9758 例健康体检者血糖与血脂的关系分析

目的:探讨健康体检人群血糖与血脂现况及两者之间的相关性。方法:采集我院9758例健康体检者的空腹静脉血,检测其空腹血糖(FPG)、总胆固醇(TC)、甘油三酯(TG)、高密度脂蛋白(HDL-C)和低密度脂蛋白(LDL-C)水平,比较不同FPG水平组间各血脂水平,分析FPG水平与血脂的相关性。结果:各年龄组FPG、TC、TG、HDL-C和LDL-C水平差异均具有统计学意义(P0.05);FPG均与TC、TG和LDL-C水平呈现正相关(r=0.127,0.189,0.141,P0.005),而与HDL-C呈现负相关(r=-0.112,P0.005);根据FPG水平由高到低分为糖尿病(DM)组,血糖调节受损(IFG)组及血糖正常组,其中对TC和LDL-C水平异常率而言,IFG组DM组血糖正常组;对TG、HDL-C水平异常率而言,DM组IFG组血糖正常组。结论:健康人群中血糖和血脂水平呈现一定的相关性,两者的水平异常会增加慢性疾病的发生风险。     

妊娠合并乙型肝炎患者血脂及雌激素水平检测的临床意义

目的:探讨妊娠合并乙型肝炎患者血脂及雌激素水平检测的临床意义。方法:选择2014年8月到2017年4月我院收治的妊娠合并乙型肝炎孕妇80例作为观察组,同期选择无乙型肝炎的80例孕妇作为对照组,比较两组的血清HDL-C、TC、TG、LDL-C及雌激素水平,对比两组不同妊娠结局血脂和血清雌激素水平,并以妊娠不良结局作为因变量,以收集的资料、血脂及雌激素水平作为自变量,分析妊娠合并乙型肝炎患者妊娠不良结局的危险因素。结果:与对照组相比,观察组血清LDL-C、TC、TG含量均显著升高,而HDL-C含量明显降低(P0.05)。观察组与对照组的血清雌激素含量分别为154.20±10.82 pmol/L和88.14±8.98pmol/L,观察组明显高于对照组(P0.05)。与对照组相比,观察组剖宫产、产后出血、新生儿窒息、胎儿窘迫、妊娠期高血压疾病的发生率均显著增高(P0.05)。观察组和对照组中妊娠不良结局患者的血清TC、TG和LDL-C含量都明显高于妊娠正常结局患者,而HDL-C含量明显低于妊娠正常结局患者。LDL-C、雌激素、年龄、乙肝发病年限为导致妊娠合并乙型肝炎患者妊娠不良结局的危险因素(P0.05)。结论:妊娠合并乙型肝炎患者妊娠不良结局的发生率较高,且伴随有血脂异常与雌激素高表达,二者与妊娠合并乙型肝炎的不良预后相关。     

脑梗塞患者血清hs-CRP、TNF-α、血脂水平的变化及其临床意义

目的:观察脑梗塞患者血清超敏C反应蛋白(hs-CRP)、肿瘤坏死因子(TNF-α)及血脂水平的变化,并探讨其临床意义.方法:选择我院2010年6月～2012年6月收治的86例急性脑梗塞患者(轻型脑梗塞组27例、中型脑梗塞组34例、重型脑梗塞组25例)为实验组和同期40例健康体检者为对照组,检测和比较两组血清超敏C反应蛋白(hs-CRP)、肿瘤坏死因子(TNF-α)、甘油三酯(TG)、总胆固醇(TC)、低密度脂蛋白(LDL-C)和高密度脂蛋白(HDL-C)的水平,并进行相关性分析.结果:与健康对照组比较,实验组血清hs-CRP、TNF-α及TC、TG、LDL-C水平显著升高,而血清HDL-C水平显著降低,差异均具有统计学意义(P＜0.05).与轻型脑梗塞组比较,中、重型脑梗塞组血清hs-CRP、TNF-α及TC、TG、LDL-C等血脂水平均显著升高,而血清HDL-C水平显著降低,其异均具有统计学意义(P＜0.05);与中型脑梗塞组比较,重型脑梗塞组血清TC、TG、LDL-C等血脂水平均显著升高,血清HDL-C水平显著降低,其差异亦均具有统计学意义(P＜0.05).脑梗塞患者血清hs-CRP与TNF-α水平呈显著正相关(P＜0.05),与TC、TG、LDL-C等血脂水平均亦呈显著正相关(P＜0.05),与血清HDL-C水平呈显著负相关(P＜0.05).脑梗塞患者血清hs-CRP、TNF-α水平与病情严重程度呈显著正相关(P＜0.05).结论:检测血清hs-CRP、TNF-α及血脂指标水平对评估脑梗塞患者病情具有重要的临床意义.     

甲状腺功能减退患者血清甲状腺激素、同型半胱氨酸及血脂水平测定的临床意义

目的:探讨甲状腺功能减退患者血清同型半胱氨酸(Hcy)、甲状腺激素(TH)及血脂水平测定的临床意义。方法:选取2016年2月-2017年2月期间我院收治的甲状腺功能减退患者101例为观察组,选取同期于我院体检的健康志愿者80例为对照组。检测所有研究对象甲状腺素(FT4)和三碘甲状腺原氨酸(FT3)、Hcy及血脂[甘油三酯(TG)、总胆固醇(TC)、高密度脂蛋白胆固醇(HDL-C)、低密度脂蛋白胆固醇(LDL-C)]变化水平。比较观察组治疗前后、对照组与观察组治疗前FT3、FT4、Hcy及血脂水平,采用Pearson相关性分析血清Hcy与FT3、FT4、血脂水平的相关性。结果:观察组患者治疗后FT3、FT4均较治疗前升高,Hcy、TC、LDL-C均较治疗前降低(P0.05),而观察组患者治疗前后TG、HDL-C比较差异无统计学意义(P0.05)。观察组治疗前FT3、FT4、HDL-C水平明显低于对照组,而Hcy、TG、TC、LDL-C则明显高于对照组(P0.05)。经Pearson相关性分析显示,甲状腺功能减退患者Hcy与FT3、FT4呈负相关(P0.05),与TC、TG呈正相关(P0.05),而与LDL-C、HDL-C无相关性(P0.05)。结论:甲状腺功能减退患者的FT3、FT4、Hcy及血脂水平表达异常,且Hcy与FT3、FT4、血脂水平密切相关,临床上可通过监测甲状腺功能减退患者的上述指标,有助于评估患者的病情程度。     

甲状腺功能异常患者血清同型半胱氨酸及血脂水平检测的临床意义

目的:研究原发性甲状腺功能减退症患者和甲状腺功能亢进患者血清同型半脱氨酸(Hey)、血脂水平与心血管疾病的关系.方法:检测29例原发性甲减者、35例甲亢患者以及30例健康体检者(对照组)的空腹血清游离三碘甲状腺原氨酸(FT3)、游离甲状腺素(FT4)、Hcy、甘油三酯(TG)、总胆固醇(Tch)、高密度脂蛋白胆固醇(HDL-C)、低密度脂蛋白胆固醇(LDL-C)水平,并对其进行相关分析.结果:原发性甲减患者Hcy、TG、Tch、LDL-C水平明显高于对照组(p＜0.01、0.01、0.01、0.01),而HDL-C水平却与对照组相比明显降低(p＜0.01);相关分析表明,甲减患者Hey与FT3、FT4水平间呈显著负相关(r=-0.432、-0.354,p＜0.01、0.01),与TG、Tch水平呈显著正相关(r=0.339、0.452,p＜0.01、0.01);而与HDL-C、LDL-C均无相关性.甲亢组Hcy和Tch水平较正常对照组明显降低(p＜0.01、0.01),Hcy与FT4水平间呈显著负相关(r=-0.408,p＜0.01).结论:血清同型半胱氨酸水平可能对判断甲状腺功能有辅助作用;甲状腺激素水平影响了Hcy及血脂水平的代谢;血清Hcy水平升高是甲减患者易患心血管疾病的危险因素.     

高血压患者颈动脉粥样硬化与血脂、血压和血尿酸水平的相关性分析

目的:探讨高血压患者颈动脉粥样硬化(CAS)与血脂、血压以及血尿酸水平的相关性。方法:选择2017年2月至2018年8月在我院就诊的高血压患者117例作为研究组,另选择同期在我院进行体检的健康志愿者50例作为对照组。采用彩色多普勒超声诊断仪测定所有受试者的颈动脉内中膜厚度(IMT),并根据研究组患者的颈动脉IMT将其分为斑块组(IMT≥1.3 mm,33例)、IMT增厚组(1.0 mm≤IMT1.3 mm,49例)和IMT正常组(IMT1.0 mm,35例)。比较研究组与对照组受试者IMT,同时分别比较研究组与对照组受试者以及不同IMT高血压患者平均收缩压(SBP)、平均舒张压(DBP)、血清总胆固醇(TC)、甘油三酯(TG)、低密度脂蛋白胆固醇(LDL-C)、高密度脂蛋白胆固醇(HDL-C)以及尿酸水平,并采用Pearson相关性分析法分析高血压患者IMT与各指标的相关性。结果:与对照组比较,研究组IMT、SBP、DBP、TC、TG、LDL-C、血尿酸水平升高,HDL-C水平降低,差异均有统计学意义(P0.05)。斑块组患者SBP、DBP、TC、TG、LDL-C、血尿酸水平高于IMT增厚组和IMT正常组,HDL-C水平低于IMT增厚组和IMT正常组,差异均有统计学意义(P0.05);IMT增厚组患者SBP、DBP、TC、TG、LDL-C、血尿酸水平高于IMT正常组,HDL-C水平低于IMT正常组,差异均有统计学意义(P0.05)。Pearson相关性分析显示,高血压患者的IMT与SBP、DBP、TC、TG、LDL-C、血尿酸均呈正相关,与HDL-C呈负相关(P0.05)。结论:高血压患者IMT与血脂、血压和血尿酸水平均有明显相关性,血压、血脂、血尿酸参与了高血压患者CAS的发生与发展。     

肾移植术后患者同型半胱氨酸、肾功能和血脂水平的变化及其相关性分析

目的:分析肾移植术后患者血清的同型半胱氨酸(Hcy)、肾功能和血脂水平的变化和相关性,探讨其在肾移植术后评价肾功能的应用价值。方法:将2013年10月~2016年9月就诊于我院确诊慢性肾衰并进行肾移植手术的300例术后随访患者作为观察组,选择同期健康志愿者100例作为对照组。检测并比较两组Hcy、总胆固醇(TC)、三酰甘油(TG)、低密度脂蛋白胆固醇(LDL-C)、高密度脂蛋白胆固醇(HDL-C)水平。根据观察组患者Hcy水平的不同将其分成Hcy正常组与Hcy异常组,并对比两组患者的血脂指标水平;测定半胱氨酸蛋白抑制剂C(CysC)的水平并计算肾小球滤过率(eGFR);对观察组血清Hcy与eGFR值、血脂指标水平进行相关性分析,并采用Logistic回归分析分析观察组肾移植术后eGFR下降的影响因素。结果:观察组患者的血清Hcy、TC、TG、HDL-C、LDL-C水平均明显高于对照组(P0.05)。Hcy异常组血清LDL-C水平明显高于Hcy正常组,而HDL-C水平明显低于Hcy正常组(P0.05)。观察组患者血清Hcy与eGFR、HDL-C水平呈负相关关系(r=-0.573、-0.414,P0.05);与TG水平呈正相关(r=0.432,P0.05),与TC、LDL-C无相关(P0.05)。多元Logistic回归分析显示,Hcy、TG、LDL-C水平均与患者eGFR下降有关(P0.05)。结论:在肾移植术后,慢性肾衰患者的TG、LDL-C、Hcy水平均升高,且伴有eGFR水平的降低;肾移植术后肾功能的改变与血清TG、LDL-C、Hcy水平相关;检测肾移植患者血脂指标、Hcy的水平可以评估移植肾功能受损情况。     

成人原发肾病综合征患者血尿酸与血脂代谢的关系

目的:研究成人原发肾病综合征(PNS)患者高尿酸血症的患病率及其与血脂代谢的关系。方法:将109例成人PNS患者根据其尿酸水平分为高尿酸血症组与血尿酸正常组,检测患者的血脂、血清脂蛋白、ALB及24小时尿蛋白定量,分析成人PNS患者高尿酸血症的患病率,比较高尿酸血症组与血尿酸正常组PNS患者的一般情况及血脂水平,并分析PNS患者血尿酸水平的相关因素。结果:成人PNS患者高尿酸血症的发病率为24.77%;高尿酸血症组患者TG及24小时尿蛋白定量水平明显高于血尿酸正常组(P0.01),两组患者TC、LDL-C、HDL-C、Apo AI及Apo B比较差异无统计学意义(P0.05);成人PNS患者血尿酸水平与TG及24小时尿蛋白定量水平呈正相关(r=0.350,P=0.001;r=0.533,P=0.014),与TC、LDL-C、HDL-C及ALB无明显相关性(P0.05)。结论:成人PNS患者高尿酸血症的发生率较高,高尿酸血症患者具有更高的TG及尿蛋白水平,且成人PNS患者血尿酸水平与TG及24小时尿蛋白定量具有相关性,应高度重视成人PNS患者的血尿酸水平。     

冠心病患者的血脂、胆红素、UA及Fib水平变化及临床意义

目的:研究冠心病(CHD)患者的血脂、胆红素、血尿酸(UA)及纤维蛋白原(Fib)水平变化及临床意义。方法:选取2014年4月到2015年4月我院收治的CHD患者110例(研究组),另选取同期健康体检者110例(对照组),检测两组受检者血清总胆固醇(TC)、甘油三酯(TG)、高密度脂蛋白胆固醇(HDL-C)、低密度脂蛋白胆固醇(LDL-C)、直接胆红素(DBIL)、间接胆红素(IBIL)、总胆固醇(TBIL)、UA以及Fib水平。结果:研究组TC、TG、LDL-C、UA以及Fib水平均显著高于对照组,两组比较差异具有统计学意义(P0.05);研究组HDL-C、DBIL、IBIL以及TBIL均显著低于对照组,两组比较差异具有统计学意义(P0.05)。结论:血脂水平异常,胆红素水平降低,UA以及Fib水平增高与CHD的发病有关。     

阿托伐他汀对急性心肌梗塞患者hs-CRP及血脂水平的影响

目的:研究阿托伐他汀对急性心肌梗塞患者超敏C反应蛋白(hs-CRP)及血脂水平的影响。方法:选取2012年1月到2015年1月我院收治的急性心肌梗塞患者80例,按照随机数字表法将患者分为研究组和对照组,每组40例,对照组给予常规治疗,研究组在对照组的基础上给予阿托伐他汀治疗,比较治疗前后两组hs-CRP和总胆固醇(TC)、甘油三酯(TG)、低密度脂蛋白胆固醇(LDL-C)和高密度脂蛋白胆固醇(HDL-C)水平。结果:两组治疗后hs-CRP较治疗前显著降低(P0.05),且研究组治疗后hs-CRP显著低于对照组,(P0.05);治疗后两组TC、TG和LDL-C显著低于治疗前,HDL-C显著高于治疗前(P0.05),且治疗后研究组TC、TG和LDL-C显著低于对照组,HDL-C显著高于对照组(P0.05)。结论:阿托伐他汀治疗急性心肌梗塞具有较好的效果,能有效降低hs-CRP水平,改善患者血脂水平。     

Study of the components of reverse cholesterol transport in lecithin:cholesterol acyltransferase deficiency

Enzymatic and lipid transfer reactions involved in reverse cholesterol transport were studied in healthy and lecithin:cholesterol acyltransferase (LCAT), deficient subjects. Fasting plasma samples obtained from each individual were labeled with [3H]cholesterol and subsequently fractionated by gel chromatography. The radioactivity patterns obtained corresponded to the elution volumes of the three major ultracentrifugally isolated lipoprotein classes (very low density lipoproteins (VLDL), low density lipoproteins (LDL), and high density lipoproteins (HDL)). In healthy subjects, the LCAT activity was consistently found in association with the higher molecular weight portion of HDL. Similar observations were made when exogenous purified LCAT was added to the LCAT-deficient plasma prior to chromatography. Incubation of the plasma samples at 37 degrees C resulted in significant reduction of unesterified cholesterol (FC) and an increase in esterified cholesterol (CE). Comparison of the data of FC and CE mass measurements of the lipoprotein fractions from normal and LCAT-deficient plasma indicates that: (i) In normal plasma, most of the FC for the LCAT reaction originates from LDL even when large amounts of FC are available from VLDL. (ii) The LCAT reaction takes place on the surface of HDL. (iii) The product of the LCAT reaction (CE) may be transferred to either VLDL or LDL although VLDL appears to be the preferred acceptor when present in sufficient amounts. (iv) CE transfer from HDL to lower density lipoproteins is at least partially impaired in LCAT-deficient patients. Additional studies using triglyceride-rich lipoproteins indicated that neither the capacity to accept CE from HDL nor the lower CE transfer activity were responsible for the decreased amount of CE transferred to VLDL and chylomicrons in LCAT-deficient plasma.     

兔主动脉平滑肌细胞低密度脂蛋白受体相关蛋白(LRP)的诱导表达调节

在兔主动脉平滑肌细胞 ( SMC)培养基中分别加入正常低密度脂蛋白 ( N- LDL)、氧化低密度脂蛋白 ( ox- LDL)、正常极低密度脂蛋白 ( N- VLDL)、氧化极低密度脂蛋白 ( ox- VLDL)和 β-极低密度脂蛋白 (β- VLDL )培养 2 4 h后 ,用定量 RT- PCR和配体结合实验检测平滑肌细胞 LRP的m RNA和蛋白质水平的表达 .结果表明 :五种脂蛋白均能在转录和翻译水平诱导兔主动脉平滑肌细胞的 LRP表达 ,尤以富含胆固醇的 N- LDL ,ox- LDL和β- VLDL的刺激作用更明显 .用胆固醇单独或与脂蛋白共同温育 SMC后 ,发现胆固醇本身可促进 SMC的 LRP蛋白水平的表达 ,脂蛋白与胆固醇的共同刺激作用更为显著 .结果提示 :上述五种脂蛋白对 SMC上 LRP的表达有上调作用 ,其机制可能主要是通过其中的胆固醇来实现的 .     

Neutral glycosphingolipids of serum lipoproteins in Fabry's disease.

The neutral glycosphingolipid compositions of lipoprotein fractions of serum from eight healthy male volunteers and three patients with Fabry's disease were determined. Four fractions were studied: very low density lipoprotein (VLDL, d less than 1.006); low density lipoprotein (LDL, d 1.006-1.063); high density lipoprotein (HDL, d 1.063-1.21); and ultracentrifugal residue (Residue, d less than 1.21). All lipoprotein fractions contained the four major neutral glycosphingolipids (glucosylceramide, lactosylceramide, galactosylgalactosylglucosylceramide and N-acetylgalactosaminylgalactosylgalactosylglucosylceramide). The LDL and HDL, however, accounted for most of the total glycosphingolipid (69 and 20%, respectively); only small amounts were demonstrated in the VLDL and Residue. The relative distributions of the glycosphingolipids within the LDL and HDL fractions were similar to the distribution in unfractionated serum. Galactosylgalactosylglucosylceramide levels were 3-5 times normal in all three patients with Fabry's disease, and in two the distribution of the excess lipid among the major lipoprotein fractions was similar to that in the control group. In the third patient, who exhibited the presence of "sinking pre-beta lipoprotein", the amount of glycosphingolipid isolated with the HDL was greater than that in the LDL.     

Dietary lipids and blood cholesterol: quantitative meta-analysis of metabolic ward studies.

OBJECTIVE: To determine the quantitative importance of dietary fatty acids and dietary cholesterol to blood concentrations of total, low density lipoprotein, and high density lipoprotein cholesterol. DESIGN: Meta-analysis of metabolic ward studies of solid food diets in healthy volunteers. SUBJECTS: 395 dietary experiments (median duration 1 month) among 129 groups of individuals. RESULTS: Isocaloric replacement of saturated fats by complex carbohydrates for 10% of dietary calories resulted in blood total cholesterol falling by 0.52 (SE 0.03) mmol/l and low density lipoprotein cholesterol falling by 0.36 (0.05) mmol/l. Isocaloric replacement of complex carbohydrates by polyunsaturated fats for 5% of dietary calories resulted in total cholesterol falling by a further 0.13 (0.02) mmol/l and low density lipoprotein cholesterol falling by 0.11 (0.02) mmol/l. Similar replacement of carbohydrates by monounsaturated fats produced no significant effect on total or low density lipoprotein cholesterol. Avoiding 200 mg/day dietary cholesterol further decreased blood total cholesterol by 0.13 (0.02) mmol/l and low density lipoprotein cholesterol by 0.10 (0.02) mmol/l. CONCLUSIONS: In typical British diets replacing 60% of saturated fats by other fats and avoiding 60% of dietary cholesterol would reduce blood total cholesterol by about 0.8 mmol/l (that is, by 10-15%), with four fifths of this reduction being in low density lipoprotein cholesterol.     

中老年食蟹猴群中糖尿病相关基因的表达状态

该研究选择10岁以上健康中老年食蟹猴138只,按空腹血糖值(FPG)将其分为低血糖组、血糖正常组和高血糖组。采用全自动血液生化仪分别检测各组血清中总胆固醇(TCHO)、甘油三酯(TG)、高密度脂蛋白胆固醇(HDL-C)和低密度脂蛋白胆固醇(LDL-C)的水平变化;采用荧光定量PCR分析食蟹猴外周血白细胞中37个糖尿病相关基因的mRNA表达情况。结果表明,血清血脂水平HDL-C、LDL-C、TCHO和TG都与FPG分组无显著相关性(P>0.05),而外周血白细胞中ACE、ACLY、PRKCB1、SLC2A4、SNAP23、VAPA、IGF2BP2、IFNG8个基因的mRNA表达水平随FPG的升高而显著上调(P<0.05)。     

Inhibition of proteolytic degradation of low density lipoprotein in human fibroblasts by chloroquine, concanavalin A, and Triton WR 1339.

The proteolytic degradation of 125I-labeled low density lipoprotein by monolayers of cultured human fibroblasts was prevented by exposure of the cells to chloroquine, an agent that has been reported previously to inhibit lysosomal degradative processes. Chloroquine did not inhibit the binding of low density lipoprotein to its cell surface receptor. However, the two regulatory actions that normally follow low density lipoprotein binding to its receptor, namely suppression of 3-hydroxy-3-methylglutaryl coenzyme A reductase activity and stimulation of cholesteryl ester formation, were both prevented when degradation of the lipoprotein was inhibited by chloroquine. Two other agents affecting lysosomal function, Triton WR 1339 and concanavalin A, also inhibited the proteolytic degradation of low density lipoprotein in intact fibroblasts and simultaneously prevented low density lipoprotein-mediated suppression of 3-hydroxy-3-methylglutaryl coenzyme A reductase activity and stimulation of cholesteryl ester formation. Unlike chloroquine, however, these two agents also affect the binding of low density lipoprotein to the cells. The inhibitory action of chloropuine, concanavalin A, and Triton WR 1339 could each be reversed by removal of the agent from the culture medium. These in vivo culture data, together with the observation that cell-free extracts of fibroblasts maximally degrade 125I-labeled low density lipoprotein at pH 4 and do not form acid-soluble material above pH 6, are consistent with the hypothesis that the proteolytic degradation of low density lipoprotein by monolayers of fibroblasts occurs within lysosomes. The data also suggest that normal lysosomal function is required in order for low density lipoprotein to regulate cholesterol synthesis and cholesteryl ester formation in the fibroblast system.     

Antimicrobial activity of lipoprotein particles containing apolipoprotein Al

Human plasmain vitro inhibits the growth of coagulase negative staphylococci,S. epidermidis, which may be pathogenic in the immunocompromised host. To determine the antimicrobial components, serum was fractionated by column chromatography, which revealed that elution areas where lipoproteins can be yielded had high antimicrobial activity againstS. epidermidis. Therefore, lipoprotein fractions, including very low density lipoprotein (VLDL), low density lipoprotein (LDL) and high density lipoprotein (HDL), were separated by ultracentrifugation and incubated withS. epidermidis. All 3 lipoprotein fractions suppressed bacterial growth within the first 3 h but VLDL enhanced bacterial growth after 9 h of incubation compared with the control. HDL, however, inhibited bacterial growth throughout 21 h of incubation.To confirm these results, serum from healthy volunteers was separated by ion exchange column chromatography and again by HPLC to purify the antimicrobial fraction. In the protein analysis with gradient polyacrylamide-SDS gel, apolipoprotein Al (apo Al), which is a major apolipoprotein of HDL, was detected in the antimicrobial fraction. Therefore, this fraction was loaded onto an immunoaffinity column coupled with the anti-apo Al monoclonal antibody (Mab). Unbound fraction had no antimicrobial activity, but anti-S. epidermidis activity was recovered from the bound fraction which consisted mainly of apo Al, All and apo C in protein composition.These results indicated that the antimicrobial activity was associated with the apo Al-containing lipoprotein particles (HDL). This property of HDL may directly affect bacterial growth and promote the self-defense mechanisms of normal and immunocompromised individuals.     

Comparative effects of khellin and timefurone on serum parameters in normal male cynomolgus monkeys

Timefurone and khellin (10 mg/kg/day, gavage, 14 days) significantly lowered low density lipoprotein cholesterol, high density lipoprotein cholesterol, and total cholesterol. Khellin-induced changes were significantly greater than those induced by timefurone. Neither drug altered body weights or clinical chemistry parameters. Monkeys treated with khellin, however, exhibited elevated levels of very low density lipoprotein cholesterol and marked emesis, while no changes were observed with timefurone. On the basis of these data, timefurone has a better therapeutic ratio and further study with this promising drug appears warranted.     

Effects of several common long chain fatty acids on the properties and lipid composition of the very low density lipoprotein secreted by the perfused rat liver.

1. Livers from normal fed male rats were perfused in vitro with a bloodless medium which contained intially 3% bovine serum albumin and 100 mg% glucose. Albumin alone, or myristate (14 : 0), palmitate (16 : 0), palmitoleate (16 : 1), stearate (18 : 0), oleate (18 : 1), or linoleate (18:2) was infused at a constant rate (496 mumol/4 h), as a complex with albumin, during the experiment. 2. The very low density lipoprotein secreted by the liver after infusion of unsaturated fatty acids (16 : 1, 18 :1, 18 : 2) has a faster rate-zonal mobility in the ultracentrifuge and is, therefore, probably a larger particle with fewer moles of phospholipid and cholesterol relative to triacyglycerol (triacyglycerol/phospholipids/cholesterol = 100/25.1/16.4) than the very low density lipoproteins produced after infusion of saturated (14 : 0, 16 : 0, 18 : 0) fatty acids (triacyglycerol/phospholipids/cholesterol = 100/30.1/19.1). The molar ratio of phosphoipids/cholesterol of the very low density lipoprotein was similar regardless of which fatty acid was infused. The predominant fatty acid of the very low density lipoprotein or hepatic triacyglycerol, in all cases, was the infused acid. 3. We conclude that free fatty acid regulates the quantity and proportions of triacyglycerol, phospholipids, and cholesterol secreted by the liver in the very low density lipoprotein, and therefore, may secondarily influence concentrations of lipids in the very low density lipoprotein and other plasma lipoproteins circulating in vivo.     

Distribution of apolipoprotein E in the plasma of insulin-dependent and noninsulin-dependent diabetics and its relation to cholesterol net transport

Noninsulin-dependent diabetics, whose plasma contained no detectable beta-VLDL (very low density lipoprotein), had a proportion (0.23 +/- 0.04) of plasma apolipoprotein E in the form of an abnormal lipoprotein not recognized by antibodies to apoB-100 from LDL (low density lipoprotein) or apoA-I from HDL (high density lipoprotein). This lipoprotein, abnormally rich in free cholesterol and apoE, had a calculated particle density within the low density lipoprotein range. It competed with LDL at the apoB,E receptor of normal fibroblasts and stimulated cholesteryl ester accumulation in mouse peritoneal macrophages. However, it did not compete with the binding of labeled rabbit beta-VLDL to macrophages. A much lower proportion of apoE (0.04 +/- 0.03) was in this form in the plasma of patients with insulin-dependent diabetes who had a comparable degree of hyperglycemia. The diabetic lipoprotein was absent in normoglycemic control subjects. The net transport of cholesterol from cell membranes to the plasma of noninsulin-dependent diabetics (and to a lesser extent, insulin-dependent diabetics) was inhibited relative to control values, and the magnitude of this inhibition was well correlated with the concentration of the abnormal lipoprotein of diabetes in plasma (r = 0.66 and 0.75, respectively). These findings suggest that diabetic plasma contains an abnormal and novel low density lipoprotein that mediates the abnormal cholesterol transport characteristic of human diabetes mellitus.