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Biomedical subjects

S Kawata

Publications and source records attributed to S Kawata.

At least 127 records · Page 7Linked to original sources
PubMed1993

Decrease of hepatic triglyceride lipase levels and increase of cholesteryl ester transfer protein levels in patients with primary biliary cirrhosis: relationship to abnormalities in high-density lipoprotein.

Serum levels of high-density lipoprotein cholesterol are often increased in patients with primary biliary cirrhosis. To elucidate the mechanism of the elevation of high-density lipoprotein cholesterol levels in this disease, lipoprotein abnormalities were analyzed in 10 patients subdivided into two groups according to concentration of high-density lipoprotein cholesterol. Activities and protein masses of lipoprotein lipase, hepatic triglyceride lipase and cholesteryl ester transfer protein were also determined. Serum high-density lipoprotein cholesterol concentration exceeded 90 mg/dl in 5 of 10 patients. Lipoprotein particles in the high-density lipoprotein2 fraction (with density between 1.063 and 1.125 gm/ml) were enriched with apolipoprotein E and larger in size than those of normal controls. In patients with and without hyperalphalipoproteinemia, hepatic triglyceride lipase activity was significantly decreased (p < 0.05); this was due to the reduction of its protein mass. Lipoprotein lipase activity and protein mass were normal. It is noteworthy that increases in cholesteryl ester transfer protein activity and mass were observed. The enhancement of cholesteryl ester transfer protein activity was more remarkable in the patients with hyperalphalipoproteinemia than in those without hyperalphalipoproteinemia. Because a significant positive correlation was demonstrated between activity and protein mass (r = 0.90, p < 0.001), the increase of cholesteryl ester transfer protein activity may be attributed to the increase of its protein mass. These data suggest that the decrease of hepatic triglyceride lipase levels at least partly explains the appearance of apolipoprotein E-rich large high-density lipoprotein particles in patients with primary biliary cirrhosis.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

[Molecular biology in development of fatty liver--regulation of apolipoprotein B synthesis].

Apolipoprotein B (apo B) synthesis in fatty liver was described in this review. Apo B synthesis has not been intensively studied in fatty liver. Recently, we demonstrated that hepatic apo B mRNA level increased in two experimental models of fatty liver. Davidson et al. reported that apo B mRNA editing was enhanced in fatty liver induced by refeeding after fasting. However, further investigation is needed to clarify whether alteration in apo B gene regulation participates in development of fatty liver.

Animals↗
PubMed1992

Changes in lipid composition of erythrocyte membranes with administration of S-adenosyl-L-methionine in chronic liver disease.

This study was undertaken to determine whether S-adenosyl-L-methionine (SAMe) changes the lipid composition and fluidity of erythrocyte membranes in chronic liver disease. SAMe was administered intravenously at a daily dose of 600 mg for 2 weeks to 10 patients; 6 patients with cirrhosis and four with primary biliary cirrhosis. The elevated free cholesterol to phospholipid molar (C/PL) ratio of the erythrocyte membranes of the patients (0.857 +/- 0.018) significantly decreased after the administration of SAMe (1 week, 0.823 +/- 0.021; 2 weeks, 0.823 +/- 0.013). In all of the four patients whose erythrocyte membrane fluidity was measured, fluidity improved with the administration of SAMe and correlated with the C/PL ratio of the membranes. These results suggest that SAMe decreases the C/PL ratio of erythrocyte membranes and thus improves membrane fluidity in chronic liver disease.

Adult↗
PubMed1992

Effect of dietary fiber on cytochrome P450IA1 induction in rat colonic mucosa.

The effect of dietary fiber on the induction of cytochrome P450IA1 in rat colonic mucosa after a single intragastric injection of 3-methylcholanthrene (3MC, 20 mg/kg) was investigated by examining the drug-metabolizing enzyme activity, immunoblotting for cytochrome P450IA1 and immunohistochemistry. 7-Ethoxycoumarin-O-deethylase activities were approximately 20-fold higher in microsomes from both proximal and distal portions of the colonic mucosa of control diet-fed 3MC-treated rats compared with those of control diet-fed untreated rats. Strong immunofluorescence for cytochrome P450IA1 was localized in the cytoplasm of the colonic mucosa surface epithelium from the control diet-fed 3MC-treated rats. 7-Ethoxycoumarin-O-deethylase activity and cytochrome P450IA1 content determined by immunoblotting were significantly lower in wheat bran-fed 3MC-treated rats than in control diet-fed 3MC-treated rats. Immunohistochemical analysis showed much weaker immunofluorescence for cytochrome P450IA1 in the surface epithelium of the colonic mucosa of the wheat bran-fed 3MC-treated rats. These observations suggested that dietary fiber can affect the induction of cytochrome P450IA1 in colonic mucosa by dietary inducers or carcinogens.

7-Alkoxycoumarin O-Dealkylase↗
PubMed1992

Elevated levels of plasma transforming growth factor-beta in patients with hepatocellular carcinoma.

We measured the plasma transforming growth factor-beta (TGF-beta) concentration in 14 patients with human hepatocellular carcinoma (HCC) and 9 age-matched normal subjects using growth inhibition assay of mink lung epithelial cells. The calculated plasma TGF-beta concentration in the patients with HCC was 28.6 +/- 27.9 ng/ml (mean +/- SE), showing significant elevation compared with that in 9 normal subjects (5.3 +/- 3.3 ng/ml, P less than 0.01). In three cases, we could measure plasma TGF-beta levels before and after their treatment for HCC. The plasma TGF-beta levels decreased from 59.0 to 18.2 ng/ml after hepatic resection in one case, and from 24.0 to 10.7 ng/ml and from 12.4 to 3.4 ng/ml after transhepatic arterial embolization in the other two cases. These data indicate that plasma TGF-beta level is elevated in patients with HCC, probably due to release from HCC tissues.

Animals↗
PubMed1992

Effect of pravastatin, a potent 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitor, on survival of AH130 hepatoma-bearing rats.

3-Hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitor is known to have an inhibitory effect on cell growth in addition to a cholesterol-lowering effect. This study examined the effect of pravastatin, a potent inhibitor of HMG-CoA reductase, on the survival of AH130 hepatoma-bearing rats. Pravastatin (1, 2, or 8 mg/kg body weight) was intraperitoneally injected once a day into tumor-bearing rats. The difference in the survival curves was significant between the controls and the rats treated with 8 mg/kg of pravastatin (P < 0.019 by logrank test) but not between the controls and the rats treated with 1 or 2 mg/kg of the inhibitor. The tumor volume was significantly decreased in the rats treated with 8 mg/kg of pravastatin (P < 0.05). These observations showed that intraperitoneal injection of pravastatin could improve the survival of AH130 hepatoma-bearing rats and had an inhibitory effect on the growth of the ascites form tumor.

Animals↗
PubMed1992

Transthyretin (prealbumin) in the pancreas and sera of newly diagnosed type I (insulin-dependent) diabetic patients.

We investigated transthyretin (TTR) in the pancreases and sera of 10 newly diagnosed type I diabetic patients by immunohistochemistry and nephelometry. In the type I diabetic pancreases, glucagon-positive A-cells showed strong immunoreactivity for TTR, the intensity and distribution pattern of which corresponded to those in normal subjects. Morphometric analysis revealed that the amount of strongly TTR-positive A-cells was not significantly different from that in normal subjects. On the contrary, insulin-positive B-cells, which normally show uneven and weak TTR immunoreactivity, decreased in number, and only a few residual B-cells showed faint immunoreactivity. Neither somatostatin cells nor pancreatic polypeptide cells were positive for TTR. The serum TTR concentration showed a significant decrease in type I diabetic patients compared with that in normal subjects (P less than 0.005). These data suggest that the synthesis or storage of TTR in A-cells is not affected, but that in B-cells is impaired in type I diabetes. The decrease in serum TTR might be one of the features of metabolic disorders in type I diabetes.

Adult↗
PubMed1992

Application of the environmental SEM in human dentin bleached with hydrogen peroxide in vitro.

The environmental SEM (E-SEM) can be used unfixed biological samples under a low vacuum and wet condition. In this study, the fractured dentin of unfixed human teeth was treated with a 30% hydrogen peroxide solution (H2O2) for the examination of tooth-bleaching prior to the E-SEM and a conventional SEM. The peritubular matrix (PM) always showed a few cracks along the long axis of a dentinal tubule, and the ends of fine fibrils rose to the smoothly changed surface of the intertubular matrix (IM). The E-SEM with non-fixation and the conventional SEM following fixation indicated that the hydrogen peroxide solution easily permeated the PM and dissolved the non-fibrillar substance including the cracks of the PM by the constriction. In the IM, the solution may partially dissolve the organic parts within mineralized fibrils as well as non-fibrillar substance between the fibrils, although these remnants might precipitate again there.

Adolescent↗
PubMed1991

Elevated levels of transforming growth factor beta messenger RNA and its polypeptide in human hepatocellular carcinoma.

Malignant cells in culture express elevated levels of transforming growth factor beta 1 (TGF-beta 1) mRNA and secrete an abundant amount of TGF-beta protein, but little is known about the production of TGF-beta in human malignant tissues in vivo. We estimated the levels of TGF-beta 1 mRNA expression by Northern hybridization and measured TGF-beta protein using a radioreceptor assay in tumor tissues surgically obtained from six patients with hepatocellular carcinoma (HCC). TGF-beta 1 mRNA was expressed at much higher levels in HCC tissues from all the cases compared with normal human liver, suggesting an association of the activated TGF-beta 1 gene transcription with hepatocarcinogenesis. The content of TGF-beta was 207 +/- 121 ng/g wet tissue in the HCC tissue, and it showed correlation with the level of TGF-beta 1 mRNA in the tissue (r = 0.69; P less than 0.05). An immunohistochemical study demonstrated that TGF-beta 1 staining could be observed in HCC cells. These observations suggest that human HCC strongly expresses TGF-beta 1 mRNA in vivo, leading to a high content of TGF-beta protein.

Aged↗
PubMed1991

Preferential distribution of group-II-like phospholipase A2 in mononuclear phagocytic cells in rat spleen and liver.

The localization of calcium-dependent phospholipase A2, (PLA2) immunochemically closely related to the enzyme of the viperid and crotalid type (group II), in cells isolated from rat spleen and liver was examined using a polyclonal antibody directed against rat spleen group II, PLA2 (PLA2M). In isolated spleen cells, the monocyte/macrophage fraction had the highest PLA2 activity (1.28 +/- 0.35.min-1.10(6) cells-1) which was almost completely inhibited by the anti-PLA2M antibody. An immunoblot analysis confirmed the presence of the enzyme in this fraction. An immunocytochemical study revealed that the PLA2 was present in spleen macrophages. In the isolated liver cells, Kupffer cells (0.92 +/- 0.22 nmol.min-1.10(6) cells-1) contained higher anti-PLA2M-antibody-inhibitable PLA2 activity than parenchymal cells (0.26 +/- 0.06.min-1.10(6) cells-1). The immunocytochemical study showed that cells immunopositive with anti PLA2M antibody were Kupffer cells. These results suggest that the mononuclear phagocytic cells in rat spleen and liver have relatively high activity of group-II-like PLA2. Subcellular distribution patterns of the anti-PLA2M-antibody-inhibitable phospholipase A2 activity in different cell populations from spleen and liver were compared. A mode of the distribution of the enzyme in the spleen macrophages was essentially similar to that in the spleen lymphocytes. The distribution in Kupffer cells was similar to that in parenchymal cells.

Animals↗
PubMed1991

Modulation of cholesterol 7 alpha-hydroxylase activity by nonspecific lipid transfer protein in human liver--possibly altered regulation of its cytosolic level in patients with gallstones.

Nonspecific lipid transfer protein (nsLTP) partially purified from human liver stimulated human microsomal cholesterol 7 alpha-hydroxylase activity. Addition of the nsLTP preparation to the reaction mixture enhanced the activity two-fold. Treatment of the nsLTP preparation with anti-rat nsLTP antiserum, which cross-reacts with human nsLTP, reduced the 7 alpha-hydroxylase-stimulating ability. These observations suggested that nsLTP plays a role in regulating the 7 alpha-hydroxylase activity in the human liver. 7 alpha-Hydroxylase activity in eight patients with cholesterol gallstones (4.7 +/- 1.6 pmol/min per mg microsomal protein) was significantly lower than that in five controls (7.9 +/- 3.4) (P less than 0.05). The amount of nsLTP in the cytosolic fraction (105,000 X g supernatant) of human liver was determined by dot-blotting immunoquantitation with the antiserum. The cytosolic level of nsLTP in the liver of the patients (716 +/- 239 cpm/3 micrograms protein) was higher than that in the controls (438 +/- 184) although the difference between the two groups was not statistically significant. This suggested that control of the cytosolic level may be affected in patients with cholesterol gallstones.

Adult↗
PubMed1991

Induction of group II-like phospholipase A2 by lipopolysaccharide in the liver of BCG-primed rat.

The specific activity of phospholipase A2 (PLA2) in the liver homogenate was elevated 1.7-fold in bacillus Calmette-Guerin (BCG)-treated rats, 1.6-fold in lipopolysaccharide (LPS)-treated rats, and 2.4-fold in BCG-infected rats treated with LPS, compared with that of control rats. These increased activities were almost completely inhibited by the antibody directed against rat splenic group II PLA2 (PLA2M) but not by anti-pancreatic PLA2 antibody. The results of immunoblot analysis confirmed that the PLA2 immunochemically related to the group II enzyme was induced by treatment with BCG and/or LPS. The anti-PLA2M antibody-inhibitable PLA2 activity per a single cell was elevated not only in nonparenchymal cell fraction but also in hepatocyte fraction, as in the case of whole liver. On the contrary, the PLA2 concentration and its specific activity did not change by the same treatment both in spleen homogenate and in isolated spleen cell fractions although a 3-fold increase in spleen mass occurred by BCG treatment. These results suggested that a tissue-specific mechanism of the PLA2 induction by these inflammatory mediators may operate in liver.

Animals↗
PubMed1991

Animal model of systemic carnitine deficiency: analysis in C3H-H-2 degrees strain of mouse associated with juvenile visceral steatosis.

We analyzed carnitine profiles in C3H-H-2 degrees strain of mouse associated with fatty liver, hyperammonemia and hypoglycemia (Koizumi et al., 1988). Carnitine levels in serum, liver and muscle of mouse with fatty liver were markedly decreased in comparison with those of control mouse (littermates without fatty liver). This is a useful animal model to analyze the role of carnitine in lipid, amino acid and carbohydrate metabolism.

Aging↗