Our findings show that the incidence of recent HDV infection in HIV/HBV-coinfected patients increased significantly from 1992-2001 to 2007-2011, and was associated with hepatitis flares and syphilis.

The actively transported sugar D-glucose binds to brush borders disrupted with tris(hydroxymethyl)aminomethane in preference to D-mannose and L-glucose, which are not actively transported. This preferential binding of D-glucose is not dependent on either added Na(+) or adenosine triphosphatase activity stimulated by Na(+) with K(+) and Mg(2+), but it is temperature-dependent and is completely inhibited by 0.1 millimolar phlorizin and 1 millimolar mercuric chloride.

A transformed human hepatoma cell line was examined to determine if it was an appropriate model system for studying the mechanism of action of two peroxisome proliferators that lower blood lipids. Cultures of HepG2 cells were exposed to four different concentrations of either the hypolipidemic drug, clofibric acid (CLO), or the adrenal steroid, dehydroepiandrosterone (DHEA). Activities of two peroxisomal enzymes, palmitoyl-CoA oxidase and catalase, and two mitochondrial enzymes, carnitine palmitoyl-CoA transferase and succinate-INT-reductase, were measured in CLO- and DHEA-treated cells. In general, as the concentration of these hypolipidemic agents increased from 0 to 1000 microM, the specific activities of peroxisomal palmitoyl-CoA oxidase and catalase increased, and mitochondrial carnitine palmitoyl-CoA transferase and succinate-INT-reductase decreased. The activity of lactate dehydrogenase was significantly higher in the medium of cultures exposed to the 500 and 1000 microM concentration of DHEA compared with the control cultures, indicating the cytotoxic effects of this steroid at millimolar levels in vitro. In summary, the peroxisomal proliferators, DHEA and CLO, inversely altered peroxisomal and mitochondrial beta-oxidation in HepG2 cultures, but not to the extent reported for rat hepatocytes in vitro. In vitro concentrations of DHEA greater than 500 microM adversely affected the viability of HepG2 cells. The results of this study suggest that beta-oxidation in this human hepatoma cell line may not be as sensitive to hypolipidemic agents as are primary cultures of rat hepatocytes.

Everted sacs of rat and hamster jejunum were used to measure, simultaneously, fluid and glucose movement in the presence of various concentrations of bile salts. Low concentrations of sodium taurocholate or glycocholate did not affect the rates of fluid absorption or transport by either rat or hamster jejunum. Under these conditions, in some cases, while glucose absorption was unaffected, glucose transport was inhibited. High concentrations of bile salts reduced fluid and glucose absorption and transport by both rat and hamster jejunum. Although the transport of glucose against a concentration gradient is completely inhibited at low concentrations of bile salts with rat jejunum, it still occurs with hamster jejunum even in the presence of high bile salt concentrations. In the absence of glucose i n the incubation medium, the rates of fluid absorption by rat and hamster jejunum were greatly reduced. Under these conditions, fluid transport by rat jejunum was completely abolished, whereas fluid transport by hamster jejunum was greatly reduced, but not completely inhibited. However, addition of bile salts to the glucosefree incubation medium did produce a complete inhibition of fluid absorption and transport by both rat and hamster jejunum. Bile salts, within the concentration range used in this investigation, have no effect upon glucose utilization and lactic acid production by either rat or hamster jejunum. Sodium taurocholate and glycocholate, a t the low Concentration of 1 mM, reduced the ATP levels in both rat and hamster jejunal sacs. This reduction of ATP levels in whole sacs was also observed to occur in the mucosal layer in the presence of low concentrations of bile salts. A greater reduction in tissue ATP levels was observed when the bile salt concentration was increased. The amount of ATP i n unincubated rat and hamster jejunum was reduced by approximately 40% when incubated in bicarbonate saline containing glucose. Tissue ATP levels were also reduced when sacs were incubated in a glucose-free medium, a greater reduction being observed i n rat jejunum. In the absence of glucose, bile salts were capable of decreasing ATP levels i n hamster, but not in rat jejunum. The effects of bile salts on fluid and glucose movement by rat and hamster jejunum were discussed in relation to tissue energy sources for these processes. Also, the possible role played by bile salts i n regulating the transference of various substances across the intestinal wall was discussed.