类固醇激素合成急性调节蛋白与动脉粥样硬化

类固醇激素合成急性调节蛋白StAR在胆固醇转化为类固醇激素的过程中具有重要作用。StAR表达于血管内皮细胞中，影响胆固醇代谢并受胆固醇、低密度脂蛋白、25-羟基胆固醇等脂类物质的调节，StAR可能参与脂质代谢平衡并在动脉粥样硬化的防治中起到重要作用。     

StAR在雌性SD大鼠海马、基底前脑及前额叶皮层中的表达与ChAT正相关

目的:探讨基底前脑胆碱能系统(basal forebrain cholinergic system,BFCS)中是否存在神经甾体的合成及局部合成的神经甾体与BFCS功能之间的关系。方法:利用免疫荧光及Western Blot方法检测甾体合成急性调节蛋白(steroidogenic acute regulatory protein,StAR)及胆碱乙酰转移酶(choline acetyltransferase,ChAT)在1月龄、6月龄及24月龄雌性SD大鼠海马、基底前脑及前额叶皮层中的表达情况,并对StAR与相应脑区中ChAT的表达量进行相关性分析。结果:海马、基底前脑及前额叶皮层多种形态的细胞中均存在StAR的表达。StAR与ChAT在1月龄及24月龄组的表达量均显著低于6月龄组(P0.05),24月龄组的表达量均略低于1月龄组(P0.05),且StAR的表达量均与相应脑区中ChAT的表达量正相关。结论:BFCS中存在神经甾体的合成,且局部合成的神经甾体与BFCS功能状态密切相关。     

类固醇生成急性调控蛋白作用的分子病理机制研究进展

类固醇生成急性调控蛋白（steroidogenic acute regulatory protein,StAR)基因突变是引起先天性类脂性肾上腺皮质增生症（congenital lipoid adrenal hyperplasia,CLAH)的原因。CLAH是一种常染色体隐性遗传病，患者从胆固醇向孕酮转换的能力严重受损，主要临床表现包括：基因型为46，XY或46，XX患者均呈女性外生殖器表现型，在出生后可有失盐型表现且严重程度不等，肾上腺及性腺细胞内胆固醇聚集，导致细胞损伤。近年来StAR作用的分子病理生理学机制研究取得了系列进展，本文拟对此进行综述。     

LXR激活对大鼠原代培养海马神经元胆固醇代谢关键酶基因表达的影响

为了探讨肝X受体(LXR)激活对海马神经元胆固醇代谢关键酶基因表达和胆固醇外流的影响,本研究取当天新生大鼠海马神经元行体外培养7d,随机分为TO组(培养液含2.0μmol/L的TO901317)和正常对照组(CON),继续培养48h。用胆固醇氧化酶-比色法检测TO组胆固醇的排出量;应用RT-PCR方法检测两组海马神经元ATP结合盒转运体A1(ABCA1)、HMG-CoA还原酶(HMGR)、胆固醇24-羟化酶(CYP46)、P450侧链裂解酶(P450scc)、固醇生成急性调节蛋白(StAR)和酰基辅酶A-胆固醇酰基转移酶1(ACAT1)等胆固醇代谢关键酶基因的mRNA的表达。结果显示:TO组mRNA表达上调的酶有HMGR、P450scc和StAR(P<0.01);表达下调的酶是ACAT1(P<0.01);表达不受影响的酶是CYP46。上述结果表明LXR激活、促进细胞内胆固醇外流时,海马神经元可能通过协调胆固醇代谢关键酶基因的表达,增加胆固醇的合成和向神经甾体的转化,抑制胆固醇的储备,而不影响胆固醇排出血脑屏障,从而维持细胞内胆固醇的动态平衡,保证神经元的正常生理功能。     

姜黄素衍生物B06对2型糖尿病大鼠睾酮合成的影响

 目的: 研究姜黄素衍生物B06对2型糖尿病大鼠睾酮合成的影响。方法: 雄性SD大鼠35只,随机均分为正常对照组(C组)、高脂组(H组)、高脂治疗组(HT组)、糖尿病组(D组)和糖尿病治疗组(DT组),后4组高脂喂养4周后,D组及DT组用低剂量链脲佐菌素诱导糖尿病,HT组和DT组用0.2 mg·kg^-1·d^-1的B06灌胃8周。微量血糖仪测定大鼠血糖浓度;ELISA法测定血胰岛素水平,并计算胰岛素抵抗指数;光镜和电镜观察睾丸形态;放射免疫法测定血睾酮、雌二醇水平;免疫组化检测Leydig细胞的类固醇激素合成急性调节蛋白(StAR)表达;RT-PCR检测睾丸Leydig细胞StAR、胆固醇侧链裂解酶(P450scc)、细胞色素P450 17A1(P450c17)、细胞色素P450芳香化酶(P450arom)、3β-羟基类固醇脱氢酶(HSD)及17β-HSD的mRNA表达水平。结果: H组及D组血糖、胰岛素抵抗指数升高,血清睾酮水平降低,经B06治疗后好转;H组及D组睾丸曲细精管变形,生精细胞脱落,Leydig细胞内线粒体肿胀,内质网减少且扩张,胞核皱缩,染色质稀疏,经B06治疗后病变减轻;D组的StAR蛋白表达减弱,经B06治疗后表达增强;H组及D组Leydig细胞StAR、P450scc mRNA表达降低,经B06治疗后升高,P450c17、P450arom、3β-HSD及17β-HSD mRNA表达未见明显差异。结论: B06可缓解2型糖尿病大鼠睾丸病变,提高血清睾酮水平,这可能与B06改善机体代谢紊乱并上调Leydig细胞StAR及P450scc mRNA表达水平相关。     

巴戟天对微波致雄鼠生精功能损伤的影响

目的探讨巴戟天对微波致雄鼠生精功能损伤的修复功效。方法将24只雄性大鼠随机均分为空白组、辐射组、给药组。用微波信号发生器辐射辐射组和给药组2周;给药组在辐射后巴戟天灌胃2周。3组均在相同条件下饲养。4周后观察各组雄鼠的睾丸指数、附睾指数、精子密度、血清睾酮、睾丸组织类固醇合成急性调节蛋白（sterodiogenic regulatory protein,StAR）mRNA水平等指标的变化。结果辐射组相对其他两组相比,在睾丸指数、精子密度、血清睾酮、StAR mRNA降低（P〈0．05）,附睾指数变化没有统计学意义（P〉0．05）;给药组相对空白组在睾丸指数、附睾指数、精子密度、血清睾酮、StAR mRNA变化没有统计学意义（P〉0．05）。结论巴戟天可促进微波辐射损伤的生精功能的修复。     

银杏叶提取物对2型糖尿病大鼠睾酮水平、LHR和StAR mRNA表达的影响

目的： 探讨银杏叶提取物(EGB)在2型糖尿病大鼠睾酮合成中的作用及其对黄体生成素受体(LHR)、类固醇激素合成急性调节蛋白(StAR)基因表达的影响。方法: 雄性SD大鼠30只，随机均分成3组：正常对照组、2型糖尿病组、EGB 治疗组。后2组给以高脂饮食加小剂量(30 mg/kg)链脲佐菌素(STZ)诱导2型糖尿病大鼠模型，EGB治疗组予EGB50mg·kg^-1·d^-1灌胃12周，正常对照组及2型糖尿病组灌服等容积生理盐水。测定各组大鼠血葡萄糖、血胰岛素、血LDL-c含量；称各组大鼠睾丸重量，并用光镜和透射电镜观察大鼠睾丸组织的形态学改变； ELISA法检测血清黄体生成素(LH)、睾酮(T)水平；RT－PCR检测睾丸组织中LHR、StAR mRNA表达水平。结果: 与正常组相比，糖尿病组大鼠血清T、LH含量及睾丸组织的StAR mRNA含量明显降低，血糖、血胰岛素、LDL-c及LHR mRNA含量显著升高，睾丸重量明显减轻；光镜下主要表现为睾丸曲细精管内生精细胞数量减少及生精阻滞，透射电镜下主要见到间质细胞(Leydig cell)及支持细胞内线粒体、内质网等细胞器空泡样变及扩张。EGB治疗组睾丸组织病理改变较轻，血清T 、LH含量及睾丸组织StAR mRNA含量明显高于糖尿病组，血糖、血胰岛素、LDL-c及睾丸组织LHR mRNA含量低于糖尿病组。结论: EGB可提高2型糖尿病大鼠T的合成，其机制可能与改善糖脂代谢紊乱，调节LHR、StAR mRNA表达有关。     

胆固醇代谢调控的研究进展

胆固醇的合成、分解及逆向转运与动脉粥样硬化密切相关。又头转录因子的0亚型3（forkheadbox03,Fox03）／去乙酰化酶6复合物（Sirt6complex）、3β-脱氢胆固醇-A24还原酶（3p—hydroxysterolA（24）．reductase,DHCR24,Seladin．1）和死亡结构域相关蛋白（deathdomainassociatedprotein,Daxx）可以通过调控核转录激活因子一甾醇调节元件结合蛋白（sterolregulatoryelement—bindingproteins,SREBPs）的表达和活化来调节胆固醇合成限速酶[如3-羟基3．甲基戊二酰辅酶A还原酶β-hydroxy-3。methvlggutaryl—coenzymeAreductase,HMGCR）]等的转录,最终调控胆固醇的合成;外周组织的胆固醇逆向转运至肝脏后在细胞色素P450超家族（cytochromeP450proteins,CYP）的作用下分解成胆汁酸或类固醇激素。胆固醇的分解代谢则受精脒／精胺-N1-乙酰基转移酶、Prospero相关同源蛋白1和Daxx等的严密调控;胆固醇逆向转运是防止动脉粥样硬化斑块和坏死中心形成的关键因素。肿瘤坏死因子α和红细胞很可能在巨噬细胞介导的胆固醇逆向转运中起着非常重要的作用。     

何首乌饮对运动疲劳大鼠睾丸组织P450胆固醇侧链裂解酶和类固醇激素急性调节蛋白的影响

目的 探讨何首乌饮对运动疲劳大鼠睾丸组织细胞色素P450胆固醇侧链裂解酶(P450scc)和类固醇激素急性调节蛋白(StAR)的影响.方法 60只雄性SD大鼠,随机分为安静对照组(A组)、安静何首乌饮组(B组)、模型组(C组)、自然恢复组(D组)、何首乌饮治疗组(E组);何首乌饮预防组(F组),每组10只.C、D、E和F组大鼠复制运动疲劳动物模型,其中F组每天训练前给何首乌饮20g/(kg·d)(含生药4.8kg/L)灌胃60 d.模型成功后E组给何首乌饮20 g/(kg·d)(含生药4.8kg/L)灌胃治疗60 d.采用美国Beckmancoulter Unicel Dxl 800仪器测定睾酮水平; 采用RT-PCR、Western blotting和免疫组织化学法检测各组睾酮合成限速酶P450scc和StAR的表达变化.结果 P450scc免疫组织化学阳性颗粒主要表达于间质细胞及精母细胞,B组和F组表达最强,C组最弱,与其余各组相比差异有统计学意义.P450scc蛋白和mRNA表达变化为B、F组明显高于E、D和A组(P<0.05),C组明显低于A组(P<0.05),A组和D组以及B组和F组两两之间差异无显著性;StAR免疫组织化学阳性颗粒主要表达于睾丸间质细胞胞质,阳性强度表现为E组和F组最强,C组最弱.StAR蛋白和mRNA表达变化为E和F组明显高于A、D组(P<0.05),C组明显低于A组(P<0.05),A、D组之间无差异.结论 何首乌饮可以提高睾酮合成限速酶P450scc和StAR的表达.     

膜脂组成改变及内源性胆固醇合成抑制对淋巴细胞功能的影响

细胞通过低密度脂蛋白受体（ＬＤＬ－Ｒ）介导的ＬＤＬ内吞及自身合成而保持胞内胆固醇的平衡。本研究以人工脂双层膜与人外周血淋巴细胞孵育，将外源性胆固醇导入细胞内，同时用ＨＭＧ－ＣｏＡ还原酶抑制剂抑制内源性胆固醇合成。结果显示，随细胞胆固醇含量升高，有丝分裂期细胞增多，细胞增殖转化能力增强。用Ｌｏｖａｓ－ｔａｔｉｎ抑制内源性胆固醇合成，淋巴细胞大部分受阻于Ｇ０／Ｇ１期，细胞增殖活性降低，且这种抑制作用不能被外源性重组ＩＬ－２所逆转。膜胆固醇过高，淋巴细胞功能反而降低。淋巴细胞活化中期标志物ＣＤ７１分子在膜上的表达及其与配体的结合容量也受细胞胆固醇含量调节。     

The role of the intestinal mucosa in cholesterol metabolism: its relation to plasma and luminal cholesterol

Interrelationships of cholesterol in the intestinal mucosa, lumen, and plasma were studied in three groups of rats, i.e., fed a sterol-free diet, a 2% cholesterol diet, and a sterol-free diet followed by biliary diversion. All rats received an intracardiac injection of cholesterol-4-¹⁴C and were sacrificed sequentially. Amounts and specific activities (SA) of cholesterol in the plasma, mucosa, and luminal contents were determined and the following results obtained. (1) Plasma cholesterol SA was greater than mucosal cholesterol SA which in turn was greater than luminal cholesterol SA suggesting that there were two pools of cholesterol in the mucosa: one was active in cholesterol synthesis, while the other was not. (2) Without cholesterol feeding, 79% of the cholesterol in the active mucosa was derived from de novo synthesis which contributed 77% of the fecal cholesterol. Transport of cholesterol from mucosa to lumen was not merely by desquamation of epithelium but primarily by active secretion. (3) Cholesterol feeding did not affect the mucosal cholesterol content, nor its SA and transport to the lumen. (4) Expansion of the cholesterol pool in active mucosa and increase of luminal cholesterol content were found throughout the intestinal tract as a consequence of biliary diversion.     

Shunts,channels and lipoprotein endosomal traffic: a new model of cholesterol homeostasis in the hepatocyte

The liver directs cholesterol metabolism in the organism. All the major fluxes of cholesterol within the body involve the liver: dietary cholesterol is directed to the liver; cholesterol from peripheral cells goes to the liver; the liver is a major site of cholesterol synthesis for the organism; cholesterol is secreted from the liver within the bile, within apoB lipoproteins and translocated to nascent HDL. The conventional model of cholesterol homeostasis posits that cholesterol from any source enters a common, rapidly exchangeable pool within the cell, which is in equilibrium with a regulatory pool. Increased influx of cholesterol leads rapidly to decreased synthesis of cholesterol. This model was developed based on in vitro studies in the fibroblast and validated only for LDL particles. The challenges the liver must meet in vivo to achieve cholesterol homeostasis are far more complex. Our model posits that the cholesterol derived from three different lipoproteins endosomes has three different fates: LDL-derived cholesterol is largely recycled within VLDL with most of the cholesterol shunted through the hepatocyte without entering the exchangeable pool of cholesterol; high density lipoprotein-derived CE is transcytosed into bile; and chylomicron remnant-derived cholesterol primarily enters the regulatory pool within the hepatocyte. These endosomal channels represent distinct physiological pathways and hepatic homeostasis represents the net result of the outcomes of these distinct channels. Our model takes into account the distinct physiological challenges the hepatocyte must meet, underlie the pathophysiology of many of the apoB dyslipoproteinemias and account for the sustained effectiveness of therapeutic agents such as statins.     

Enhanced placental cholesterol efflux by fetal HDL in Smith-Lemli-Opitz syndrome

Previous studies from this laboratory have shown that maternal-derived cholesterol can be effluxed from trophoblasts to fetal HDL and plasma. We had the opportunity to study for the first time the ability of HDL and plasma from a fetus with the Smith-Lemli-Opitz syndrome (SLOS) to efflux cholesterol from trophoblasts. It was unclear whether cholesterol could be effluxed to fetuses with SLOS since lipoprotein levels are often very low. To answer this question, cord blood was collected from the placentas of an SLOS fetus and unaffected fetuses just after delivery. Plasma cholesterol concentrations were very low in the affected fetus; cholesterol, 7-dehydrocholesterol, and 8-dehydocholesterol concentrations were 14.1, 4.5, and 5.2 mg/dl, respectively. The HDL from the fetal SLOS effluxed approximately 50% more cholesterol from a trophoblast cell line, were smaller in size, and had a lower cholesterol to phospholipid ratio as compared to HDL from unaffected fetuses or adults. Plasma from the SLOS fetus effluxed cholesterol to a similar percentage as unaffected fetal plasma or adult plasma, possibly due to fewer HDL particles as demonstrated in previous SLOS patients. These novel data demonstrate that the cholesterol-deficient SLOS fetus is able to obtain cholesterol from trophoblasts at a time when cholesterol is playing a critical role in development, and has implications for design of treatments for cholesterol deficiency syndromes as well as understanding of prenatal cholesterol transport in humans.     

Cell cholesterol esters and high-density lipoprotein plasma levels during liver hyperplasia in choline-fed male and female rats

Sexual dimorphism exists in the response of rats to lead nitrate, liver hyperplasia occuring earlier and being more pronounced in males. Excess dietary choline in females shifted the growth pattern towards that of males. To determine whether phosphatidylcholine-induced growth modulations could be related to a derangement of cholesterol metabolism, liver accumulation of cholesterol esters and plasma lipoprotein patterns were investigated. In males, lead-induced liver hyperplasia was associated with increased total cholesterol hepatic content, accumulated cholesterol esters and reduced concentration of plasma High Density Lipoprotein (HDL) cholesterol. Females were less responsive to the liver mitogenic signal of lead nitrate; there was no elevation of cholesterol content nor any marked accumulation of cholesterol esters. This is consistent with the lack of change in the plasma levels of HDL cholesterol. Continuous choline feeding displaced the liver cholesterol ester pattern and plasma HDL cholesterol levels in females, and in parallel that of DNA synthesis, towards those of males. Choline was not observed to have any effect in males. These results suggest that the derangement of phosphatidylcholine metabolism induces growth-related changes in cholesterol turnover; they are consistent with the proposal that the intracellular content of cholesterol esters may have a role in regulating liver growth rates.     

Effects of a high-fat,high-cholesterol diet on brain lipid profiles in apolipoprotein E ɛ3 and ɛ4 knock-in mice

Apolipoprotein E (ApoE) is important in facilitating the transport of lipids (cholesterol, phospholipids, and sulfatides) and plays a fundamental role in normal lipid metabolism. High cholesterol levels increases the risk of developing Alzheimer's disease. In this study, we investigated the effects of a high-fat high cholesterol (HFHC) diet on brain lipid profiles in 95 young and aged APOE ?3 and ?4 knock-in mice to determine whether diet leads to altered brain levels of a number of glycerophospholipids, sphingolipids, cholesterol precursors, cholesterol, cholesterol oxidation products, and cholesterol esters. The results in this study revealed significant changes in lipid levels. The HFHC-enriched diet influenced the levels of cholesterol esters. A sharp increase in cholesterol ester levels, particularly in the aged APOE ?4 diet-enriched group, might be suggestive of abnormal acyl-coenzyme A:cholesterol acyltransferase 1 (ACAT) activity and/or levels. Age exerts appreciable effects on the brain lipidome, especially with regard to polar lipid species.     

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.     

Effect of combined clofibrate-cholestyramine treatment on serum and tissue cholesterol pools and on cholesterol synthesis in hypercholesterolemic swine.

The effect of clofibrate on whole-body cholesterol synthesis was studied in cholestyramine-treated hypercholesterolemic male Yorkshire swine and swine with normocholesterolemia or mild hypercholesterolemia.Daily whole-body synthesis rates were calculated by methods developed for the non-steady-state condition using various parameters of cholesterol balance; dietary cholesterol intake, fecal excretion of steroids, and cholesterol retention or loss in the body.After 16 days of treatment, the cholestyramine group showed reductions in serum cholesterol level and carcass cholesterol concentration, and increases in fecal steroid excretion and whole-body cholesterol synthesis, as compared with pretreatment values. The group which received both cholestyramine and clofibrate showed the same changes in all parameters listed above, but showed a greater reduction in serum cholesterol levels and greater increases in fecal excretion and whole-body cholesterol synthesis as compared with the group receiving cholestyramine alone.Unfortunately for the therapeutic implications, the increased output of steroids resulting from treatment with the combination of the two drugs was largely offset by a corresponding increase in cholesterol synthesis. The increase in synthesis might have been caused by a direct effect of clofibrate on the biosynthetic process. However, it seemed more likely that the increased synthesis was secondary to the increased output of steroids.The effect of clofibrate alone in hypercholesterolemic swine treated for 64 days revealed restraint in increase of serum cholesterol levels as compared to untreated controls, and an increase in total steroid excretion. No reduction in the whole-body cholesterol synthesis was observed in the clofibrate-treated group.In the other experiment, clofibrate even under mildly hypercholesterolemic or normocholesterolemic conditions did not result in a reduction of whole-body cholesterol synthesis, although serum cholesterol levels were reduced under both conditions.     

Dietary cholesterol and human coronary heart disease. The epidemiologic evidence

For decades, dietary cholesterol has been recognized as the "materia peccans" (Anitschkow) for the induction of atherosclerosis in animals. In rabbits, chickens, and monkeys, long-term feeding of small amounts of cholesterol leads to atherosclerosis despite little or no rise in serum total cholesterol, indicating an independent contribution of dietary cholesterol to atherogenesis over-and-above its influence on serum cholesterol, possibly through effects on serum cholesterol fractions (eg, increased low-density lipoprotein-cholesterol and decreased high-density lipoprotein-cholesterol). In humans, ingestion of dietary cholesterol raises serum cholesterol, largely through its effect on low-density lipoprotein-cholesterol. Over the range of intake in usual American diets, this effect is substantial, eg, with 300 mg of cholesterol intake per 1000 kcal, rather than 100, serum cholesterol is on average about 6% to 7% higher, equivalent to a 12% to 14% greater risk of coronary heart disease (CHD). In international studies based on the Food and Agriculture Organization and the World Health Organization (Geneva) data, mean per capita dietary cholesterol levels are consistently related to CHD mortality rates. In addition, since 1981, four prospective within-population studies have shown that dietary cholesterol intake of individuals is significantly related to their long-term CHD risk, independent of and in addition to serum cholesterol, blood pressure, and cigarette use. On average, a 200-mg/1000 kcal higher intake of cholesterol at baseline was associated with a 30% higher CHD rate (95% confidence interval, 1.1 to 1.5). Conversely, lower intakes of cholesterol were associated with significantly lower risks of CHD, and of all causes mortality as well. For example, with 19 years of follow-up in the Chicago Western Electric Study, a 200-mg/1000 kcal habitual lower cholesterol intake was associated with a 37% lower risk of death from any cause, equivalent to a life expectancy longer by 3.4 years. The importance of a low-dietary cholesterol intake for prevention of CHD merits increased emphasis.     

Characteristics of cholesterol absorption by human gall bladder: relevance to cholesterolosis.

The characteristics of cholesterol uptake by 83 human gall bladders (obtained at cholecystectomy) were studied with a modified Ussing technique. Real and artificial biles labelled with 14C-cholesterol and 3H-dextran (the latter to correct for adherent mucosal bile) were used; all gall bladders absorbed cholesterol (average 3.5 nmol/cm2/minute). Recovery of the absorbed cholesterol from the tissue showed that about 4% was esterified over 60 minutes. In artificial bile the rate of absorption of cholesterol increased as the bile saturation index rose, but became constant once supersaturation was achieved. In contrast, supersaturated real bile permitted greater absorption of cholesterol, possibly due to enhanced cholesterol solubilisation. Preincubation of gall bladder tissue in sodium cyanide (5 mM) caused a 30% reduction in cholesterol uptake indicating that, although absorption is predominantly a "passive" process, there is a partial "active" component. There were no pronounced differences in the rate of cholesterol absorption as gall bladders became more diseased, but there was a reduction in the amount of cholesterol ester formed.     

Factors associated with changes in serum cholesterol during a community-based hypertension programme

A cohort of 1019 male and 1232 female hypertensives, aged 25-59 years, based on a random population sample, was followed for five years during a community-based cardiovascular prevention programme. A small mean reduction in serum cholesterol level was found. The observed changes in casual serum cholesterol values were partly due to the regression to the mean. The reductions were most marked in elderly people and in those with high baseline serum cholesterol values. The partial regressions of the cholesterol change were computed in subgroups by age, sex and baseline serum cholesterol level. Changes in weight in men and in age in women were the strongest independent predictors of the change in serum cholesterol. Changes in dietary fat intake were also associated with the change in serum cholesterol. Only a small part of the total variation in the change in serum cholesterol was explained by the regression models. The results indicate that reduction of the serum cholesterol level among hypertensive persons, especially men, was caused by changes in their dietary habits.