ApoE 基因多态性与中国人非胰岛素依赖型糖尿病血脂水平的关系

为研究ＡｐｏＥ基因对中国人非胰岛素依赖型糖尿病（ＮＩＤＤＭ）患者血脂水平的影响，应用聚合酶链反应（ＰＣＲ）扩增出ＡｐｏＥ基因第４外显子内的２９２ｂｐ片段，继以限制性内切酶ＨｈａⅠ酶解消化，最后行８％聚丙烯酰胺凝胶电泳，根据电泳带型判断ＡｐｏＥ基因型。共检测了１１２例非胰岛素依赖型糖尿病患者的ＡｐｏＥ基因型。通过比较不同ＡｐｏＥ基因型与血脂水平的关系发现：ＡｐｏＥ基因多态性与ＴＧ，ＨＤＬ－Ｃ，ＡｐｏＡⅠ，ＡｐｏＢ及Ｌｐ（ａ）水平无相关性，而与ＴＣ（Ｐ＝０．００２９）及ＬＤＬ－Ｃ（Ｐ＝０．００２１）水平相关，携带ε４等位基因者具有较高的ＴＣ及ＬＤＬ－Ｃ水平，而携带ε２等位基因者具有较低的ＴＣ及ＬＤＬ－Ｃ水平。     

载脂蛋白E基因多态性与血管性痴呆关系的研究

为探讨载脂蛋白Ｅ（ＡｐｏＥ）基因多态性与血管性痴呆（ｖａｓｃｕｌａｒｄｅｍｅｎｔｉａ，ＶＤ）的关系，采用单链构象多态性分析（ＰＣＲ－ＳＳＣＰ）检测了３７例ＶＤ患者的ＡｐｏＥ基因型，并与４０例同龄对照组及４０例非痴呆脑梗塞组比较，同时检测血脂、脂蛋白及部分载脂蛋白。结果表明，ＶＤ组ε４基因频率明显高于对照组（Ｐ＜０．０１）和非痴呆脑梗塞组（Ｐ＜０．０５），ＶＤ患者中携ε４等位基因者血ＴＣ及ＬＤＬ－Ｃ水平显著高于携ε２、ε３者。提示：ε４基因可能是ＶＤ的危险因子，其机理可能与大脑血管性和变性性损害有关。     

ApoE基因多态性与中国人非胰岛素依赖型糖尿病血脂水平的…

为研究ＡｐｏＥ基因对中国人非胰岛素依赖型糖尿病（ＮＩＤＤＭ）患者血脂水平的影响，应用聚合酶链反应（ＰＣＲ）扩增出ＡｐｏＥ基因第４外显子内的２９２ｂｐ片段，继以限制性内切酶ＨｈａⅠ酶解消失，最后行８％聚丙烯酰胺凝胶电泳，根据电泳带型判断ＡｐｏＥ基因型。共检测了１１２例非胰岛素依赖型糖尿病患者的ＡｐｏＥ基因型。通过比较不同ＡｐｏＥ基因与血脂水平的关系发现：ＡｐｏＥ基因多态性与ＴＧ，ＨＤＬ－Ｃ，ＡｐｏＡ     

长寿老人血脂,脂蛋白和载脂蛋白价值的研究

对９０岁以上３６例长寿老人的血脂、脂蛋白和载脂蛋白进行了测定，并与陈旧性心肌梗塞（ＯＭＩ）和成人组对比。结果显示：与ＯＭＩ组比较，长寿老人血清ＨＤＬ－ｃ／ＴＣ、ＨＤＬ－ｃ／ＬＤＬ－Ｃ和ＡｐｏＡ１／ＡｐｏＢ１００比率明显高于ＯＭＩ，而ＴＣ、ＴＧ、ＬＤｃ、ＶＬＤＬ－ｃ、ＡｐｏＢ１００和ＡｐｏＡ１明显低于ＯＭＩ，ＨＤＬ－ｃ在两组间无显著性差异，与成人组比较，长寿老人血清ＴＧ、ＶＬＤＬ－ｃ、ＡｐｏＡ、／Ａ     

丙型肝炎病毒基因型与血清HCV RNA含量关系及与干扰素应答的研究

目的探讨丙型肝炎病毒（ＨＣＶ）基因型与血清ＨＣＶＲＮＡ含量的关系及其对干扰素应答的影响。方法应用定量荧光ＰＣＲ（Ａｍｐｌｉｓｅｎｓｏｒ－ＰＣＲ）技术检测了１３５例不同基因型ＨＣＶ感染的慢性丙型肝炎患者血清ＨＣＶＲＮＡ含量，另对其中７７例进行干扰素治疗并随访１２个月以上。结果ＨＣＶ－Ⅱ型感染血清ＨＣＶＲＮＡ水平（１０７．８±３．４拷贝／ｍｌ）显著高于ＨＣＶ－Ⅲ型感染（１０６．３±２．５拷贝／ｍｌ）（Ｐ＜０．０１），Ⅲ型感染的应答率（７／１３，５３．８％）显著高于Ⅱ型感染（２０／６４，３１．３％）（Ｐ＜０．０５）。应答组治疗前血清ＨＣＶＲＮＡ含量（１０６．８±２．７拷贝／ｍｌ）显著低于无应答组（１０８．３±３．２拷贝／ｍｌ）（Ｐ＜０．０１）。ＨＣＶＲＮＡ含量低于１０６．５拷贝／ｍｌ者，无论何种型别ＨＣＶ感染均应答较好，而ＨＣＶＲＮＡ高于１０８．０拷贝／ｍｌ者则应答极差。结论ＨＣＶ基因型及病毒血症水平是预测干扰素疗效的重要因素，且后者比前者意义更大。Ⅱ型感染病毒血症水平较高可能是影响其疗效的原因之一。     

α-2b干扰素治疗不同基因型丙肝疗效与免疫指标的关系

根据Ｏｋａｍｏｔｏ基因分型法对２８例丙肝患者的病毒基因进行了分型，１８例为ＨＣＶ－Ⅱ型，１０例为ＨＣＶ－Ⅲ型。重点研究了α－２ｂＩＦＮ治疗ＨＣＶ－Ⅱ型患者和ＨＣＶ－Ⅲ型患者免疫功能的不同改变：在α－２ｂＩＦＮ治疗前，ＨＣＶ－Ⅱ型患者和ＨＣＶ－Ⅲ型患者之间ＩｇＧ、ＩｇＭ、ＩｇＡ、ＣＤ４百分比、ＣＤ８百分比及ＣＤ４／ＣＤ８比值６项指标无明显差别。α－２ｂＩＦＮ治疗８ｗ时，ＨＣＶ－Ⅲ型患者ＣＤ４／ＣＤ８比值明显高于ＨＣＶ－Ⅱ型患者ＣＤ４／ＣＤ８比值。α－２ｂＩＦＮ治疗１个疗程（１２ｗ）时，ＨＣＶ－Ⅲ型患者ＣＤ４百分比，ＣＤ４／ＣＤ８比值明显高于ＨＣＶ－Ⅱ型患者。α－２ｂＩＦＮ治疗１个疗程后第４周（１６ｗ）时，ＨＣＶ－Ⅲ型患者ＣＤ４百分比，ＣＤ４／ＣＤ８比值仍明显高于ＨＣＶ－Ⅱ型患者，但在整个治疗过程中，ＨＣＶ－Ⅲ型和Ⅱ型患者ＩｇＧ、ＩｇＭ、ＩｇＡ和ＣＤ８百分比４项指标改变无显著差异。α－２ｂＩＦＮ治疗ＨＣＶ－Ⅲ型患者，其ＣＤ４百分比，ＣＤ４／ＣＤ８比值改变明显高于ＨＣＶ－Ⅱ型患者。这可能是α－２ｂＩＦＮ治疗ＨＣＶ－Ⅲ型患者疗效明显好于ＨＣＶ－Ⅱ型患者重要原因之一。     

载脂蛋白AI基因的基因型与冠心病临床表现型的关系

对４３例经冠状动脉造影证实的冠心病患者及６０例正常人载脂蛋白（Ａｐｏ）ＡＩ基因ＰｓｔＩ酶切位点限制性片段长度多态性（ＲＦＬＰｓ）进行检测，结果表明：冠心病组中少见Ｐ２等位基因的相对频率为０．１４，明显高于正常对照组的０．０５；Ｐ２等位基因的相对频率随冠状动脉病变支数的增多而增高，以３支病变增高最为明显；冠心病组中具Ｐ１Ｐ２基因型得与具Ｐ１Ｐ１基因型者比较，ＨＤＬ－Ｃ和ＳＯＤ水平明显降低，而ＴＣ及Ｌ     

自身免疫性疾病患者T细胞表面抗原CD2,CD4和CD8mRNA的表达

用斑点杂交技术检测了１８例系统红斑狼疮（ＳＬＥ），２２例干燥综合征（ＳＳ）、２１例类风湿性关节炎（ＲＡ）患者及１６例正常人外周血淋巴细胞ＣＤ２，ＣＤ４和ＣＤ８ｍＲＮＡ的表达水平，结果表明，这３种病人ＣＤ２ｍＲＮＡ水平均较正常人有明显升高，ＳＬＥ和ＲＡ患者ＣＤ４／ＣＤ８ｍＲＮＡ比值也明显升高，而ＳＳ患者ＣＤ４／ＣＤ８ｍＲＮＡ比值在正常范围，在Ｔ细胞发育过程中，ＣＤ２先天ＣＤ４和ＣＤ８的表达，结果提示     

T细胞受体Vβ基因在识别HSV—2过程中的表达水平和特点

本课题主要研究Ｔ细胞受体（ＴＣＲ）识别抗原后Ｖβ基因发生重排，ｍＲＮＡ表达水平改变。用紫外线处理的单纯疱疹病毒－２型（ＨＳＶ－２）、ＨＳＶ－２及ＰＨＡ分别感染或刺激正常人的ＰＢＬｓ，培养４～６天后，提取ｍＲＮＡ，并采用ＲＴ－ＰＣＲ、Ｓｏｕｔｈｅｒｎ杂交发现识别ＨＳＶ－２的ＴＣＲＶβ２、６、７、８基因在体外选择性扩增。在采用ＨＳＶ－２攻击皮肤病患者发作期、缓解期以及再发作期的ＰＢＬｓ时，发现ＴＣＲＶβ基因表达随着病程变化而改变，尤其Ｖβ７亚家族表达水平显著高于其它亚家族基因，这显示了ＴＣＲＶβ基因的变化是恒定特异性的。     

α—2b干扰素治疗不同基因型肝疗效与免疫指标的关系

根据Ｏｋａｍｏｔｏ基因分型法对２８例丙肝患者的病毒基因进行了分型，１８例为ＨＣＶ－Ⅱ型，１０例为ＨＣＶ－Ⅱ型，重点研究了α－２ｂＩＦＮ治疗ＨＣＶ－Ⅱ型患者和ＨＣＶ－Ⅱ型患者免疫功能的不同改变，在α－２ｂＩＦＮ治疗前，ＨＣＶ－Ⅱ型患者和ＨＣＶ－Ⅱ型患者之间ＩｇＧ，ＩｇＭ，ＩｇＡ，ＣＤ４百分比，ＣＤ８百分比及ＣＤ４／ＣＤ８比值６项指标无明显差别，α－２ｂＩＦＮ治疗８ｗ时，ＨＣＶ－Ⅲ型患者ＣＤ４／ＣＤ８     

Low-density lipoproteins isolated from the blood of patients with coronary heart disease induce the accumulation of lipids in human aortic cells

Smooth muscle cells cultured from the intima of unaffected human aorta accumulate lipids during incubation with the blood serum of patients with coronary heart disease (CHD). Blood sera of most healthy subjects fail to induce the deposition of lipids in cultured cells. Very-low-density lipoproteins (VLDL), low-density lipoproteins (LDL), and high-density lipoproteins of two subclasses (HDL2 and HDL3) were isolated from the blood of healthy subjects and CHD patients. LDL from the blood of healthy individuals did not raise intracellular lipid levels within 24 hr of cultivation (the maximal concentration used, 1000 micrograms/ml). During the same incubation period, LDL obtained from the blood of CHD patients (200 to 1000 micrograms/ml) caused a 2- to 5-fold rise in cholesteryl esters as well as a 1.5- to 3-fold rise in free cholesterol and triglycerides, whereas intracellular phospholipid levels remained unchanged. There was a direct correlation (r = 0.95) between cholesterol accumulation in the cells incubated with whole sera of CHD patients and cholesterol level in the cells incubated with LDL isolated from these sera. In one of the three cases, the ability to raise the intracellular level of cholesteryl esters was demonstrated by VLDL (500 micrograms/ml) derived from CHD patients' blood. HDL2 and HDL3 did not affect lipid levels in smooth muscle cells cultured from unaffected intima. HDL3 from the blood of CHD patients and healthy subjects (50 to 250 micrograms/ml) reduced cholesteryl ester levels in cells cultured from atherosclerotic plaques 1.5- to 2-fold. HDL2 also decreased the content of cholesteryl esters in plaque cells, though less effectively than HDL3. The data obtained suggest that circulating LDL and, possibly, VLDL in the blood of CHD patients are capable of inducing the accumulation of fat in vascular wall cells.     

ApoE polymorphism may determine low-density lipoprotein cholesterol level in association with obesity and metabolic syndrome in postmenopausal Korean women

Purpose

We investigated how serum low-density lipoprotein (LDL) level is related to various isoforms of apolipoprotein (ApoE) polymorphism in association with obesity and metabolic syndrome.

Materials and Methods

We gathered total 332 sample of postmenopausal Korean women and analyzed ApoE isoforms, serum lipid level including LDL, blood pressure, fasting glucose, and anthropometry. The relationship between ApoE isoforms and serum lipid level, metabolic syndrome, and obesity was investigated.

Results

Six ApoE isoforms were found, ApoE2 [E2/2 (n=1), E2/3 (n=54), E2/4 (n=14)], ApoE3 (E3/3, n=200), ApoE4 [E3/4 (n=55), and E4/4 (n=8)]. The prevalence of metabolic syndrome and obesity showed higher ApoE3 isoform than that of other isoforms. In additon, ApoE3 isoform was related to higher serum LDL and total cholesterol level than to ApoE2 isoform. The odds ratio of having the highest LDL cholesterol quartile in ApoE3 with obesity, compared to ApoE2 without obesity, was 3.46 [95% confidence interval (CI); 1.07-11.14, p=0.037], and odds ratio of ApoE3 with metabolic syndrome compared to ApoE2 without metabolic syndrome was 5.06 (95% CI; 1.14-22.29, p=0.037). Serum LDL cholesterol was positively associated with obesity or metabolic syndrome in ApoE3 isoform.

Conclusion

This study suggests that obesity or metabolic syndrome risk should be effectively managed in ApoE3 isomform groups to reduce serum LDL in postmenopausal Korean women.     

Correlation between various lipid and apolipoprotein parameters and clinical severity in arteriopathy of the lower limbs

We have compared the serum levels of lipids (cholesterol, triglycerides, high density lipoprotein cholesterol), apolipoproteins (Apo Al and Apo B) and two ratios (HDL cholesterol/VLDL + LDL cholesterol and Apo Al/Apo B) between a population of 180 patients with atheromatous member lesions, divided into four sub-groups with respect to clinical severity, and one of 121 controls without lesions. It seems that the most discriminative values linking to the severity of atherosclerotic manifestations are levels of Apo B, ratio Apo Al/Apo B and with a lower efficiency ratio HDL cholesterol/VLDL + LDL cholesterol.     

Apolipoprotein E gene polymorphism and serum lipids in patients with superficial fungal disease

Superficial mycosis, including dermatophytic infections, tinea versicolor, and cutaneous candidiasis is mostly limited to the outer layers of the skin, nails, and mucous membranes. In this study, Apolipoprotein E (ApoE) polymorphism and lipoprotein cholesterol concentrations were compared between 42 patients with superficial fungal disease and 27 control subjects. Both the patients and controls were found to be normolipemic. The patients with superficial fungal disease had significantly higher concentrations of high-density cholesterol (HDL) compared to the control group (p=0.0462). However, there was no difference in the serum triglyceride, low-density lipoprotein (LDL) and very low-density lipoprotein (VLDL) cholesterol concentrations. A significantly higher incidence of heterozygosity E2/3 was found in the patients (p=0.0228), and significantly lower incidence of homozygosity E3/3 in all patients, and those with candidiasis and dermatophytosis (p=0.0139, 0.0194 and 0.0337, respectively) compared to the control group. The E3/4 genotype differences between patients and controls were not statistically significant. There were slight differences in the allele frequencies between the two groups, but these did not reach statistically significant levels. It was concluded that the presence of apoE2/3 genotype, high HDL-cholesterol levels and the absence of apoE3/3 genotype can be regarded as risk factors for superficial fungal disease, especially dermatophytosis.     

Metabolic disorders of lipoproteins--influences of compositional changes of lipoproteins upon their metabolic behavior

Compositional changes of apoproteins and lipids in lipoproteins influence their affinities for receptors and enzymes. Decrease of apo C proteins and increase of apo E in chylomicron and very low density lipoproteins (VLDL) during their catabolism might promote the binding to remnant receptor. On the other hand, the affinity for lipoprotein lipase (LPL) gradually decreases and that for hepatic lipase increases. However, the responsiveness of VLDL to LPL might be under the control of triglyceride (TG)/surface component ratios but not of the apoprotein ratios in ordinary circumstances judging from the results of the releases of fatty acids from VLDL by LPL in vitro. Responses of VLDL from diabetic patients to LPL significantly decreased compared with those from non-diabetic subjects. Glycation of VLDL in vitro impaired their responses to LPL. Therefore, delayed catabolism of VLDL in diabetes might partially depend upon glycation of VLDL besides the decreased LPL activity. Low density lipoproteins (LDL), apoproteins of which consist mostly of apo B protein and had a low TG level, showed a high affinity to the LDL receptor. However, LDL from hypertriglyceridemic subjects, in which the TG contents was increased, had a low affinity to the receptor. Since high density lipoproteins (HDL) from patients in acute phases contain a large amount of serum amyloid A protein (SAA), the percentages of apo A proteins markedly decreased. When SAA-rich HDL were incubated with leucocytes, SAA were degraded rapidly, although other apoproteins remained to be unchanged. Therefore, such HDL become unstable, and this might induce low HDL levels in the acute phase.     

HDL cholesterol levels in patients with molecularly defined familial hypercholesterolemia

Familial hypercholesterolemia (FH) is the most common genetic disorder leading to premature atherosclerosis. Typically, it is due to mutations in the LDL receptor gene resulting in elevated total and LDL cholesterol levels. The type of the LDL receptor gene mutations may affect the severity of hypercholesterolemia and consequently the incidence of coronary atherosclerosis. Furthermore, high-density lipoprotein (HDL) cholesterol levels have been recently shown to be an independent risk factor for coronary heart disease in this population. We examined the effect of the type of the LDL receptor gene mutations and of common gene polymorphisms possibly affecting HDL metabolism [cholesterol ester transfer protein (CETP), apolipoprotein A-IV (ApoA-IV), angiotensin converting enzyme (ACE), and apolipoprotein E (ApoE)] on HDL cholesterol levels in patients with molecularly defined heterozygous FH who were attending our lipid clinic (n=84). The nature of the LDL receptor gene mutation (81T>G, n=12; 858C>A, n=13; 1285G>A, n=12; 1646G>A, n=22; and 1775G>A, n=25) did not significantly influence HDL cholesterol levels. Unlike other gene polymorphisms, the apolipoprotein (apo) E gene polymorphism did significantly affect these levels. In fact, the presence of the E4 allele was associated with lower HDL cholesterol levels compared to patients not carrying this allele. We conclude that HDL cholesterol levels in heterozygous FH patients may be affected by the apoE gene polymorphism.     

A case of hyper-HDL-cholesterolemia presenting peculiar lipoprotein patterns in agarose gel electrophoresis

Lipoprotein metabolism was analyzed in a patient with marked hyper-HDL-cholesterolemia. A 50 year old male with no symptom of ischemic heart disease or xanthoma had a serum cholesterol level between 293 and 410 mg/dl, and a markedly elevated, HDL-cholesterol level (160-190 mg/dl). The cholesterol content of ultracentrifugally separated HDL2 was exclusively increased, while it was normal in the HDL3 fraction. Analytical ultracentrifugation and HPLC revealed that HDL particles became remarkably larger than the control and, on the contrary, LDL particles became smaller. LPL and LCAT activities were higher in this case, but H-TGL activity was normal. Agarose gel electrophoresis of lipoproteins showed an abnormal broad band which was located between alpha and pre beta band. Serum levels of apolipoprotein A-I, A-II, C-II, C-III and E were higher, while apolipoprotein B level was slightly lower than the control. Cholesteryl ester transfer protein (CETP) activity was demonstrated to be completely deficient in this case, as determined in 10 microliters serum using [3H] CE-labeled HDL3 as donor and VLDL + LDL fraction as acceptor. Since CETP was considered to catalyze the cholesteryl ester transport from HDL to VLDL and LDL, the deficiency of this activity might be the cause of the marked hyper-HDL-cholesterolemia in this patient.     

The effects of trimazosin and pindolol on serum lipids, blood glucose and serum insulin levels

The effects on plasma lipids, blood glucose and serum insulin levels of oral administration of trimazosin and pindolol over a 6-month period were studied in 11 patients with essential hypertension. Total plasma cholesterol and LDL cholesterol concentrations were higher (p less than 0.05) after one month's treatment with trimazosin than basal values, but the significance of changes disappeared with continuation of treatment. The concentrations of plasma triglycerides, VLDL cholesterol, HDL cholesterol and free fatty acids and the HDL cholesterol/total cholesterol ratio remained about constant during treatment with trimazosin. During pindolol treatment the plasma levels of total cholesterol and LDL cholesterol were slightly but not significantly lowered at 3 and 6 months. The levels of plasma triglycerides, VLDL cholesterol and HDL cholesterol remained about constant and the ratio of HDL cholesterol to total cholesterol had increased slightly (p less than 0.05) at 3 months. Serum free fatty acid concentration decreased significantly. There were no significant differences between plasma lipid levels during either trimazosin or pindolol treatment. Blood glucose concentrations showed a slight tendency to increase during the treatment periods, but no impairment in insulin release was found.     

Comparative effects of two HMG-CoA reductase inhibitors (lovastatin and pravastatin) on serum lipids and lipoproteins

The effects of the HMG-CoA reductase inhibitors lovastatin and pravastatin were studied over 4 months on serum lipids and lipoproteins in 35 patients with severe primary hypercholesterolaemia. In 17 patients 20 mg of lovastatin/day lowered the total cholesterol level by 18% (baseline 373 mg/dl) and LDL cholesterol by 20% (baseline 300 mg/dl). The corresponding data for 40 and 80 mg of lovastatin/day were respectively -23% and -29% for total cholesterol, and -30% and -36% for LDL cholesterol. Pravastatin at 20 mg/day lowered the total cholesterol in 18 patients by 20% (baseline 373 mg/dl) and LDL cholesterol by 24% (baseline 307 mg/dl). The corresponding data for 40 mg of pravastatin per day were 24% for total cholesterol and 30% for LDL cholesterol. So the effects of both HMG-CoA reductase inhibitors on total and LDL cholesterol are comparable. HDL (high-density lipoprotein) cholesterol was increased by lovastatin, whereas pravastatin showed no influence on HDL cholesterol. The reduction of serum triglycerides, VLDL triglycerides and VLDL cholesterol was more pronounced under treatment with lovastatin than under pravastatin.     

Genetic and environmental variation in serum lipoproteins in relation to coronary heart disease

Variation in the serum concentration of VLDL, IDL, LDL, and HDL was studied in (a) 192 survivors of myocardial infarction under the age of 50 living in the north-east of Scotland; (b) 250 relatives, mostly first degree; and (c) 259 unrelated individuals, comprising mostly spouses and their relatives.

The biochemical characterisation of the lipids, which were separated by preparative ultracentrifugation, included (a) determination of total serum cholesterol and triglyceride; and (b) determination of the content of cholesterol in the four fractions, and also of triglyceride in the VLDL fraction.

In male survivors of infarction there is a significant negative regression of VLDL and a significant positive regression of HDL on peak aspartate aminotransferase activity in blood samples taken within 24 hours of the incident. In later samples correlations were not evident.

Serum lipoprotein concentrations have been compared in samples taken at different times after the incident. The average value of samples taken within 24 hours is similar to the mean scores for LDL and VLDL of repeat samples taken, on average, 9 months later.

The incidence of hyperlipidaemia in samples taken within 24 hours of the infarction is about the same for total cholesterol and triglyceride and LDL or VLDL. Respectively, 18·3%, 16·1%, and 7·5% of the survivors exceed the 90th centile value for either LDL, VLDL, or both fractions, while, for the 95th centile limit, the corresponding figures are 8·6%, 9·7%, and 2·2%.

In samples taken within 24 hours of the incident, the LDL concentration is, on average, 20 to 30% higher, and the VLDL concentration 50 to 60% higher, than the controls. The corresponding HDL difference in males, though negative, is trivial and statistically insignificant, but in females the difference is greater and significantly so.

VLDL levels are substantially increased in regular cigarette smokers in both sexes, especially in males. HDL levels tend to be lower, though not significantly so. The frequency of persons who are or have been regular cigarette smokers is higher in index cases than in controls.

Correlation analysis of individual variation of controls and index case relatives indicates a substantial level of independence between the major lipoprotein fractions. There is no correlation between LDL and HDL. There are positive correlations between VLDL, IDL, and LDL, though when IDL is held constant by multiple regression, the correlation between VLDL and LDL is removed. There is a low but consistent negative correlation between VLDL and HDL cholesterol.

About a quarter of the variance of VLDL in males is accounted for by multiple regression on measures of body fatness, that is, relative weight and subscapular skinfold thickness. In females only about 10% of the variance is thus accounted for, and only in males do LDL levels show correlated changes with fatness. There are no significant differences for either relative body weight or subscapular skinfold thickness between the means of first degree relatives of survivors of infarction and controls.

The concentrations of VLDL and LDL in first degree relatives of survivors of infarction are significantly higher than the control means. HDL shows no significant difference.

The evidence for genetic variation in serum lipoprotein is based on the polygenic model and the analysis of the correlation between parents and offspring and the correlation between sibs. From the pooled regression on single parents, heritabilities for HDL, LDL, and VLDL work out at 0·67 ± 0·21, 0·36 ± 0·18, and 0·23 ± 0.20, respectively. The lower heritability of VLDL is consistent with the variance of repeat measurements on the same control individuals, which is much higher for VLDL than for LDL or HDL. The high correlation between VLDL and measures of fatness, for which heritability estimates are statistically insignificant, as well as the association between raised VLDL concentration and smoking, also provide confirmatory evidence of the major importance of non-genetic causes in the variation of VLDL.

The results are discussed in relation to the origin of the effects of smoking, variation in proneness to coronary disease, and the biological significance of differences in HDL concentration.