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K Oida

Publications and source records attributed to K Oida.

At least 73 records · Page 4Linked to original sources
PubMed1987

Expression of a monoclonal antibody-defined aminoterminal epitope of human apoC-I on native and reconstituted lipoproteins.

Nine distinct mouse monoclonal antibodies were produced in two fusions using holo-human very low density lipoprotein (VLDL) as antigen. On immunoblotting first with human VLDL and then with isolated human apoC-I, seven of the antibodies, representing three isotypes, manifested specificity for apoC-I. Two antibodies were directed against apoB. To assess whether the seven anti-apoC-I antibodies were directed against the same or distinctively different epitopes, cross-competition assays were performed wherein 125I-labeled monoclonal antibodies were made to compete with unlabeled antibodies for occupancy on immobilized VLDL-associated apoC-I. All antibodies cross-competed to varying extents implying that they were directed against closely spaced epitopes, but based on these experiments three different epitopes were defined. On immunoblotting with CNBr fragments, all of the epitopes were assigned to the CNBr I fragment of human apoC-I (amino acids 1-38) suggesting that the NH2-terminal region of apoC-I is more immunogenic in mice than other parts of the molecule when apoC-I is associated with VLDL. A competitive solid-phase radioimmunoassay (RIA) was developed employing one of the anti-apoC-I antibodies (A3-4). VLDL was adsorbed to plastic microtiter wells, and a limiting amount of the antibody was reacted with the adsorbed VLDL. The amount of monoclonal antibody that bound to the immobilized VLDL-apoC-I was determined with a 125I-labeled goat anti-mouse IgG antibody. The addition of competitor apoC-I complexed with lipids resulted in reduced binding of the anti-apoC-I antibody to the immobilized VLDL-apoC-I. Competitor complexes consisted of an artificial lipid emulsion (Intralipid) incubated with apoC-I at phospholipid/apoC-I ratios of 1:1 to 60:1 (w/w). As the lipid/protein ratios were increased, the competitive displacement curves produced by the complexes become progressively steeper, while isolated lipid-free apoC-I produced curves with very shallow slopes, suggesting that a conformation-dependent epitope was being probed. Other apoproteins (C-II, C-III, A-I, A-II, and E) whether lipid-free or complexed with lipids did not compete. Fractionation of the 30:1 apoC-I-Intralipid complex by gel permeation chromatography suggested that apoC-I bound to phospholipids was the most effective competitor. This was confirmed by testing of apoC-I-DMPC complexes, which yielded curves that paralleled those produced by apoC-I-Intralipid.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1986

Characteristics of lipoprotein receptors of the isolated liver parenchymal cells prepared from the streptozotocin-induced diabetic rats.

Characteristics of lipoprotein receptors of the isolated liver parenchymal cells prepared from the streptozotocin-induced diabetic rats were investigated. Streptozotocin-induced diabetic rats fed 1.0% cholesterol showed the exaggerated hypercholesterolemia as compared to control rats fed 1.0% cholesterol. The present study was designed to elucidate the role of lipoprotein receptor mechanisms of liver parenchymal cells in the diabetic dyslipoproteinemia. 125I-labeled lipoproteins (rat beta-VLDL, human LDL2 or rat HDL3) were incubated with liver parenchymal cells isolated by liver perfusion using collagenase. According to the Scatchard analysis, the apparent dissociation constant (kd) and maximum beta-VLDL binding (Bmax) for the higher affinity binding site in the diabetic rats (n = 6) were (11.9 +/- 5.1) X 10(2) ng/ml and 307.5 +/- 145.2 ng/10(6) cells, respectively. These binding characteristics of the diabetic rats were not significantly different from the control rats. Furthermore, there were no significant differences in the binding characteristics of human LDL2 and rat HDL3 between the diabetic rats and the control rats. The data presented suggest that significant role of alteration of lipoprotein receptor characteristics in liver parenchymal cells is not played in the diabetic dyslipoproteinemia.

Animals↗
PubMed1985

Effects of insulin on hypercholesterolemia in the streptozotocin-induced diabetic rats fed a high cholesterol diet.

The effect of dietary cholesterol (Ch) on plasma lipoprotein and apolipoproteins (apo) in diabetic rats was investigated. Ch-fed diabetic rats were severely hypercholesterolemic and hypertriglyceridemic. They had higher concentrations of very low density lipoprotein (VLDL), intermediate density lipoprotein (IDL) and low density lipoprotein (LDL). Concentration of high density lipoprotein (HDL) was decreased. beta-VLDL increased predominantly in Ch-fed diabetic rats, whereas IDL increased in the Ch and propylthiouracil-fed control rats. According to sodium dodecyl sulfate polyacrylamide gel electrophoresis, VLDL and IDL from Ch-fed diabetic rats were unusual in that they contained more apo E, A-I and A-IV. Concentrations of plasma apo A-I and apo E were measured by radioimmunoassay. The diabetic rats fed a labo chow showed a significantly lower concentration of plasma apo E than control rats. Plasma apo E was extremely higher in the diabetic rats fed a cholesterol diet. Plasma apo A-I was significantly increased in the diabetic rats fed a labo chow and those fed a cholesterol. Insulin treatment significantly decreased the concentrations of VLDL, IDL and LDL and plasma concentration and distribution of apolipoproteins in lipoprotein subfractions changed toward normal. However, decreased HDL in the Ch-fed diabetic rats was not recovered by insulin treatment.

Animals↗
PubMed1984

Lipoprotein lipase activities in heart muscle of streptozotocin-induced diabetic rats.

Triglyceride lipase (TGL) activities in the homogenates of the rat heart muscle were studied. TGL activity per mg protein of heart muscle was the highest in heart muscle homogenate utilizing 2.1 M glycine buffer, pH 8.3 among the assays investigated. The effects of NaCl, serum and heparin on TGL activities in heart muscle homogenates indicated the characteristics of lipoprotein lipase (LPL). Twelve-hour fasting increased heart muscle LPL activity, while enzyme activities in 48 hour- and 72 hour-fasted rats were lower than those in fed rats. LPL activities in heart muscle homogenates in streptozotocin (STZ)-induced diabetic rats either 3 days or 4 weeks after STZ injection, were decreased significantly as compared with those of control rats.

Animals↗
PubMed1984

The effect of insulin-dextran complexes on the protein synthesis in the primary monolayer culture of adult rat hepatocytes.

The purpose of the present study was to investigate the mechanisms of the long-term effects of insulin on protein synthesis in rat liver parenchymal cells. Three kinds of soluble and stable insulin-dextran complexes (I: Mr 150,000; II: Mr 450,000; III: Mr 2,000,000) were prepared. The effects of insulin or insulin-dextran complexes on protein synthesis were evaluated in the primary monolayer culture of adult rat liver. To avoid the effects of serum factors, the primary monolayer culture of adult rat liver in serum free medium was established. The cultured hepatocytes well maintained the metabolic and morphological characteristics of the adult rat liver. The incorporation of [14C]-leucine into trichloroacetic acid insoluble proteins and immunoprecipitates by anti-rat albumin serum were measured in cultured hepatocytes prepared either from the control or streptozotocin-induced rats. An addition of insulin-dextran complexes to the culture medium of the hepatocytes from diabetic rats stimulated the protein synthesis as well as the native insulin. The maximal effect of insulin-dextran complex (I) on protein synthesis was comparable to native insulin. However, insulin-dextran complex (II) caused a 67% stimulation of native insulin. Insulin-dextran complexes (III) induced only a slight increase of protein synthesis. Furthermore, an addition of insulin-dextran complexes into the medium caused a more tight cellular attachment to the dish and more extensive spreading. These results favor the view that the stimulation by insulin of protein synthesis in rat hepatocytes does not require the entry of insulin into cells.

Albumins↗
PubMed1984

Plasma lipoproteins of monosodium glutamate-induced obese rats.

The plasma lipids and lipoproteins of rats developing obesity after neonatal administration of monosodium glutamate (MSG) were compared with those obtained from controls. The MSG-treated rats, in addition to being stunted and having enlarged adipose tissue stores, showed reduced body weight and food intake. These rats revealed a marked increase of plasma triglyceride and a slight but significant increase of phospholipids in both male and female. There was no significant difference in plasma cholesterol between MSG-treated rats and controls. The lipids and protein concentrations of very low density lipoprotein (VLDL: d less than 1.006 g/ml) were significantly greater in the MSG-treated rats than in the controls. There were no changes in the composition of these increased VLDL, which indicated that the number of VLDL particles was increased. Plasma triglyceride and lipids components of VLDL were significantly greater in males than in females. In spite of hypophagia, both male and female MSG-treated rats had higher plasma glucose levels than sex-matched controls. Plasma insulin level was higher in male MSG-treated rats (49.3 +/- 6.6 microU/ml [s.e.]) than in female MSG-treated rats (14.3 +/- 3.2 microU/ml) or in male control rats (34.6 +/- 6.6 microU/ml). These results suggested that hyperinsulinemia plays an important role in the increase of VLDL observed in the MSG-treated male rats.

Animals↗
PubMed1982

Effects of niceritrol (pentaerythritol tetranicotinate) on plasma lipoprotein concentration: increment of high density lipoprotein(HDL) cholesterol and HDL-cholesterol/low density lipoprotein cholesterol ratio in hypo-high density lipoproteinemia.

The purpose of the present study was to investigate the effects of niceritrol on HDL metabolism. In study (A), niceritrol, 750 mg/day was given for initial period of 12 weeks and 1,500 mg/day was prescribed for an additional 12 weeks to 12 subjects. In six of them, the HDL cholesterol (Ch) levels were less than 45 mg/100 ml with normal plasma cholesterol levels and with plasma triglyceride levels of less than 250 mg/100 ml. In the remaining six subjects, HDL-Ch, plasma cholesterol and triglyceride levels were all within normal limits except in one subject having a higher triglyceride level, 213 mg/100 ml. Plasma lipoproteins were fractionated by sequential ultracentrifugation and analyzed for cholesterol, triglyceride (TG), phospholipid(PL), apolipoprotein(Apo) B and Apo A-I, every 4 weeks. Niceritrol decreased plasma-Ch, VLDL-Ch, LDL-Ch, plasma-TG, VLDL-TG, plasma-PL, VLDL-PL and LDL-PL. Niceritrol increased HDL-Ch and the HDL-Ch/LDL-Ch ratio. These effects were more significant for the dose of 1,500 mg/day than 750 mg/day and were more marked in the patients with lower pretreatment HDL-Ch levels. Apo B level at 20 weeks was significantly lower than that before treatment. Initial plasma Apo A-I levels of the patients were approximately one-half of the control plasma. After treatment with niceritrol, Apo A-I concentration tended to increase. In study (B), changes of lipids concentration in HDL2 and HDL3 fraction were investigated in 5 patients during treatment with niceritrol, 1,500 mg/day for 8 weeks. Lipoproteins were analyzed every 2 weeks. HDL2-Ch levels tended to increase without significant changes of HDL3-Ch levels and HDL2-Ch/HDL3-Ch ratio showed a tendency to increase. A significantly but weakly inverse correlation between changes of VLDL-TG and HDL-Ch was observed, suggesting that the increment of HDL might be due partly to promoted lipolysis of TG-rich lipoproteins. However, it was suggested that the effects of niceritrol on lipoprotein synthesis in the liver and HDL catabolism should be considered.

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