Triglyceride droplets

Figure 4-2. Photomicrograph of a portion of a hepatocyte from a cholestatic infant with PIZ phenotype.Amorphous a 1-antitrypsin (AT) is in the transitional zone between rough and smooth endoplasmic reticulum. B, bile T, triglyceride droplet.

R. Zechner, and E. Steyrer, Intracellular distribution and mobilization of unesterified cholesterol in adipocytes triglyceride droplets are surrounded by cholesterol-rich ER-like surface layer structures, /. Cell. Sci., 2000, 3 33, 2977-2989. 

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. 

As a result, membranes or triglyceride droplets whose components are high In unsaturated fatty acids (e.g., liquid corn and olive oils) tend to be more fluid at room temperature than those with a high proportion of saturated fatty acids (e.g., solid animal fats). Because humans cannot synthesize certain essential polyunsaturated fatty acids, such as linoleic acid and linolenlc acid, we must obtain them from our diets. 

Lipoprotein lipase catalyzes the complete hydrolysis of triglycerides to free fatty acid and glycerol. This reaction occurs in the bloodstream, while the chylomicron particle is in proximity to the endothelial surface of the capillary wall. Cholesterol ester is not a substrate for lipoprotein lipase. Therefore, with the selective loss of triglycerides, the particle becomes more enriched in cholesterol ester. The free fatty acids are then taken up and oxidized in muscle or re-esterified and stored as triglyceride droplets in adipose tissue. The abundance of the adipose form of lipoprotein lipase is increased by insulin, thus promoting uptake of free fatty acids and storage as cytoplasmic triglyceride droplets (see Fig. 4). 

In Type I diabetes mellitus, there is a severe deficiency (or total absence) of insulin due to an autoimmune attack on the cells that produce insulin, pancreatic j8-cells. The absence of insulin produces a deficiency in adipose tissue lipoprotein lipase. This causes sluggish catabolism of VLDL and leads to hypertriglyceridemia. Another mechanism by which insulin deficiency promotes increased VLDL levels is the failure to inhibit the activity of adipose tissue hormone-sensitive lipase. This enzyme hydrolyzes cytoplasmic triglyceride droplets. The fatty acids then go to the liver, where they are re-esterified to form triglycerides. These triglycerides are exported on VLDL particles. Since adipose tissue-derived fatty acids are an important substrate for hepatic VLDL triglycerides, the failure to suppress adipose tissue lipolysis is an important contributor to the enhanced rate of VLDL triglyceride secretion. 

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