Concentrative liver parenchymal cell

There is abundant evidence that glucagon elevates cAMP levels in isolated liver parenchymal cells, in perfused liver and in the liver in vivo [58,59], As illustrated in Fig. 2, this occurs rapidly and with concentrations of the hormone [59] within the range found in portal venous blood in vivo i.e., 0.2-2 x 10-10 M. When sufficiently sensitive and accurate methods are employed to measure cAMP, an increase in the nucleotide is consistently observed in situations where the hormone induces metabolic responses [58,59]. However, an increase of only 2- to 3-fold is capable of inducing full stimulation of some major hepatic responses, e.g., phos-phorylase activation (Fig. 2) and gluconeogenesis [58,59]. Since higher concentrations of the hormone can elevate cAMP 10-fold or more [59] it appears that there is considerable receptor reserve for these responses. 

Up-regulation of the high-affinity pyrimidine-preferring nucleoside transporter concentrative nucleoside transporter 1 by tumor necrosis factor-alpha and interleukin-6 in liver parenchymal cells. Journal of Hepatology, 41 (4), 538-544. 

Fernandez-Veledo, S., Huher-Ruano, I., Aymerich, I., Duflot, S., Casado, F.J., and Pastor-Anglada, M. (2006) Bile acids alter the subcellular localization of CNT2 (concentrative nucleoside cotransporter) and increase CNT2-related transport activity in liver parenchymal cells. The Biochemical Journal, 395 (2), 337-344. 

Bile is formed and secreted continuously by polygonally shaped liver parenchymal cells called hepatocytes. An aqueous buffer component (e.g., HCOj") is added to the bile by the hepatic bile duct cells that carry the secretion toward the common bile duct. The membrane of the hepatocytes in contact with the blood has microvilli that facilitate the exchange of substances between plasma and the cells. Hepatocytes are rich in mitochondria and endoplasmic reticulum. Hepatic bile flows into the gallbladder, where it is concentrated, stored, and emptied into the duodenum when the partially digested contents of the stomach enter... 

Much of the pharmacology of FPL-55712 is ascribed to its antagonism of SRS-A however, at concentrations only slightly higher than those needed to inhibit SRS-A, FPL-55712 also inhibits thromboxane synthetase and lipoxygenase in broken cell, but not intact cell preparations. FPL-55712 also inhibits the extensive necrosis of liver parenchymal cells and death in animals injected with endotoxin and D-galactosamine. ... 

Liver. In humans, chronic Cd exposure does not typically result in hepatotoxicity. In laboratory animals, the liver accumulates the largest concentrations of Cd after acute or chronic exposures. In chronically exposed rats, liver injury occurs prior to renal dysfunction. Chronic Cd effects in the liver include increased plasma activities of alanine and aspartate aminotransferases, structural irregularities in hepatocytes, and decreased microsomal mixed function oxidase and CYP450 activities. Acute exposures in rats result in hepatic necrosis, particularly in parenchymal cells. Additionally, rough endoplasmic reticulum deteriorates, while smooth endoplasmic reticulum proliferates. Mitochondria are also degraded. As is the case with chronic exposure, microsomal mixed function oxidases and CYP450s are inhibited. 

In the liver, isoprenaline-stimulated adenylate cyclase has been found to be located almost exclusively on the surface of the parenchymal cells, with little or no deposit on the surface of the reticulo-endothelial cells. In contrast, the predominant effect of glucagon resulted in the deposition of reaction product on the reticulo-endothelial cell surface, although deposits were also present on the parenchymal cells. In the presence of F , there were substantial deposits on the surface of both types of cells. These results demonstrate that distinct enzyme systems are present in parenchymal and reticulo-endothelial cells. No theories concerning the function of adenylate cyclase in the liver have considered its role in the endothelial cells which act mainly on phagocytes. These cells contribute 35% of the cells in the liver and can be expected to contribute substantially to biochemical measurements of adenylate cyclase activity and cyclic AMP concentrations when liver slices, homogenates, or cell fractions constitute the enzyme source. 

More frequently encountered are acquired defects in bUe acid synthesis, which have been noted in Liver diseases such as hepatitis and cirrhosis. In acute hepatitis, alterations of bile acid synthesis and conjugation occur because of hepatic parenchymal cell disease. In cirrhosis, there is a marked reduction in cholic acid synthesis with a low concentration of biliary deoxycholic acid. These abnormalities are due both to decreased synthesis and to portosystemic shunting. The... 

In the plasma, vitamin A is transported from its major depots in the liver to tissues in several forms, primarily as a 1 1 molar complex of all-frans-retinol with RBP. Low concentrations of dll-trans- and 13-ds-retinoic acid, probably bound to albumin, and retinyl and retinoyl p-glucuronides, are also present. Holo-RBP also interacts strongly with transthyretin in the plasma. All of these forms of vitamin A can be taken up by various tissue cells. Several tissues besides the parenchymal cells of the liver can also synthesize RBP, as evidenced by the presence of mRNA for RBP within such cells. Thus, the extensive recycling of retinol between the liver and peripheral tissue cells may well occur as complexes with RBP. Another possibility is that retinyl ester, which is synthesized in essentially all cells of the body, might be carried back to the liver in lipoproteins. 

---