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Biomedical subjects

T Tamai

Publications and source records attributed to T Tamai.

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

Aged↗
PubMed1981

The effects of glibenclamide and insulin on plasma high density lipoprotein in diabetics.

The purpose of the present study was to investigate the effects of various types of treatment such as glibenclamide and insulin on plasma lipids and lipoprotein concentration in diabetics. Treatment of diabetes mellitus was reevaluated from the standpoint of high density lipoprotein (HDL) metabolism. Twenty-one diabetic patients (6 men and 15 women) who have been admitted in the hospital and kept on Japanese standard diet for diabetes mellitus, have been studied. Changes of plasma lipoprotein in diabetic patients were followed up before and after treatment with glibenclamide or insulin. Very low density lipoprotein (VLDL) and low density lipoprotein (LDL) were decreased and HDL was increased with insulin treatment. However, glibenclamide induced a significant decrease in HDL- cholesterol (Ch). Relationship between triglyceride (TG)-rich lipoproteins and HDL metabolism was studied. A significant negative correlation was found between pretreatment VLDL-TG and changes of VLDL-TG with insulin treatment, indicating an accelerated catabolism of VLDL-TG with possible increase of triglyceride lipases. There was a significant negative correlation between VLDL-TG and HDL-Ch before insulin treatment, but not after treatment. There was no negative correlation between changes of VLDL-TG and changes of HDL-Ch with insulin therapy. These results indicate that an increment of HDL with insulin treatment can not be explained solely by increased HDL formation from TG-rich lipoprotein and that insulin might increase synthesis and secretion of HDL in liver and/or intestine.

Cholesterol↗
PubMed1981

Plasma lipids and lipoproteins of Japanese adults and umbilical cord blood.

By means of sequential ultracentrifugation of plasma from 85 control healthy Japanese subjects and from 15 maternal infant pairs, very low density lipoprotein (VLDL: d less than 1.006 g/ml), low density lipoprotein (LDL: 1.006 less than d less than 1.063 g/ml) and high density lipoprotein (HDL: d greater than 1.063 g/ml) were obtained and analyzed for cholesterol (Ch), triglyceride (TG), phospholipid (PL) and apolipoprotein B (Apo B). These results were compared to values in Western countries reported in the literature. HDL-Ch/LDL-Ch of adult Japanese was much higher than that of subjects in Western countries, especially in males. Umbilical cord (U) plasma-Ch, TG, PL and Apo B were 73.3 +/- 15.9, 51.0 +/- 10.4, 110.0 +/- 21.0 and 47.6 +/- 15.7 (mean +/- S.D.) mg/100 ml, respectively. In cord blood the concentrations of Ch, TG and PL in all lipoprotein density classes were less than one half of those in normal adults. Cord blood has higher levels of HDL-Ch and lower levels of LDL-Ch than normal adults. Therefore, HDL-Ch/LDL-Ch ratio in cord blood (1.58 +/- 0.32 was far higher than the ratio in normal adults (0.50 +/- 0.11). In cord blood, HDL was the predominant Ch, TG and PL carrying lipoprotein. HDL-Ch/LDL-Ch ratios were 1.58 in Japan, 1.14 in USA, 0.89 in Australia and 0.69 in GDR. HDL-Ch/LDL-Ch ratio in Japanese cord blood was the highest among the values reported in the literature. The relationships between maternal and infant lipoproteins were more significant in HDL than in VLDL or LDL. The positive correlation between maternal HDL and infant HDL may suggest the possibility of placental transfer of intact HDL particles.

Adolescent↗
PubMed1981

Hypertensive effects on pregnancy in spontaneously hypertensive rats (SHR) and stroke-prone SHR (SHRSP).

We studied the hypertensive effects on mothers and newborns in Wister Kyoto rats (WKY), spontaneously hypertensive rats (SHR), and stroke-prone SHR (SHRSP). The average blood pressure of pregnant rats in WKY, SHR, and SHRSP was 100, 180, and 210 mmHg, respectively. The average adult female weight and weight gain during pregnancy were inversely proportional to the increase of hypertension. The rate of delivery, reproduction, litter size and their weight were lowest in the SHRSP.

Animals↗
PubMed1979

The effects of streptozotocin diabetes on hepatic triglyceride lipase activity in the rat.

The function of the hepatic triglyceride lipase (H-TGL) is not yet clear. The purpose of the present study was to investigate the possible hormonal regulation of H-TGL. Postheparin plasma was obtained 3 min after the intravenous injection of 50 U/250 g body weight of heparin into male Wistar rats. The lipase activities were measured using substrate containing [14C] triolein emulsified with gum arabic and were expressed in mumoles of free fatty acid released/ml/hour (mean +/- SD). H-TGL was the lipase activity remaining after inhibition of lipoprotein lipase (LPL) by 1.0 M NaCl. Diabetic rats were prepared by intravenous injection of streptozotocin (STZ), 65 mg/kg body weight. The contributions of H-TGL and LPL to the total plasma triacylglycerol hydrolase (TGH) activity depend on the amount of heparin injected and the time of blood withdrawal after heparin injection. H-TGL was maximally released at higher heparin (50 U/250 g body weight) concentrations, compared to LPL which was maximally released at lower heparin (5 U/250 g body weight) concentrations. H-TGL was significantly higher at 3 min after the injection of 50 U of heparin/250 g body weight than at 20 min. Twenty-four-hour fasting produced a significant fall in H-TGL compared to H-TGL in fed rats. Total TGH was significantly lower in diabetic rats 3 days after STZ injection. In diabetic rats 3, 5, and 7 days after STZ injection, H-TGL were significantly lower than those in control rats. H-TGL and H-TGL/total TGH were 9.49 +/- 0.99 and 0.551 +/- 0.071, respectively, in rats 3 days after STZ injection, compared to H-TGL (13.46 +/- 0.69) and H-TGL/total TGH (0.739 +/- 0.052) in control nondiabetic rats. When diabetic rats were treated with insulin, total TGH (14.37 +/- 3.01) and H-TGL (6.77 +/- 4.12) rose to 25.16 +/- 1.02 (total TGH) and 16.49 +/- 1.13 (H-TGL), that were comparable to activities in control nondiabetic rats. Separation of H-TGL and LPL was performed using heparin-Sepharose affinity chromatography of postheparin plasma. The enzyme activity of peak I from STZ rats, which is eluted by 0.72 M NaCl-Veronal buffer, pH 7.4 and corresponds to H-TGL, was approximately half the activity from control rats. TGH released by heparin from isolated rat liver parenchymal cells was investigated. The enzyme activites released from isolated liver parenchymal cells prepared from STZ rats was approximately half that from control rats. The role of insulin in the regulation of LPL has been well documented. Our findings suggest that H-TGL also is under hormonal regulation by insulin in rats.

Animals↗