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Biomedical subjects

H Mabuchi

Publications and source records attributed to H Mabuchi.

At least 253 records · Page 14Linked to original sources
PubMed1982

Lecithin: cholesterol acyl transfer rate in hypothyroidism and hyperthyroidism.

The initial rate of lecithin: cholesterol acyl transferase and serum concentration of lipids were determined in euthyroid, hypothyroid and hyperthyroid subjects. In hyperthyroid subjects, the serum levels of total and free cholesterol were significantly lower than in normal subjects and the fractional lecithin: cholesterol acyl transfer rate was significantly higher than in normal subjects. The molar lecithin: cholesterol acyl transfer rate was also higher than in normal subjects, but not significantly. The free cholesterol/total cholesterol ratio in hypothyroid females and the serum levels of triglyceride and free fatty acid in hypothyroid male were significantly higher than in normal subjects. The fractional lecithin: cholesterol acyl transfer rates in hypothyroid females were significantly lower than in normal females. After treatment of the thyroid disease the fractional and molar lecithin: cholestorol cholesterol acyl transfer rate approached the normal values. There was a positive correlation between fractional and molar lecithin: cholesterol acyl transfer rate and thyroxine. These results suggest that thyroid hormone influences the cholesterol esterification through the activation of lecithin: cholesterol acyltransferase.

Adult↗
PubMed1982

The incidence and pathogenesis of hyperlipidaemia in 16 consecutive acromegalic patients.

Serum lipids were analyzed in 16 patients with active acromegaly. Of these 62.5% had hyperlipidaemia defined as exceeding and 90% fiducial limits of normal controls. The mean serum cholesterol (5.50 mmol/l) and triglyceride (4.09 mmol/l) levels of the patients were significantly higher than those of age-matched normal controls. Type V hyperlipoproteinaemia was observed in two cases and type III hyperlipoproteinaemia in one. There was no difference in the incidence of diabetes between the normolipidaemic (n = 6) and hyperlipidaemic (n = 10) groups. Serum levels of growth hormone in hypercholestelaemic patients (n = 3) were significantly higher than those of normolipidaemic patients and combined hyperlipidaemic patients (n = 5 tended to have higher levels of growth hormone than normolipidaemic patients. In cases developing type III or type V hyperlipoproteinaemia, the activity of hepatic triglyceride lipase of lipoprotien lipase was decreased, but in increased when serum GH levels fell after therapy for acromegaly. It is suggested that 1) growth hormone may play some role on the pathogenesis of hyperlipidaemia associated with acromegaly, and 2) growth hormone has an inhibitory effect on H-TGL and LPL, and so hyperlipoproteinaemia in some cases of acromegaly might be caused by low H-TGL or LPL activity resulting from high growth hormone levels.

Acromegaly↗
PubMed1982

Secondary type V hyperlipoproteinemia in an acromegalic patient without overt diabetes.

A rare case of acromegaly developing gross hyperlipidemia not associated with overt diabetes was presented. Gross hyperlipidemia revealed type V hyperlipoproteininemia, according to agarose gel electrophoretic pattern of serum lipoprotein. Before pituitary surgery, the serum levels of cholesterol and triglyceride were 320 mg/dl and 1830 mg/dl respectively, and the basal level of growth hormone was markedly elevated, ranging from 129 to 231 ng/ml with the mean +/- SD of 168 +/- 39 ng/ml. The enzymatic activities of hepatic triglyceride lipase (H-TGL) and lipoprotein lipase (LPL) were 14.2 and 1.50 mumoles/ml/hour, respectively. H-TGL activity was normal, while LPL activity was extremely low compared to those of normal subjects. After combined therapy with pituitary surgery and 60Co radiation, the serum level of growth hormone was decreased to 35.9 +/- 8.6 ng/ml in the mean +/- SD, but not normalized. However, the serum level of triglyceride was decreased and both H-TGL and LPL activities were increased to 19.3 and 2.7 mumoles/ml/hour, respectively. LPL activity was increased 79% compared to the level of pretreatment. Agarose gel electrophoretic pattern of lipoprotein changed from type V to type IV and ultracentrifugal analysis showed that very low density lipoprotein (VLDL)-cholesterol was decreased and intermediate density lipoprotein (IDL)-cholesterol, low density lipoprotein (LDL)-cholesterol and high density lipoprotein (HDL)-cholesterol were increased.

Acromegaly↗
PubMed1981

Systematic separation of medium-sized biologically active peptides by high-performance liquid chromatography.

The systematic separation of medium-sized biologically active peptides by high-performance liquid chromatography (HPLC) is described. Three steps are involved: first, high-performance sodium dodecyl sulphate (SDS) gel chromatography on a newly developed column. TSK-GEL 2000SW; secondly, ion-pair reversed-phase HPLC using stepwise elution mobile phases containing SDS and tetrabutylammonium phosphate; thirdly, high-performance cation-exchange chromatography on a Partisil SCX column for purification, using stepwise gradient elution with volatile buffers. Removal of SDS was possible in the final step. This systematic method is fast, reproducible and gives excellent separations and recoveries.

Body Fluids↗
PubMed1981

Effects of an inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A reductase on serum lipoproteins and ubiquinone-10-levels in patients with familial hypercholesterolemia.

We studied the effects of ML-236B, a competitive inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, on serum levels of lipoproteins and ubiquinone-10-in seven heterozygous patients with familial hypercholesterolemia. ML-236B was given at doses of 30 to 60 mg per day for 24 weeks. Serum cholesterol decreased from 390 +/- 9 to 303 +/- 8 mg per deciliter (101 +/- 0.2 to 7.88 +/- 0.2 mmol per liter, mean +/- S.E.M.; p less than 0.001) and serum triglyceride decreased from 137 +/- 18 to 87 +/- 9 mg per deciliter (1.55 +/- 0.20 to 0.98 +/- 0.01 mmol per liter; p less than 0.05). Intermediate-density-lipoprotein (DL) cholesterol, IDL triglyceride, low-density-lipoprotein (LDL) cholesterol, and LDL triglyceride decreased significantly (p less than 0.01, P less than 0.001, and P less than 0.001, respectively). However, there were no significant changes in very-low-density-lipoprotein (VLDL) cholesterol and triglyceride or high-density-lipoprotein (HDL) cholesterol. Serum ubiquinone-10 levels did not change, and LDL levels of ubiquinone-10 decreased by 50 per cent, from 0.39 +/- 0.07 to 0.20 +/- 0.01 microgram per milliliter (P less than 0.05). No adverse effects were observed. We conclude that ML-236B is effective in lowering serum cholesterol without lowering serum ubiquinone-10 in heterozygous patients with familial hypercholesterolemia.

Adult↗
PubMed1981

Intermediate-density lipoprotein and cholesterol-rich very low density lipoprotein in angiographically determined coronary artery disease.

The relationship between the concentrations of intermediate-density lipoprotein (IDL) and other lipoproteins and the extent of coronary artery disease (CAD) was studied in 182 consecutive patients evaluated by selective coronary cineangiography. On univariate analysis, the extent of CAD correlated significantly and positively with very low density lipoprotein (VLDL) cholesterol, IDL cholesterol and low-density lipoprotein (LDL) cholesterol, and negatively with high-density lipoprotein (HDL) cholesterol. Analysis of four subgroups divided by IDL cholesterol and LDL cholesterol levels indicated that moderately increased levels of IDL cholesterol were closely associated with a high frequency of CAD. Moreover, multi-variate regression analysis demonstrated that IDL cholesterol for men, LDL cholesterol for men and women and HDL cholesterol for men were significant variables of use in the final weighting procedure. IDL cholesterol was closely associated with cholesterol-rich VLDL. This study shows that IDL and cholesterol-rich VLDL combine to contribute to the development of CAD.

Adult↗
PubMed1981

Effects of ML-236b (compactin) on sterol synthesis and low density lipoprotein receptor activities in fibroblasts of patients with homozygous familial hypercholesterolemia.

We studied biochemical genetics of low density lipoprotein (LDL) receptor mutations in fibroblasts from six homozygous and five heterozygous patients with familial hypercholesterolemia (FH). Three of six homozygotes are receptor-negative type and the other three homozygotes are receptor-defective type. In the cells from three receptor-negative homozygotes, the receptor binding, internalization, and degradation of (125)I-LDL were 0.5+/-0.3 ng/mg protein (mean+/-SEM), 14+/-8 and 8+/-6 ng/mg protein per 6 h (four normal cells; 44+/-3, 386+/-32, and 1,335+/-214 ng/mg protein per 6 h), respectively. In the cells from three receptor-defective homozygotes, the receptor binding, internalization, and degradation of (125)I-LDL were 6+/-2, 29+/-8, and 90+/-32 ng/mg protein per 6 h, respectively. In these six homozygotes, two pairs of siblings are included. Two siblings in the same family were classified as receptor-negative and two siblings in another family were classified as receptor-defective. The receptor-negative phenotypes and the receptor-defective phenotypes bred true in individual families. The cells from five heterozygotes showed approximately 46% of the normal activities of receptor.ML-236B, competitive inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMG-CoA reductase), completely inhibited the incorporation of [(14)C]acetate into digitonin-precipitable sterols in fibroblasts from normal subjects and heterozygous and homozygous patients with FH with the concentration of 0.5 mug/ml. However, at 0.05 mug/ml of ML-236B sterol synthesis in fibroblasts from homozygotes was not completely suppressed in contrast to normal and heterozygous cells. Moreover, after preincubation with 0.05 mug/ml of ML-236B for 24 h in medium containing lipoproteins, sterol synthesis in the cells from receptor-negative homozygote showed 75% of the initial activity compared with that of 25% without preincubation. In the cells from a normal subject and a heterozygote, sterol synthesis was inhibited even after preincubation. These results suggest that (a) the inhibitory effect of ML-236B is overcome in homozygote cells by their high intracellular levels of HMG-CoA reductase and (b) that a higher dose of ML-236B may be required to lower serum cholesterol levels in FH homozygotes than in heterozygotes.

Anticholesteremic Agents↗