lead to poor product performance. Comparisons of emulsions under perikinetic (at rest) and orthokinetic (under shear) conditions were made in an effort to understand the role of shear on the stability of the systems studied. Davies et al. (22) found stability of triglyceride emulsions containing crystals to be sensitive to both shear and crystal concentration. Crystal morphology also plays an important role in the destabilization of emulsions under shear. Boode and Walstra (4) reported the presence of needle-like... 

Pancreatic lipase, in the presence of bile salts and coUpase, acts at the oil-water interface of the triglyceride emulsion to produce fatty acids and 2-monoacylglycerols. Cohpase is secreted in pancreatic juice as an inactive proenzyme, which is converted to the active form by trypsin. Other significant enzymes involved in the breakdown of fats within the intestinal lumen are cholesterol ester hydrolase, phospholipase A, and a nonspecific bile salt-activated lipase. 

Adolph M, Hailer S, Echart J. Serum phospholipid fatty acids in severely injured patients on total parenteral nutrition with medium chain/long chain triglyceride emulsions. Ann Nutt Metab 1995 39 251-260. 

It may well be that the same mechanism can act in crystallizing triglyceride emulsion droplets, but the author is unaware of clear evidence. 

Lipoprotein lipases are so called because, unlike normal lipases, they do not hydrolyze, or hydrolyze very slowly, triglyceride emulsions, unless a lipoprotein complex is also present. The normal substrate is the turbid chylomicron-containing, or lipemic, plasma formed after a fatty meal. Since this substrate is clarified by the enzyme, the term clearing factor is used to describe a lipoprotein lipase. 

J, Nordenstrom. A, Thome, and T. Olivecrona. Metabolic effects of infusion of a structured triglyceride emulsion in healthy subjects. 

Although apoprotein A-IV exhibits the properties of an apolipoprotein [2], and recent data on its sequence [11, 12, 21] have shown that it contains 14.5 tandemly repeated docosapeptides that possess the potential to form amphipathic a-helices [11], it is mainly found unassociated with lipoproteins in human plasma [4,18,19,36]. The Apo A-IV fraction in the lipoprotein-free plasma compartment is still able to bind lipids, as shown by Weinberg and Scanu [37], who were able to reassociate Apo A-IV from the d = 1.21 g/ml infranate to a phospholipid-triglyceride emulsion. After reassociation Apo A-IV could be isolated by flotation in chylomicron-like particles upon ultracentrifugation. 

The possible mechanism of Apo A-IV displacement from the surface of chylomicrons upon entry into the plasma was studied in an in vitro model by Weinberg and Spector [41]. They used Apo A-IV associated with a phospholipid-triglyceride emulsion for displacement studies. When these chylomicron-like particles were incubated with HDL, they found a displacement of Apo A-IV from these particles, mainly by Apo C-III. Thus, one of the mechanisms responsible for the dissociation of Apo A-IV frbm chylomicrons upon entry into the plasma compartment could be a displacement by other circulating apoproteins that have a higher affinity for chylomicrons (or their remnants after attack by hpoprotein lipase). In contrast to Apo A-IV, which decays and is later mostly found in the lipoprotein-free plasma compartment, the other major chylomicron apoprotein, A-I, reassociates with HDL, as shown by tracer kinetic studies [20, 29]. It thus remains puzzling why the bulk of Apo A-IV, despite its apoprotein structure, does not reassociate with lipoproteins. In addition, lymph and plasma Apo A-IV have similar a-helical contents and properties in solution [10]. This seems to be an unexplained phenomenon since we were able to show that apoprotein A-IV, isolated either from chylomicrons or from lipoprotein-free plasma, recombines with hpids to form stable complexes [34]. 

Ostwald Ripening in Triglyceride Emulsions with Added Ethanol... 

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