Triglyceride lipase function

In functional lipoprotein lipase deficiency there appears to be a normal removal rate for VLDL from the plasma (B31, F19, N7), and an unimpaired rate for the conversion of VLDL apoB to LDL apoB (N7). It may be that VLDL is hydrolyzed by hepatic triglyceride lipase (unaffected in lipoprotein lipase deficiency) (N7). Hepatic triglyceride lipase does not require apoC-II as a cofactor (E2). 

ApoC-I is expressed mainly in liver but also in lung, skin, testis, spleen, neural retina, and RPE. Its multiple functions include the activation of lecithin cholesterol acyltransferase (LCAT) and the inhibition, among others, of lipoprotein and hepatic lipases that hydrolyze triglycerides in particle cores. Notably, both LCAT and lipoprotein lipases are expressed in RPE and choroid (Li et al., 2006). Moreover ApoC-I has been shown to displace ApoE on the VLDL and LDL and thus hinder their binding and uptake via their corresponding receptors (Li et al., 2006). 

Serum amylase, bilirubin, cholesterol, lipase, and triglyceride levels blood glucose level CBC CD4+ cell count and liver function test results... 

Figure 3 Function of CETP, LPL (lipoprotein lipase) and HTGL (hepatic triglyceride...

Apolipoprotein C-II can also be isolated from VLDL or HDL (H20, L5, N3). It contains 78 residues (J3) and has been shown by Chou-Fasman analysis to bind phospholipids (M26, M40), with three predicted helical sequences (M26). ApoC-II has attracted a great deal of attention because it activates one of the most important enzymes in plasma lipid metabolism, lipoprotein lipase, responsible for the hydrolysis of triglyceride in chylomicrons and VLDL. Sparrow and Gotto have summarized a number of studies on structure-function relationships (S52). These, taken together, indicate that there are separate functional domains in apoC-II, in that lipoprotein lipase activation is mediated by residues 55-78 and phospholipid binding by... 

Figure 26-5. Principle of the 13C-mixed triglyceride breath test. Absorption of 13C-mixed triglycerides requires prior hydrolysis by pancreatic lipase (1), which leads to production of free fatty acids (stearic acid) and monoacylglycerol [2-(l-13C)octanoylglycerol]. These metabolites are incorporated into micelles, absorbed, and transported to the liver (2). Further degradation by hepatic enzymes and P-oxidation results in formation of 13C02, which is absorbed into the bloodstream, transported to the lung, and exhaled (3). Thus, exhalation of 13C02 reflects intestinal lipolysis and is a marker of pancreatic exocrine function.

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