Secretion by hepatocytes

Prokopenko et al described that some naphthoquinones normalized or increased the immune response in rats after intensive physical load. The naphthoquinones induced the development of immunostimulating properties in heavy red blood cells by direct action on cell membranes or indirectly through proteolytic enzymes secreted by hepatocytes [212]. Other activities described for several naphthoquinones related to lapachol are antipsoriatic [213], larvicidal and insecticidal, [214-215] molluscicidal [216], and mutagenicity in salmonella [217]. The potential use of lapachol in cosmetics has been published too [218]. 

Schmidt There is a coincidence between those two comments. Hepatocyte growth factor (HGF) is actually produced by the lung, so what results when you do a two-thirds hepatectomy is that the HGF secreted by the lung brings the fiver back up to its size. 

Bile is produced continuously by the liver bile salts are secreted by the hepatocytes and the water, sodium bicarbonate, and other inorganic salts are added by the cells of the bile ducts within the liver. The bile is then transported by way of the common bile duct to the duodenum. Bile facilitates fat digestion and absorption throughout the length of the small intestine. In the terminal region of the ileum, the final segment of the small intestine, the bile salts are actively reabsorbed into the blood, returned to the liver by way of the hepatic portal system, and resecreted into the bile. This recycling of the bile salts from the small intestine back to the liver is referred to as enterohepatic circulation. 

Figure 2.2 Secretion of bile acids and biliary components. Bile acids (BA) cross the hepatocyte bound to 3a-hydroxysteroid dehydrogenase and are exported into the canaliculus by the bile-salt export protein (BSEP). Phosphatidylcholine (PC) from the inner leaflet of the apical membrane is flipped to the outer layer and interacts with bile acids secreted by BSEP. BA, PC, together with cholesterol from the membrane form mixed micelles that are not toxic to epithelial membranes of the biliary tree. Aquaporins (AQP) secrete water into bile.

Figure 2.3 Absorption of bile acids by the cholangiocyte in the cholehepatic shunt. Bile acids are absorbed at the apical membrane of the cholangioc5de by the apical sodium-dependent bile-acid transporter (ASBT) that causes cholehepatic shunting of bile acids back to the hepatocyte. Absorbed bile adds are exported across the basolateral membrane by multi-drug-resistance-associated protein 3 (MRP3), a truncated form of ASBT or by the het-eromeric organic solute (OST) a and p forms. Bile adds cause choleresis that is rich in bicarbonate ions secreted by the chloride/bicarbonate ion exchanger.

A major pathway by which LDL are catabolized in hepatocytes and other cells involves receptor-mediated endocytosis. Cholesteryl esters from the LDL core are hydrolyzed, yielding free cholesterol for the synthesis of cell membranes. Cells also obtain cholesterol by de novo synthesis via a pathway involving the formation of mevalonic acid by HMG-CoA reductase. Production of this enzyme and of LDL receptors is transcriptionally regulated by the content of cholesterol in the cell. Normally, about 70% of LDL is removed from plasma by hepatocytes. Even more cholesterol is delivered to the liver via remnants of VLDL and chylomicrons. Thus, the liver plays a major role in the cholesterol economy. Unlike other cells, hepatocytes are capable of eliminating cholesterol by secretion of cholesterol in bile and by conversion of cholesterol to bile acids. 

Ammonia (NH3) and the ammonium ion (NH4"1") are highly toxic to mammalian cells. In vivo, ammonium is secreted by the cells and transported to the mitochondria of hepatocytes, where it is converted into urea via the urea cycle. Urea production occurs almost exclusively in the liver and is the fate of most of the ammonium channeled there. The urea passes into the bloodstream and thus to the kidneys and is excreted into the urine. Mammalian cells in culture secrete ammonium into the culture medium, where its concentration increases gradually because there is no ammonium recycling pathway (Newland et al., 1990). 

ApoSAA is secreted by mouse hepatocytes in vitro apparently independently of lipid and of apoA-I. However, when HDL is added the bulk of the apoSAA is recovered in the HDL fraction, with apoA-I. In mouse plasma, apoSAA and apoA-I appear to reside together on a population of HDL3 particles (H26, H27). 

Kll. Kempen, H. J. M., Lipoprotein secretion by isolated rat hepatocytes characterization of... 

AUister, E. M., Borradaile, N. M., Edwards, J. Y., Huff, M. W. (2005). Inhibition of microsomal triglyceride transfer protein expression and apolipoprotein BlOO secretion by the citms flavonoid naiingenin and by insulin involves activation of the mitogen-activated protein kinase pathway in hepatocytes. Diabetes, 54, 1676-1683. 

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V.A.Kosykh, V.Z.Lankin, E.A.Podrez, D.K.Novikov, S.A.Volgushev, A.V.Victorov, V.S.Repin and V.N. Smirnov, Very low density lipoprotein secretion by cultured hepatocytes of rabbits fed purified or autoxidized cholesterol. Lipids 24 (1989) 109-115. 

Phung.T. I.., Rod cone, A Jensen, K., Sparks, C, and Sparks,]. D. (1997). Phosphoinositldc 3-kinase activity Ls nsKCSSary for insulin-dependent inhibition of apolipoprOtein B secretion by rat hepatocytes and localizes to the endoplasmic reticulum. /. Biof. Cheof, 271, 30693-3(17112. 

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