The HDL-cholesterol (HDL-Ch) concentration of 153 cerebrocascular patients within 1 year from onset and 257 controls were determined in the supernatant of serum in heparin-Ca⁺⁺ precipitation method. In some patients, serum HDL-phospholipid (HDL-PL) concentrations were also determined. Liver function tests (GOT, GPT, TTT, ZST) were normal in all of these subjects, and control subjects had no adnormalities in physical findings, blood pressure, ECG, urinalysis etc.
The average values in male and female controls were 65±20.9mg/dl and 65±22.3mg/dl, respectively. The value of female subjects over 55 years of age was lower than those of age-matched male and female under 54. There was no significant change by age in values of male control. In male patients with cerebral infarction, average HDL-Ch value was 55±18.6mg/dl and it was significantly lower than the control value. The value of female patients was 62±15.0mg/dl. In female, there was no significant difference between patients and control. Among the patients with cerebral infarction, the cases with angiographically demonstrated obstruction of internal carotid or middle cerebral arteries showed lower value as compared to those without such findings. In male and female patients with cerebral hemorrhage, average HDL-Ch concentrations were 55±13.3mg/dl and 60±16.8mg/dl respectively. Again only the value of male patients was significantly lower than that of control.
Considering the importance of balance between atherogenic and anti-atherogenic properties of cholesterol in various lipoprotein fractions, HDL-cholesterol/total cholesterol (HDL-Ch/TC) ratio was calculated in each subjects. The average values of this ratio in healthy men and women were 0.37±0.13 and 0.37±0.14, respectively. The value of male patients with cerebral infarction was 0.30±0.10, it was significantly lower than the control value. The values of female patients with cerebral infarction, male and female patients with cerebral hemorrhage were 0.33±0.09, 0.35±0.10 and 0.35±0.11, respectively. These values exhibited no significant difference when compared with each controls. From these results, it was recognized that at a given concentration of serum total cholesterol, male patients with cerebral infarction had relatively less cholesterol in their HDL fraction as compared to healthy subjects.
Serum HDL-PL concentrations in male patients either with cerebral infarction or cerebral hemorrhage, were significantly lower than the control value. The difference between female patients and control was insignificant.
These results may suggest the importance of HDL-Ch for the development of cerebral atherosclerosis and subsequent cerebral infarction at least in man.

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Modifying a heparin-Ca⁺⁺ precipitation method described by Noma et al., a rapid method for the enzymatic determination of high-density (HDL), low-density (LDL), and very low-density (VLDL) lipoprotein cholesterol was established.
HDL-cholesterol: A mixture of 0.1ml serum and 4.0ml Reagent I containing heparin (100-150mg/L) and CaCl₂ (35mM) was filtered through a Millipore filter, on which VLDL and LDL were retained. The retained fraction was suspended with Triton X-100 solution followed by enzymatic determination of cholesterol. By subtracting the cholesterol content of this fraction from serum one, HDL-cholesterol (total and free) were measured.
LDL-cholesterol: To a mixture of 0.2ml serum and 4.0ml Reagent II containing heparin (100-150mg/L) and NaCl (4g/L), 0.5g of Amberlite IRA-400 was added. The supernate containing HDL and LDL was diluted with four volumes of Reagent III. The final concentration of heparin and CaCl₂ in this solution become 100-150mg/L and 30mM respectively and the insoluble complex of LDL was formed. This complex was filtered through a Millipore filter and LDL-cholesterol was measured.
The determination of VLDL-, LDL- and HDL-cholesterol by the present method showed that the male patients with cerebral infarcts had the significantly lower levels of HDL-cholesterol than the male healthy subjects.

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Serum lipoprotein fractionations by the ultracentrifugation method were performed in 18 cases (cerebral thrombosis=CT 8 cases, cerebral haemorrhage=CH 10 cases) with CVD within a week from stroke, and 18 cases (CT 12 cases, CH 6 cases) with CVD two months or more after stroke and 34 healthy persons.
Cholesterol, triglyceride and binding hexose were measured in each lipoprotein fraction, and gel column chromatography of each lipoprotein fraction was performed.
I. VLDL fraction
1) There are no difference in each component between fresh stage and old stage in CT or CH.
2) Though lipids and binding hexose are not high in CT, these are high generally in CH.
3) The lipids in each fraction are higher in CH than these in CT but there is no difference in binding hexose between CT and CH.
4) VLDL fraction was separated into three fractions or more by sephadex G-100 column chromatography.
II. LDL fraction
1) Though there are no differences in CT between fresh stage and old stage in lipids of each fraction, binding hexose is higher in old stage than that in fresh stage. In CH cholesterol is higher in fresh stage than that in old stage but significant differences are not found in other components.
2) Cholesterol in CT is higher than that healthy persons but triglyceride is lower. Though cholesterol in CH is lower in old stage, there are no differences in fresh stage. Binding hexose in CT or CH is low in fresh stage but in old stage binding hexose is high only in CH.
3) Cholesterol is higher in CT than that in CH but no differences are found in other components.
4) LDL fraction shows a single paek as lipid sugar complex by sephadex G-100 column chromatography.
III. HDL fraction
1) In CT, cholesterol and binding hexose are higher in fresh stage than these in old stage. In CH, cholesterol is lower in old stage than that in fresh stage but triglyceride is higher in fresh stage.
2) Cholesterol in fresh stage does not show a significant difference between healthy persons and CT or CH, but triglyceride shows low tendency. In CT, lipids are low in old stage. In CT, cholesterol is low in old stage but triglyceride high. Binding hexose in CVD is high generally in both stages.
3) Triglyceride in old stage is lower in CT than that in CH but there are no differences in other components.
4) HDL fraction was separated into two fractions or more by sephadex G-100 column chromatography.
IV. In CT, triglyceride in each lipoprotein fraction is low generally but in CH high.
V. There are differences pathogenetically between CT and CH from viewpoint of ultracentrifugal fractionation about serum lipoprotein.

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In order to study the role of HDL in the pathogenesis of stroke, serum lipids and lipoprotein were determined in male and female patients aged above 55 within 30min after the onset of stroke.
The results were compared with those obtained in an age-adjusted healthy control group and coronary heart disease (CHD) group, randomly selected from the population of an old-aged institution.
While serum total cholesterol and phospholipid concentrations were almost equal among these three groups, serum HDL-cholesterol of patients with stroke were lower than these in the control group as well as in CHD group.
On the other hand, serum HDL-phospholipid were in the middle of the control group and CHD group.
However, phospholipid components in the HDL fraction measured by Thinchrograph TFG 10 type were slightly different.
Results of this study suggest that a reduction of serum HDL-cholesterol and HDL-phospholipid concentration may be playing a role in the development of stroke.

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The present investigation was undertaken to clarify a clinical significance of serum high density lipoprotein cholesterol (HDL-cholesterol) in diabetes mellitus. Serum HDL-cholesterol was determined in 100 healthy subjects and 137 diabetic patients according to the method of NIH using heparin-Mn⁺⁺. Serum HDL-cholesterol levels in diabetics were significantly lower than those in healthy subjects. In diabetic groups, no significant correlation was found between HDL-cholesterol and FBS or the duration of the disease. Serum HDL-cholesterol levels in diabetics complicated with hypertension, albuminuria and/or abnormal ECG findings were lower than those in diabetics without these complication. Furthermore, there was a reverse relationship between the degree of diabetic retinopathy and serum HDL-cholesterol level.
Our results indicate that determination of serum HDL-cholesterol may be a useful tool to estimate the degree of diabetic angiopathy.

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Many reports have showed a negative relationship between serum HDL cholesterol (ch) level and ischemic heart disease. We studied the effect of Simfibrate on the serum HDL-ch, LDL-ch and total-ch levels in the patients. Simfibrate, 1g per day, was administered for 3 months in the 15 patients.
Total-ch and Triglyceride was 223.2±246.5mg/dl, 143.7±44.3mg/dl respectively before Simfibrate and decreased to 200.8±65.3mg/dl and 116.7±44.3mg/dl respectively one month after administration. HDL-ch below 50mg/dl increased from 44.3mg/dl to 50.5mg/dl at 2 month and HDL-ch above 50mg/dl did not change. LDL-ch decreased significantly and the changes of LDL-ch was correlated with the changes of total-ch. The fraction of lipoprotein showed increase of α/β.
It was suspected that Simfibrate increased low HDL-ch and decreased LDL-ch and may influence the prognosis of atherosclerosis.

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1. In in vitro experiments, low molecular weight dextran (10w/v%)(LMD) inhibited ADP-, noradrenaline- and collagen-induced human platelet aggregation. The inhibition was particularly marked for collagen-induced aggregation.
2. Administration of 250ml or 500ml of LMD with sodium lactate to normal individuals significantly inhibited platelet aggregation when determined by the screen filtration pressure method.
3. LMD exhibited significant effect to maintain red blood cell deformation ability under exaggerated conditions in vitro. Administration of 250ml or 500ml of LMD with sodium lactate tended also to increase the deformation ability in humans.
4. LMD dose-dependently inhibited release of platelet factor 3 from the platelet.
5. Use of LMD with sodium lactate in 250ml or 500ml produced no appreciable changes in clinical laboratory tests, though plasma triglyceride and cholesterol definitely decreased.

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On 42 hyperlipidemic out-patients aged 33-69 years, the effects of dietary treatment for five weeks to serum lipoprotein were studied. Two types of diet were designed. Subjects with type IIA were kept on diet low in fat (20% of total carolies) and cholesterol (150mg daily) and high polyunsaturated/saturated (P/S) ratio (3.0). Subjects with type IIB, type III and type IV were given a low carbohydrate diet (40% of carolies) and the same content of cholesterol and P/S ratio.
Three lipoprotein classes were determined with lipoprotein electrophoresis using an internal standard (dyed carbamylated albumin). The diet caused significant reductions on mean levels of α-lipoprotein (8%↓, p<0.05) and β-lipoprotein (10%↓, p<0.05) in type IIA, α-lipoprotein (7%↓, p<0.05), pre β-lipoprotein (35%↓, p<0.01) and β-lipoprotein (14%↓, p<0.01) in type IIB and pre, β-lipoprotein (47%↓, p<0.001) in type IV.
A few cases of type IIA changed into other phenotypes, but type IIB and type IV changed more frequently into other phenotypes.
Of these, 9 hyperlipidemic patients (21%) were normalized in the lipid levels.

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It has been reported that the incidence of ischemic heart disease in Japan is much lower than that in Western countries. Contribution of genetic or environmental factors to this difference has not been established. The close association between premature atherosclerosis and increased concentrations of low density lipoprotein (LDL) or decreased concentrations of high density lipoprotein (HDL) has been indicated. By means of sequential ultracentrifugation of plasma from Japanese 15 maternal infant pairs, very low density lipoprotein (VLDL d<1.006g/ml), LDL (1.006<d<1.063g/ml) and HDL (d<1.063g/ml) were obtained and analysed 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.
Umbilical cord (U) plasma-Ch, TG, PL and Apo B were 73±16, 51±10, 110±21 and 48±16 (mean±S.D.) mg/100ml, 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 or mothers and HDL, was the predominant Ch, TG and PL carrying lipoprotein. Cord blood have 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 higher than the ratio in normal adults (0.50±0.11) and cord blood had relatively more antiatherogenic lipoprotein than adults.
Japanese cord blood contained higher levels of HDL-Ch and lower levels of LDL-Ch than those in Sweden, U.S.A. and Australia. HDL-Ch/LDL-Ch ratio were 1.58 in Japan, 1.14 in U.S.A., 0.89 in Australia and 0.69 in G.D.R. HDL-Ch/LDL-Ch ratio in Japanese cord blood was the highest in 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 indicate the possibility of placental transfer of intact HDL particle.

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Familial dyslipoproteinemias were reviewed from the viewpoint of six-step metabolism of human serum lipoproteins proposed for comprehension of various aspects of complicated serum lipoprotein metabolism. The six steps of lipoprotein metabolism consists of (i) synthesis of triglyceride-rich lipoproteins in digestive organs, (ii) conversion of triglyceride-rich lipoproteins to intermediate lipoproteins (IDL) through hydrolysis of triglycerides, (iii) transformation of IDL to LDL by hydrolysis of the remaining triglycerides, (iv) catabolism of LDL and release of cholesterol by LDL pathway in peripheral cells, (v) removal and esterification of cholesterol from cell membrane by HDL and LCAT, and (vi) catabolism of HDL in the liver lysosome and the excretion of cholesterol into the bile. The first three steps of these metabolic processes are related to the energy metabolism of the human body, while the last three to the structural metabolism of tisrues and organs.
In reviewing familial dyslipoproteinemias, abetalipoproteinemia, C-II deficiency, LPL deficiency, and Type IV and V hypertriglyceridemia have common characteristics of accumulation of triglycerides in parenchymal cells of organs, while broad beta disease, Type II hyperlipidemia, LCAT deficiency and HDL deficiency cause accumulation of esterified cholesterol in the scavenger cells of arteries, skin, and the other peripheral tissues.
The six-step theory of human serum lipoproteins, thus, shed a new light on understanding the relationship between serum lipoprotein and tissue reaction, and enables to provide a tool for an integrated approach toward the role of human lipoproteins in whole-body metabolism.

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1) We examined sterol synthesis from [¹⁴C] acetate in cultured human fibroblasts. Cultured fibroblasts were derived from skin biopsy samples of normal subjects and a patient with the heterozygous familiar hypercholesterolemia (FHC). Cells were grown in dishes containing 15% fetal calf serum. On day 4, the medium was replaced with 3ml of fresh medium containing 10% human lipoprotein deficient serum (LPDS). 24hr later, LDL was added to obtain an appropriate concentratin of cholesterol. In the presence of LPDS heterozygous FHC fibroblasts synthsized cholesterol from acetate at a rate nearly 3 times greater than that of control cells.
In addition the heterozygous FHC fibroblasts showed low response to alterations in the LDL content of medium.
2) Scanning electron microscopid (SEM) abnormalities are not being reported yet in fibroblasts expressing lipid metabolic defects.
We have studied the SEM appearance of cultured fibroblasts in monolayer during in the logaristhmic phase of growth.
In normal fibroblasts incubated with medium containing 10% LPDS and LDL at a concentration coresponding to 500μg/ml of the cholesterol, numerous microvilli on the surface of the cell and a lot of long slender processes from the cell body could be distinguished.
In normal fibroblasts incubated with LPDS, there were a marked decrease in the number of microvilli and long processes, and numerous small pit-holes appeared on the cell surface, suggestig demage of plasma membrane structure. Meanwhile in the heterozygous FEC cells, morphological changes in plasma membrane structure induced by LPDS incubation were slight. These data suggest that LDL is vital to keep plasma membrane structure of fibroblasts.
3) The following study was done in order to clarify the localization of LDL receptors on plasma membrane of human fibroblasts.
Monolayers of fibroblasts were incubated with growth medium containing 10% LPDS and LDL. Each monolayer was washed with PBS buffer and fibroblasts were incubated with T-4 bacteriophages-LDL antiserum 2hr at 37°C. Numerous T-4 bacteriophages were localized by SEM on normal fibroblasts plasma emmbrane, while few T-4 bacteriophages were observed to bind to the cell membrane in the heterozygous FHC cells.

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Clinical studies, measurement of postheparin lipolytic activity and the analysis of apolipoproteins were performed in patients with hyperchylomicronemia and those with retention of remnants in plasma.
Four patients with hyperchylomicronemia showed a deficiency in lipoprotein lipase (LPL) activity. One of them belonged to a classical form of LPL deficiency. Two other patients, brother and sister, also showed a marked deficiency in LPL activity. However, the addition of normal plasma resulted in a complete recovery of the lipolytic activity and the analysis of chylomicron and VLDL apoproteins showed a deficiency in apo CII. Analysis of apoproteins of the parents showed that apo CII was reduced to approximately half the normal control, suggesting that the parents were heterozygotes (Yamamura, T. et al.: Atherosclerosis in press). The other patient showed a marked decrease both in LPL and hepatic triglyceride lipase (H-TGL) activities and the retention of the remnant was also observed on lipoprotein electrophoresis. Three of his children were normolipidemic, but two of them showed a deficiency in LPL with a normal or increased activity of H-TGL.
Among ten patients with broad x band on PAG disc electrophoresis of lipoproteins, only three fell under a category of Type III hyperlipoproteinemia as defined by chemical indices and clinical symptoms proposed by Fredrickson and Hazzard. A 50-year-old male had a marked hyperlipemia of Type V, but the pattern was changed into broad B type ly dietary fat restriction. One of his daughter died of pancreatitis with hyperchylomicronemia. Another daughter was usually normolipidemic, while a small amount of the remnant was detected on electrophoresis of lipoproteins, and hyperlipidemia was induced by high fat diet. Both of these daughters had xeroderma pigmentosum.
Most of the patients with broad B band showed a decrease in H-TGL activity and the injection of heparin could not succeed in reducing the amount of the remnant. Disturbances in the H-TGL-mediated removal mechanism of the remnant was suggested.

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Plasma lipids and lipoproteins, glucose tolerance and insulin secretory function were examined in 81 relatives of 12 index cases with type IV hyperlipidemia, hyperinsulinemia and fatty liver as well as in 90 nonrelatives, including the spouses, as controls. Hyperinsulinemia mostly coupled with type IV or type IIb hyperlipidemia and abnormal liver function suggesting fatty liver was shown to exist in 37% of the relatives. Thus, hyperinsulinemia might be the basic trait of this form of familial hyperlipidemia, although the mode of transmission remains to be elucidated.
The electronmicroscopic morphometry was performed on the biopsied liver specimens from the hyperinsulinemic and hyperlipidemic patients. In the hepatocyte, the membrane-bound ribosomes in rough endoplasmic reticulum, which are known to produce secretory proteins, were significantly increased in the patients. Number of VLDL particles in the hepatocyte Golgi complexes was also increased significantly. A highly significant positive correlation was found between the density of the membrane-bound ribosomes and the number of VLDL per hepatocyte, suggesting that the production and secretion of VLDL in the hyperinsulinemic patients might be accelerated in relation to the increased VLDL-apoprotein synthesis. Therefore, hyperinsulinemia could be the causative factor of this form of type IV hyperlipidemia.
A glycoside-hydrolase inhibitor (Bay g 5421-Bayer AG, West Germany) was applied for treatment of hyperinsulinemia combined with hyperlipidemia. After administration of this drug, the absorption of dietary starch was shown to be delayed and the postprandial insulin elevation was markedly decreased. The administration of Bay g 5421 in the daily dosage of 300mg for 4 weeks produced no change in body weight but significant reduction in plasma lipids in the hyperinsulinemic hyperlipidemic patients.

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Clinical and biochemical features of type V hyperlipoproteinemia (HLP) were examined in our five cases of familial type V HLP. The VLDL (including chylomicron) cholesterol and triglyceride levels were significantly increased and the IDL, LDL and HDL cholesterol levels significantly reduced in type V HLP. There was no difference in the increase of serum FFA levels after intravenous injection of heparin between type V HLP and normal or other types of HLP. Reduction of serum triglyceride levels after intravenous injection of heparin was significantly smaller in type V HLP than in normal or other types of HLP. Fasting serum triglyceride levels showed significant correlations to the decrease of serum triglyceride after intravenous injection of heparin. The regression equation in normal or other types of HLP was Y (fasting serum triglyceride in mg/dl)=1.28X (decrease of serum triglyceride after heparin injection in mg/dl)+20.2 (r=0.966, p<0.01), while the regression equation in type V HLP was Y=4.56X+71.2 (r=0.964, p<0.01).
In 4 out of 5 cases of type V HLP, lipoprotein lipase (LPL) activity was definitely low, while hepatic triglyceride lipase (HTGL) activity was normal or slightly low. In one case (Y. M.) of type V HLP the LPL activity against ¹⁴C-triolein emulsion was normal, and the LPL activity against rat or human chylomicron was low. Thus, the LPL able to hydrolyze the emulsion but unable to hydrolyze rat or human chylomicrons is an “abnormal” LPL according to Schreibman et al..
From these data and the results of other reports, seven possible biochemical abnormalities in the pathogenesis of type V HLP are discussed.

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Since the first report of familial LCAT deficiency in 1967, the patients with the disease have been increasing all over the world. Originally, hypercholesterolemia or hyperlipidemia was regarded as one of the essential features of the disease, but later, non-hypercholesterolemic patients were reported. Because plasma lipids and lipoproteins may vary greatly by the living circumstances, observations on similarity and dissimilarity of lipid and lipoprotein patterns among patients within the same family may have a value to find a role of LCAT in plasma lipid metabolism. There were marked differences in terms of serum cholesterol concentration among three Japanese siblings with familial LCAT deficiency, who have been living in the same circumstances. On examining them, the following conclusions have been drawn. (1) Hypercholesterolemia may not be the essential feature in LCAT deficiency. We observed marked to moderate hypocholesterolemia in two out of three patients. (2) Triglyceride concentration in relation to cholesterol concentration is usually high in LCAT deficiency and this is especially marked in HDL and LDL fractions. (3) Lipoprotein lipase activity, in general, appeared to decrease in familial LCAT deficiency. (4) Fresh frozen plasma transfusion increased total cholesterol as well as esterified one. (5) Linoleic acid content in cholesterol ester is significantly low in all patients, and it may be directly related to LCAT deficiency. (6) Lysolecithin concentration in relation to lecithin is higher in VLDL than in HDL, and increases in VHDL in all patients. (7) On our examination of the patients, it was hardly thought that esterified cholesterol in VLDL was exclusively derived from HDL. (8) It was suggested that LCAT might directly act on nascent VLDL.

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Cuataneous manifestations in hyperlipidemia were summerized.
Lipid metabolism in epidermis, sebaceous and apocrine glands had been well investigated, however the relationships between these metabolism and hyperlipidemia are not yet well understood. lipids, xanthomatosis
Xanthoma, as one of the model of abnormal lipid metabolism in corium, was discussed. But, there still remains unknown mechanism concerning the development of xanthoma especially in relation to plant sterol levels.

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Experimental myocardial infarction (necrosis) induced by isoproterenol hydrochloride injection to rat, was made by the method of Rona. Lipoperoxide (TBARS) and vitamin E (α-tocopherol) in the serum and heart tissue were measured. TBARS in the heart tissue of isoproteronol treated rat was significantly elevated than that of the control. So, it seems that lipoperoxide are produced in the infarcted heart tissue. There was no significant difference between isoproteronol treated and control rat in the serum TBARS and α-tocopherol of the heart tissue. But, the serum α-tocopherol of isoproterenol treated rat was markedly decreased than the control. This findings were similar to the acute phase of the clinical myocardia infarction, that we already reported.

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Among 16, 759 persons, 107 persons with hyperlipidemis and with a total cholesterol level over 300mg/100ml were found. The prevalence rate of hyperlipidemia was found to be 0.64 per cent. Among them, 72 persons received reexamination; and by the electrocardiographic finding they were divided into two groups, one group with and the other without ischemic change. The results are as follows:
1) In the group with ischemic change; the average age, the degree of obesity, the mean systolic blood pressure and the mean cardiothoracic ratio were found to be larger than those of the group without ischemic change.
2) In the group with ischemic change; the mean fasting blood sugar, triglyceride and uric acid were found to be elevated compared with the group without ischemic change. The mean HDL-cholesterol level in the former group was a little lower than that of the latter group. It is presumed that the above mentioned differences of clinical findings will act additively on the) development of ischemic heart desease.

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Trapidil inhibited: TXA₂-induced platelet aggregation in rabbits, TXA₂-induced constriction of excised strips of rabbit aorta, synthesis of TXA₂ in platelets, TXA₂-induced ischemic changes of heart of rabbits and increase in TXA₂ synthesis after high cholesterol feeding in rats.
The above results show that trapidil posseses inhibitory action of TXA₂ synthesis and antagonistic actions on TXA₂, in addition to coronary dilating action.

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One handred and thirty seven patients (male 68, female 69) with diabetes mellitus were divided into three groups according to the difference of the treatment i. e., group 1 (n=37) was treated by only diet therapy, group 2 (n=52) by oral hypoglycemic agents and group 3 (n=48) by insulin therapy, respectively. Furthermore, each group was divided into two subgroups whether with or without the diabetic complications, which estimated by the presence of hypertension (over 150mmHg, systolic and/or 90mmHg diastolic), proteinuria, abnormal ECG findings and diabetic retinopathy.
Serum HDL-cholesterol was determined by the precipitation method using Heparin-Mn⁺⁺. The results obtained are as follows. All data were expressed as mean±S.E.
1) Serum HDL-cholesterol levels in group 2 (54.8±1.5mg/100ml) and group 3 (55.4±1.6) had a tendency to be low in comparison with those in group 1 (58.3±1.6).
2) Serum total cholesterol levels and the ratics of total cholesterol to HDL-cholesterol in group 2 (216.0±4.9mg/100ml, 4.1±0.2) were significantly higher than those in group 1 (207±5.4, 3.6±0.1).
3) In group 2 and 3 with diabetic complication (s) significantly low levels of serum HDL-cholesterol (group 2, 51.7±2.1mg/100ml, n=25, p<0.005; group 3, 54.4±1.6, n=23, p<0.01) and high ratios of total cholesterol to HDL-cholesterol (group 2, 4.2±0.2, n=25, p<0.01; group 3, 4.1±0.2, n=23 p<0.05) were observed in comparison with those in group 1. These observations indicate that the appearance of complications in diabetics under the hypoglycemic agents therapy for a long time accompanies with the low levels of serum HDL-cholesterol.

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