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Biomedical subjects

M Shinomiya

Publications and source records attributed to M Shinomiya.

At least 91 records · Page 5Linked to original sources
PubMed1983

Lipid metabolism in the aorta of daunomycin-induced nephrotic rats.

Several enzyme activities involved in lipid hydrolysis (acid and neutral cholesterol esterase and lipase) or synthesis (acyl-CoA synthetase, acyl-CoA: cholesterol acyltransferase and cholinephosphotransferase) were assayed in the aortas of rats with nephrosis induced by daunomycin and of rats fed on high cholesterol diet. In nephrotic rats activities of some enzymes involved in lipid hydrolysis, but not in synthesis, were increased. On the contrary, in rats fed on high cholesterol diet, the activities of all enzymes involved in lipid synthesis were significantly increased, with some increase in those involved in lipid hydrolysis. In nephrotic rats fed on high cholesterol diet all enzyme activities were markedly increased. From the view point of accumulation of cholesterol ester (CE), the ratio of hydrolysis of CE in lysosomes to CE incorporated from the blood and the ratio of hydrolysis of CE to reesterification of free cholesterol in microsomes were considered to be important. From this point of view, nephrotic hyperlipidemia was not so atherogenic as hyperlipidemia induced by the diet. The role of serum high density lipoproteins in lipid metabolism in the aorta was discussed.

Animals↗
PubMed1983

Effects of gamma-oryzanol on lipid metabolism in rats fed high-cholesterol diet.

The lipid contents of the plasma and liver and enzyme activities in the aorta were determined in rats given the following diets: Group I, normal diet (ND); Group II, high cholesterol diet (HCD, ND plus 1% cholesterol and 0.5% cholic acid); Group III, HCD plus 0.5% gamma-oryzanol; Group IV, HCD plus 2% gamma-oryzanol in the last days of the 4th, 8th and 12th week of the feeding period. Total cholesterol, low-density lipoprotein-cholesterol and very low-density lipoprotein-cholesterol in the plasma were significantly higher in rats in groups III and IV than in those in group II. High-density lipoprotein-cholesterol was increased in groups III and IV. There were no differences in the triglyceride or phospholipids concentrations in the plasma of rats in the four groups. The liver weight was higher in the HCD groups (groups II, III and IV) than in the ND group (group I). The cholesterol ester and triglyceride contents of the liver were higher in the HCD groups than in the ND group, and the increase was the least in group IV of the HCD groups. Changes in acid cholesterol esterase activity and acyl CoA: cholesterol acyltransferase activity in rat aorta homogenates to compensate for lipid deposition were greater in groups III and IV than in group II.

Animals↗
PubMed1983

In vivo effects of cis-5,8,11,14,17-20:5 (n-3) and cis-4,7,10,13,16,19-22:6(n-3) on serum lipoproteins, platelet aggregation, and lipid metabolism in the aorta of rats.

Highly purified cis-5,8,11,14,17-20:5 (n-3) or cis-4,7,10,13,16,19-22:6 (n-3) was administered to rats for 2 weeks, and serum lipoprotein lipid levels, platelet aggregation, and lipid metabolism in the aorta in vivo were investigated. 20:5 (n-3) decreased the level of low density lipoprotein phospholipid. 22:6 (n-3) increased the level of high density lipoprotein cholesterol and decreased those of low density lipoprotein triglyceride and phospholipid. Both 20:5 (n-3) and 22:6 (n-3) markedly inhibited platelet aggregation. 20:5 (n-3) decreased the acid and neutral cholesterol esterase activities, but did not affect either acyl-CoA synthetase or acyl-CoA: cholesterol acyltransferase activity. 22:6 (n-3) had no effect on any of these enzyme activities. From these results, the roles of 20:5 (n-3) and 22:6 (n-3) in the formation of atheromatous lesions and the mechanism of the decrease in cholesterol esterase activity by 20:5 (n-3) were discussed.

Animals↗
PubMed1983

Lipoprotein lipase-catalyzed hydrolysis of phosphatidylcholine of guinea pig very low density lipoproteins and discoidal complexes of phospholipid and apolipoprotein: effect of apolipoprotein C-II on the catalytic mechanism.

To elucidate the mechanism by which apolipoprotein C-II (apoC-II) enhances the activity of lipoprotein lipase (LpL), discoidal phospholipid complexes were prepared with apoC-III and di[(14)C]palmitoyl phosphatidylcholine (DPPC) and containing various amounts of apoC-II. The rate of DPPC hydrolysis catalyzed by purified bovine milk LpL was determined on the isolated complexes. The rate of hydrolysis was optimal at pH 8.0. Analysis of enzyme kinetic data over a range of phospholipid concentrations revealed that the major effect of apoC-II was to increase the maximal velocity (V(max)) some 50-fold with a limited effect on the Michaelis constant (K(m)). V(max) of the apoC-III complex containing no apoC-II was 9.2 nmol/min per mg LpL vs. 482 nmol/min per mg LpL for the complex containing only apoC-II. The effect of apoC-II on enzyme kinetic parameters for LpL-catalyzed hydrolysis of DPPC complexes was compared to that on the parameters for hydrolysis of DPPC and trioleoylglycerol incorporated into guinea pig very low density lipoproteins (VLDL(p)) which lack the equivalent of human apoC-II. Tri[(3)H]oleoylglycerol-labeled VLDL(p) were obtained by perfusion of guinea pig liver with [(3)H]oleic acid. Di[(14)C]palmitoyl phosphatidylcholine was incorporated into the VLDL(p) by incubation of VLDL(p) with sonicated vesicles of di[(14)C]palmitoyl phosphatidylcholine and purified bovine liver phosphatidylcholine exchange protein. The rates of LpL-catalyzed hydrolysis of trioleoylglycerol and DPPC were determined at pH 7.4 and 8.5 in the presence and absence of apoC-II. In the presence of apoC-II, the V(max) for DPPC hydrolysis in guinea pig VLDL(p) increased at both pH 7.4 and pH 8.5 (2.4- and 3.2-fold, respectively); the value of K(m) did not change at either pH (0.23 mm). On the other hand, the kinetic value of K(m) for triacylglycerol hydrolysis in the presence of apoC-II decreased at both pH 7.4 (3.05 vs. 0.54 mm) and pH 8.5 (2.73 vs. 0.62 mm). These kinetic studies suggest that apoC-II enhances phospholipid hydrolysis by LpL in apoC-III-DPPC discoidal complexes and VLDL(p) mainly by increasing the V(max) of the enzyme for the substrates, whereas the activator protein primarily causes a decrease in the apparent K(m) for triacylglycerol hydrolysis.-Shirai, K., T. J. Fitzharris, M. Shinomiya, H. G. Muntz, J. A. K. Harmony, R. L. Jackson and D. M. Quinn. Lipoprotein lipase-catalyzed hydrolysis of phosphatidylcholine of guinea pig very low density lipoproteins and discoidal complexes of phospholipid and apolipoprotein: effect of apolipoprotein C-II on the catalytic mechanism.

Animals↗
PubMed1982

Effect of apolipoproteins on the hepatic lipase-catalyzed hydrolysis of human plasma high density lipoprotein2-triacylglycerols.

The effect of apolipoproteins on the hepatic lipase-catalyzed hydrolysis of high density lipoprotein (HDL) triacylglycerols was studied in an in vitro system consisting of purified human post-heparin hepatic lipase, HDL2 and albumin. The apparent values of the Michaelis constant (Km) and maximal velocity (Vmax) for the hepatic lipase-catalyzed hydrolysis of HDL2-triacylglycerols were 0.18 mM and 86 nmol free fatty acids released/mg hepatic lipase per min, respectively. The addition of purified human plasma apolipoprotein A-I, A-II, E, C-I or C-III2 (containing 2 mol of sialic acid) to HDL2 caused inhibition of hepatic lipase activity. At a 1:1 weight ratio of added apolipoprotein to HDL2-protein, inhibition was 50% for apolipoprotein E and over 75% for the other apolipoproteins tested. Inhibition of enzyme activity occurred with both the unfractionated HDL2 and the HDL which were reisolated by ultracentrifugation. The major alteration in the composition of the reisolated HDL was an increase in the protein to phospholipid ratio. Based on these results, we speculate on the possible role of the apolipoproteins in the metabolism of HDL2 by hepatic lipase.

Apolipoproteins↗
PubMed1982

Lipid metabolism in arteriosclerotic arterial wall of rats.

Arteriosclerotic lesions were formed in rat aorta by the administration of vitamin D2, a high-fat diet and a thyroid suppressing agent. This treatment increased the serum total cholesterol level to 12 times the control level. In the arteriosclerotic lesions that were induced the activities of lysosomal enzymes, such as acid phosphatase and acid lipase, were higher than in controls, that of acid cholesterol esterase was decreased, those of microsomal lipid-synthesizing enzymes--such as acyl-CoA synthetase and cholesterol ester synthesizing activity--were increased and that of neutral cholesterol esterase was decreased. These data suggest that lipid metabolism in arteriosclerotic lesions was changed, resulting in the accumulation of cholesterol esters in the aorta. Administration of high-fat diet and thyroid suppressing agent also increased the serum cholesterol levels to 12-fold the control level, but did not induce arteriosclerotic lesions. After this treatment the activities of hydrolyzing enzymes, such as acid and neutral cholesterol esterase and lipase, in the aorta increased, but the activities of lipid synthesizing enzymes also increased. These data suggest that lipid metabolism in the aorta in this condition changed to compensate for the large influx of serum lipids and to prevent arteriosclerosis. The roles of the serum lipid level, cell injury and lipid metabolism in the aorta in forming arteriosclerotic lesions are discussed on the basis of these results.

Animals↗
PubMed1982

Effect of tocopherol deficiency on lipid metabolism in arterial wall of spontaneously hypertensive rats on normal and high cholesterol diets.

Lipid metabolism in the arterial wall of spontaneously hypertensive rats (SHR) fed on tocopherol-deficient diet, high-cholesterol diet or both was studied. Serum tocopherol was greatly decreased in tocopherol-deficient SHR. Lipoperoxide, determined as thiobarbituric acid-reactive substances, was higher in tocopherol-deficient SHR than in normal SHR. Tocopherol-deficient SHR showed a decrease in acid cholesterol esterase activity, but no change in neutral cholesterol esterase, acid and neutral lipase, acyl CoA synthetase, cytidine-diphosphate choline-1-2-diacyl glycerol choline phosphotransferase (CPT) or triglyceride synthesizing activity.

Animals↗
PubMed1982

Effect of hypertension on lipid metabolism and beta-oxidation in rat aorta and brain microvessels.

The effects of hypertension on various enzyme activities involved in lipid metabolism and beta-oxidation in rat brain microvessels and aorta were studied. The purity of the brain microvessel preparation was confirmed immunologically and microscopically. Activities involved in lipid synthesis, such as triacylglycerol synthesizing activity, acyl-CoA synthesizing activity, acyl-CoA: cholesterol acyltransferase and cytidine diphosphate choline:1,2-diacylglycerol cholinephosphotransferase, were significantly higher in brain microvessels than in aorta in both normotensive and hypertensive rats; lipid hydrolyzing activities, such as lipases and cholesterol esterases, were similar in the two preparations. beta-oxidation in brain microvessels was more active than in aorta in both groups. Hypertension did not alter these enzyme activities in either aorta or brain microvessels, or change beta-oxidation in the aorta. However beta-oxidation in brain microvessels was significantly lower in hypertensive rats than in normotensive rats. These results suggest that brain microvessels are metabolically more active than aorta, and that their beta-oxidation activity is more susceptible to effects of hypertension. Reduced beta-oxidation in brain microvessels might lead to angionecrosis by derangement of energy production, which in turn may cause cerebral bleeding.

Animals↗
PubMed1982

Lipid metabolism in the aorta and the brain microvessels of rabbits on high cholesterol diet.

The characteristics and properties of lipid metabolism in the aorta and the brain microvessels of rabbits were investigated to clarify the role of lipid metabolism in formation of atherosclerosis. In rabbit aorta, cholesterol esterase and lipase each had an acidic and a neutral optimum pH, whereas acyl-CoA synthetase, acyl-CoA: cholesterol acyltransferase, triglyceride synthesizing activity and choline phosphotransferase each had one neutral optimum pH. These pH optima were similar to those in rats. High cholesterol diet induced atheromatous lesions in the aorta, but not in the brain microvessels. In atheromatous aorta, the acid lipase and acid phosphatase activities were higher than in controls, but not the acid cholesterol esterase activity. Moreover the activities of neutral lipase, acyl-CoA synthetase, acyl-CoA:cholesterol acyltransferase, triglyceride synthesis and choline phosphotransferase were increased, but neutral cholesterol esterase activity was normal. These data suggest that lipis metabolism in the atheromatous aorta is changed in a manner favoring accumulation of lipids, especially cholesterol esters. In controls, most of the above enzyme activities in the brain microvessels were higher than those in the aorta. However, these enzyme activities in the brain microvessels were not changed by cholesterol feeding. Thus it is suggested that the properties of lipid metabolism in the aorta and brain microvessels, including permeability of lipoproteins into the vessel walls, are important in formation of atherosclerosis in addition to the serum factors.

Animals↗
PubMed1980

Electron-microscopic observation of adrenergic innervation in guinea pig Eustachian tube.

The precise locations of adrenergic nerve terminals in the Eustachian tube of guinea pigs have, for the first time, been demonstrated by electron microscopy, with application of a false transmitter (5-OHDA). Adrenergic nerve terminals were found in abundance near the arteries in each area of the Eustachian tube. In particular, these terminals were observed just beneath the smooth muscle layer of the arteries. The exact locations of adrenergic nerve terminals in the submucous and gland region are also discussed.

Adrenergic Fibers↗
PubMed1980

Effect of pantethine on cholesterol ester metabolism in rat arterial wall.

The total serum cholesterol level in rats fed on a high cholesterol diet (HCD) for 16 weeks was markedly higher than that in rats fed on a normal diet (ND), but pantethine reduced the increased level in rats fed on HCD (P less than 0.05). Acid cholesterol esterase activity (acid CEase) of arterial wall homogenates from rats fed on HCD was significantly lower than that of rats fed on ND (P less than 0.005). Acid CEase activity in the arterial wall of rats fed on HCD for 8 weeks and then ND for 8 weeks was less than that of rats fed on ND for 16 weeks. Acid CEase activity in the arterial wall was increased in rats fed on pantethine-containing diet. The ratio of cholesterol ester synthesizing activity to neutral cholesterol esterase (neutral CEase) activity was higher in rats fed on NCD than in those fed on ND. The ratio was lower in rats on the pantethine-containing diet than in those on NCD. The relationship between hypercholesterolemia and lipid metabolism in the arterial wall and effects of pantethine are discussed on the basis of these results.

Alanine Transaminase↗