Adipose tissue triglyceride uptake

A lipoprotein lipase inhibitor was found in the serum of hyperlipemic subjects (Klein et al. 1959). The resistance of very low density lipoproteins (1.5X 10 Crmin.) to lipolysis, may also contribute to underutilization (Angerwall et al. 1962). In contrast to adipose tissue, triglyceride uptake by rat liver apparently does not require lipolysis (Olivecrona and Belfrage 1965). Variations between tissues, and species variations mentioned previously, complicate the interpretation of lipolysis data. 

In adipose tissue glucose uptake is diminished and triglyceride breakdown is increased. The fatty acids produced are exported via the plasma and are oxidized by other tissues, while the glycerol is used for gluconeogenesis in the liver. Muscle oxidizes mainly fatty acids and ketone bodies while the brain adapts to use ketone bodies rather than glucose as a major energy source. This ability of the brain to use ketone bodies reduces the requirement for amino acids as a source of glucose, and is a factor of importance in the conservation of body protein. 

The enzyme responsible for lipolytic release of fatty acids from adipose tissue triglycerides is most likely not lipoprotein lipase. The activity of this enzyme increases under conditions of maximum uptake but decreases when maximum release is induced (Cherkes and Gordon 1959 Salaman and Robinson 1961). Any function of lipoprotein lipase in the transport of fat would therefore be in the uptake and not in the release. 

Niacin (vitamin B3) has broad applications in the treatment of lipid disorders when used at higher doses than those used as a nutritional supplement. Niacin inhibits fatty acid release from adipose tissue and inhibits fatty acid and triglyceride production in liver cells. This results in an increased intracellular degradation of apolipoprotein B, and in turn, a reduction in the number of VLDL particles secreted (Fig. 9-4). The lower VLDL levels and the lower triglyceride content in these particles leads to an overall reduction in LDL cholesterol as well as a decrease in the number of small, dense LDL particles. Niacin also reduces the uptake of HDL-apolipoprotein A1 particles and increases uptake of cholesterol esters by the liver, thus improving the efficiency of reverse cholesterol transport between HDL particles and vascular tissue (Fig. 9-4). Niacin is indicated for patients with elevated triglycerides, low HDL cholesterol, and elevated LDL cholesterol.3... 

Il.f.l.1. Insulins. Insulin is the most effective of diabetes medications. Insulin has profound effects on carbohydrate, protein, fat metabolism and electrolytes. It has anabolic and anticatabolic actions. In a state of insulin deficiency, glycogenesis, glucose transport, protein synthesis, triglyceride synthesis, LPL activity in adipose tissue, cellular potassium uptake all decrease on the other hand, gluconeogene-sis, glycogenolysis, protein degradation, ketogene-sis, lipolysis increase. 

Mechanism of Action Afibricacid derivative that inhibits lipolysis of fat in adipose tissue decreases liver uptake of free fatty acids and reduces hepatic triglyceride production. Inhibits synthesis of VLDL carrier apolipoprotein B. Therapeutic Effect Lowers serum cholesterol and triglycerides (decreases VLDL, LDL increases HDL). Pharmacokinetics Well absorbed from the GI tract. Protein binding 99%. Metabolized in liver. Primarily excreted in urine. Not removed by hemodialysis. Half-life 1.5 hr. 

Within the developing embryo, lipoprotein lipase activity is high in both heart and adipose tissue at EI4 but is absent from liver and brain. A big increase in activity occurs in adipose tissue between EI2 and EI6 and this coincides with the period of lipid uptake from the yolk and deposition in the adipocytes. More than 90% of the energy required by the developing embryo is obtained from oxidation of fatty acids present in yolk triglycerides. A further increase in lipoprotein lipase activity also occurs on hatching (Speake, Noble McCartney, 1993). 

Experiments with isolated adipose tissue which is incubated with labelled triglycerides point to the conclusion that the process of assimilation of triglycerides proceeds in two phases. An initial rapid uptake, insensitive to poisons of lipoprotein lipase, is followed by a slower, sensitive phase. It is this second phase in which hydrolysis and resynthesis takes place, as indicated by changes in the triglyceride fatty acids (Rodbell 1960) in the glycerol to fatty acid ratios of radioactivity (Rose and Shapiro 1960) and by shift of the labelled triglycerides from one compartment to another (Markscheid and Shafrir 1964). If lipoprotein lipase participates in the uptake, it is presumably at a site not accessible to the poisons in the medium. 

As in the other tissues, so far discussed, triglyceride assimilation by adipose tissue is carried out by initial uptake at a site in the tissue, followed by a facilitated transfer of the fat to other parts of the cells. This latter process involves hydrolysis and resynthesis of the triglycerides. 

The uptake of triglycerides by tissues other than adipose tissue possibly serves as an energy source in addition to the free fatty acid fraction and glucose (Gousios et al. 1963, Wood et al. 1965). 

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