Phospholipids secretion, decrease

Although interspecies differences can be circumvented through the use of primary cultures of human alveolar epithelial cells, routine use of these cells is limited by availability.58,60 Primary culture of rat type II alveolar epithelial cells is economical and demonstrates high reproducibility, and its phospholipid secretion is similar to that of human type II cells.43 P-gp is expressed in both human and rat type I cells but not in freshly isolated rat type II cells.61 It is assumed that alveolar type II cells are progenitors for regenerating type I cells in vivo, and type II cells in culture lose their cuboidal appearance, lamellar bodies, and microvilli, and the number of surfactant proteins decrease. Monolayers are formed in 5 to 8 days, and the transdifferentiation to type I-like cells is complete within 7-8 days, characterized by the development of attenuations, tighter junctions, and increasing expression of... 

Another experimental approach to gallstone therapy is the use of phenobarbital. In Rhesus monkeys it increases bile salt and phospholipid secretion into bile without significantly changing cholesterol secretion.98 Furthermore, it has been reported to decrease cholesterol saturation in hepatic bile in man.99 Phenobarbital s ability to decrease the relative cholesterol content in bile may allow dissolution of cholesterol gallstones after long-term therapy. Neither lecithin nor cholestyramine are effective in human gallstone disease.100... 

The effects of a short-time interruption (24 hours) of the enterohepatic circulation on bile composition has also bfjeu studied in man. At the time of operation on patients with cholelithiasis, Thurciborn (1962) cannulated the common bile duct with a ballenterohepatic circulation. Interruption of the EHC resulted in a decrease in the secretion of bile acid conjugates in the same way as in the bile fistula rats. In addition, the secretion of phospholipids decreased considerably, but the cholesterol output from the liver was about the same as with an intact enterohepatic circulation. Tlie decrease in phospholipid secretion is an interesting finding. Several explanations are possible. The occurrence of an enterohepatic... 

In the bile cholesterol is kept soluble by fats, phospholipids like lecithin and by bile acids. The important bile acids in human bile are cholic acid, chen-odeoxycholic acid or chenodiol and ursodeoxycholic acid or ursodiol. Bile acids increase bile production. Dehydrocholic acid, a semisynthetic cholate is especially active in this respect. It stimulates the production of bile of low specific gravity and is therefore called a hydrocholeretic drug. Chenodiol and ursodiol but not cholic acid decrease the cholesterol content of bile by reducing cholesterol production and cholesterol secretion. Ursodiol also decreases cholesterol reabsorption. By these actions chenodiol and ursodiol are able to decrease the formation of cholesterolic gallstones and they can promote their dissolution. 

Jiang XC, Qin S, Qiao C, Kawano K, Lin M, Skold A, Xiao X, Tall AR (2001) Apolipoprotein B secretion and atherosclerosis are decreased in mice with phospholipid-transfer protein deficiency. Nat Med 7 847-852... 

Phosphatidylcholine is the major phospholipid on the surface monolayer of all lipoproteins, including VLDLs. In the liver, phosphatidylcholine is synthesized by two biosynthetic pathways the CDP-choline pathway and the phosphatidylethanolamine A -methyltransferase pathway (Chapter 8). Choline is an essential biosynthetic precursor of phosphatidylcholine via the CDP-choline pathway. When cells or animals are deprived of choline, plasma levels of TG and apo B are markedly reduced and TG accumulates in the liver, resulting in fatty liver. These observations led to the widely held view that the fatty liver caused by choline deficiency is due to inhibition of PC synthesis, which in turn would decrease VLDL secretion. This hypothesis was tested in primary rat hepatocytes cultured in medium lacking choline. Upon removal of choline/methionine from culture medium, the TG content of hepatocytes was increased 6-fold, and the secretion of TG and apo B in VLDL was markedly reduced. The interpretation of these experiments was that hepatic VLDL secretion requires the synthesis of phosphatidylcholine from either the CDP-choline or methylation pathways which require choline or methionine, respectively, as precursors (D.E. Vance, 1988). However, since choline deprivation was induced in a background of methionine insufficiency, it was not clear whether the lack of choline per se, and inhibition of the choline pathway for phosphatidylcholine synthesis, decreased VLDL secretion. More recent experiments have shown, surprisingly, that deficiency of choline in primary mouse hepatocytes does not reduce, but increases, phosphatidylcholine synthesis via the CDP-choline pathway, and does not decrease VLDL secretion (J.E. Vance, 2004). Thus, a deficiency of dietary choline reduces plasma TG and apo B levels by a mechanism that does not involve reduction of phosphatidylcholine synthesis. 

Fig. 6 shows that BC-PL are able to affect in men prolactin secretion and spinal lumbar HVA suggesting an effect on dopaminergic system also in humans. Phospholipids induce a decrease of serum prolactim and an increase of HVA in the lumbar spinal fluid. Serum prolactin is believed to be under the inhibitory control of DA along the hypothalamic pituitary axis (Me Leod Lehmeyrer, 1974), while lumbar HVA may be indicative of DA turnover (Curzon, 1975). Furthermore, BC-PL reverse the chlorpromazine effect on serum prolactim. The effect of phenothiazines on prolactin secretion seems to depend on a block of dopamine receptors and it is counteracted by the administration of L-dopa and of dopamine agonists (Frantz et al., 1972). 

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