脂肪肝大鼠线粒体膜流动性改变及活血化瘀法防治的实验研究

目的:探讨脂肪肝大鼠线粒体膜流动性改变及活血化瘀法的防治作用.方法:采用高脂饲料辅以乙醇和CCl4复制脂肪肝大鼠模型,观察大鼠肝脏线粒体膜的流动性,肝组织中SOD、MDA含量及肝脂,血清肝功能,血脂等变化,并以活血化瘀法进行防治,观察其对上述指标的影响.结果:模型组肝线粒体膜流动性、SOD活性明显降低、而肝组织MDA含量、肝脂及血清ALT、AST、TG、TC显著升高,与正常组比较差异有显著性意义(P＜0.01);活血化瘀法能明显改善肝线粒体膜流动性,增强SOD活性,降低血脂、肝脂、MDA含量,改善肝功能(P＜0.05或P＜0.01).结论:脂肪肝大鼠肝脏脂质过氧化增强,线粒体膜流动性降低;活血化瘀法可通过减轻肝脏脂质过氧化并修复线粒体膜流动性,从而达到减轻肝脂变、保护肝功能的作用.     

消脂护肝方对非酒精性脂肪肝大鼠脂质过氧化的影响

目的:探讨中药"消脂护肝方"对非酒精性脂肪肝(NAEL)大鼠脂质过氧化(LP)的影响.方法:用CCl4和高脂饮食复合方法建立大鼠NAFL模型,造模期间给予中药"消脂护肝方"和西药"东宝肝泰"干预,6周后检测肝功能、血脂并观察肝组织病理变化,检测肝组织脂质含量和超氧化物歧化酶(SOD)、谷胱甘肽过氧化酶(GSH-PX)及丙二醛(MDA)的含量.结果:中药组和西药组肝组织病理改变较模型组明显减轻,肝组织脂质含量及MDA含量较模型组明显降低,SOD、GSH-PX含量则明显升高.结论:①消脂护肝方具有保护肝功能、降低血脂、抗肝脏脂质沉积的作用;②消脂护肝方具有减轻大鼠NAFL模型肝组织细胞LP反应的作用,对LP导致肝脏脂肪变性具有抑制作用.     

肝脂消煎剂对脂肪肝大鼠肝微粒体膜流动性及心肌黄酶、丙二醛的作用

目的 :探讨肝脂消煎剂治疗脂肪肝药效学机制。方法 :采用高脂饮食加白酒灌胃建立大鼠脂肪肝模型 ,以东宝肝泰作对照 ,观察肝脂消煎剂对脂肪肝大鼠肝微粒体膜流动性及心肌黄酶 (DTD)、丙二醛 (MDA)的影响。结果 :模型对照组 MDA与肝微粒体膜荧光偏振度较正常对照组明显增大 ,且两者成正相关 (r =0 .974 6 ) ,表示肝脏因脂质过氧化引起膜流动性降低 ;肝脂消煎剂能降低 MDA含量及荧光偏振度 ,拮抗膜流动性的下降 ,提高肝脏DTD活性 ,均明显优于东宝肝泰。结论 :肝脂消煎剂可抑制肝微粒体脂质过氧化 ,拮抗其膜流动性降低 ,具有良好的防治脂肪肝作用。     

保肝消脂冲剂对高糖高脂饲料诱导的大鼠非酒精性脂肪肝的治疗作用

[目的]观察保肝消脂冲剂对高糖高脂饲料诱导的大鼠非酒精性脂肪肝(NAFL)的治疗作用。[方法]雄性Wistar大鼠80只中20只作为正常对照组;其余60只用高糖高脂肪饲料喂养30d建立NAFL模型,造模成功后分组并给药治疗,连续给药8周。检测各组大鼠血清和肝脏中生化指标,做肝脏组织病理学检查。[结果]NAFL大鼠经保肝消脂冲剂治疗后,血清中三酰甘油(TG)含量和谷丙转氨酶活性显著降低(P<0.01);肝组织中TG、总胆固醇、丙二醛、游离脂肪酸含量减少,超氧化物歧化酶活力增加(P<0.01);肝细胞脂肪肝程度明显减轻,肝细胞坏死程度减轻。[结论]保肝消脂冲剂能降低NAFL大鼠血液和肝脏中TG含量,对NAFL有治疗作用,其作用机制可能与其抗氧化作用,减轻脂质过氧化引起的肝脏损伤,降低肝脏脂肪沉积有关。     

肝脂消煎剂对脂肪肝大鼠肝微粒体膜流动性及心肌黄酶、丙二醛的作用

目的探讨肝脂消煎剂治疗脂肪肝药效学机制.方法采用高脂饮食加白酒灌胃建立大鼠脂肪肝模型,以东宝肝泰作对照,观察肝脂消煎剂对脂肪肝大鼠肝微粒体膜流动性及心肌黄酶(DTD)、丙二醛(MDA)的影响.结果模型对照组MDA与肝微粒体膜荧光偏振度较正常对照组明显增大,且两者成正相关(r=0.974 6),表示肝脏因脂质过氧化引起膜流动性降低;肝脂消煎剂能降低MDA含量及荧光偏振度,拮抗膜流动性的下降,提高肝脏DTD活性,均明显优于东宝肝泰.结论肝脂消煎剂可抑制肝微粒体脂质过氧化,拮抗其膜流动性降低,具有良好的防治脂肪肝作用.     

肝细胞色素P450 2E1在大鼠非酒精性脂肪肝形成中的作用

目的 研究肝细胞色素P450 2E1在大鼠非酒精性脂肪肝形成中的作用。方法 Wistar大鼠40只，随机分为正常对照组和高脂饲料2、4、8和12周组(其中每组各8只)：HE染色光镜观察肝脏组织病理改变；硫代巴比妥酸法测定肝脏组织丙二醛(MDA)的含量变化：免疫组织化学和Westemblot方法研究高脂饲料诱导的大鼠脂肪肝形成中肝细胞色素P450 2E1表达变化。结果 高脂饲料组大鼠肝脏内MDA含量明显高于对照组，随时间延长，逐渐增加：随着脂肪肝程度的加重，MDA含量逐渐增强，肝细胞色素P450 2E1蛋白表达亦明显增强。结论 非酒精性脂肪肝大鼠肝细胞色素P450 2E1表达变化与脂肪肝引起的脂质过氧化损伤程度密切相关。     

壳聚糖和中药复方对实验性大鼠脂肪肝的防治作用

目的：观察壳聚糖和中药首乌、丹参、牛膝的复方对大鼠脂肪肝的预防作用。方法：在小剂量的四氯化碳直损伤的基础上,合并应用高脂饮食复制大鼠脂肪肝模型,同时分别给予不同浓度的药物,以肝脏的脂质含量为衡量指标,观察药物预防结果,结果：四氯化碳损伤肝脏合并高脂饮食可引起大鼠肝脏明显的脂肪变性,表现为肝组织甘油三酯（TG）、总胆固醇（TC）含量显著增加,SOD活性明显降低,镜检显示肝细胞肿胀,内部充满足大小不等的脂滴,而药物防治组大鼠与模型组相比肝组织TG、TC值显著降低,肝细胞的脂变程度明显小于模型组,表现为脂滴养活,脂变面积缩小,SOD活力逐渐升高并恢复正常,其改善程度随用药剂量的增加而增加,应用中、高剂量的药物还可使大鼠血清丙氨酸转氨酶活性明显降低,结论：药物对脂肪肝的形成具有明显的预防作用,其机理除了减少脂肪自肠道的吸收外,还可能有保护肝脏,提高肝抗氧化能力,促进其对脂质的氧化与转运功能的作用。     

脂肪肝与肝纤维化关系的实验研究

为探讨脂肪肝与肝纤维化的关系及其机制,建立Wistar大鼠高脂饮食和/或酒精、CCl_4性脂肪肝模型。结果表明,脂肪肝和肝纤维化是两种并无因果关系的病理学改变,致病因素的强度和作用时间共同决定肝纤维化的显型表达,并非肝组织脂肪本身,而是肝脂质过氧化终产物丙二醛含量与肝纤维化时x-SMA阳性细胞数以及肝胶原蛋白含量之间呈显著正相关,但肝内脂肪沉积可通过增强酒精、CCl_4等对肝脏脂质过氧化反应。促进肝纤维化的发生和发展。     

健肝消脂合剂对脂肪肝大鼠过氧化物的影响及肝脏病理学改变

[目的]进一步探讨健肝消脂合剂对高脂血症性脂肪肝大鼠肝脏脂变的改善及作用机制。[方法]采用高脂饮食建立营养性脂肪肝大鼠模型,设健肝消脂合剂大、小剂量治疗组和大、小剂量预防组,以东宝肝泰组（简称东宝组）、模型组、正常组为对照组,观察健肝消脂合剂对高脂血症性脂肪肝大鼠血清超氧化物歧化酶（SOD）、丙二醛（MDA）的影响及肝脏病理学的改变。[结果]模型组较正常血清MDA组显著升高,SOD显著降低（P〈0.01）;治疗组、预防组较模型组血清MDA显著降低,SOD升高（均P〈0.01）;模型组大鼠肝脏受损面积明显高于正常组（P〈0.01）;大、小剂量预防组和治疗组均明显低于模型组（P〈0.01）。[结论]健肝消脂合剂能有效地抑制肝细胞内氧应激-脂质过氧化损伤,显著改善脂肪肝病理变化;其作用机制可能通过减少脂质在肝脏沉积与减轻过氧化损伤改善脂肪肝。     

清肝降浊颗粒对酒精合并高脂饮食性脂肪肝大鼠的治疗作用

目的研究清肝降浊颗粒对酒精与高脂饲料联合诱导的大鼠脂肪肝是否具有治疗作用。方法采用灌服56%乙醇同时饲喂高脂饲料的方法,诱导建立复合因素导致的脂肪肝大鼠模型。给药4 w后,检测与酒精性脂肪肝密切相关的各项指标。血液生化学指标检测:天冬氨酸氨基转移酶(AST)活性,丙氨酸氨基转移酶(ALT)活性;血清及肝组织中总胆固醇(TC)含量,甘油三酯(TG)含量;肝脏组织中超氧化物歧化酶(SOD)活性,丙二醛(MDA)含量;肝脏、脾脏、胸腺及肾上腺脏器系数。结果清肝降浊颗粒对脂肪肝动物血清AST、ALT、TC和TG水平的异常升高均具有明显的降低作用(P0.01或P0.05);可以升高脂肪肝动物肝组织中SOD活性,降低TC、TG和MDA含量及肝脏系数(P0.01或P0.05)。结论清肝降浊颗粒具有保肝降酶、抑制脂质过氧化反应、降低血脂肝脂含量,从而达到治疗复合因素所致脂肪肝的作用。     

氟中毒对大鼠肝肾组织磷脂脂肪酸组成的影响

目的　研究氟中毒对大鼠肝、肾组织磷脂脂肪酸组成的影响。方法　选用 Wistar纯系大鼠 ,饲以高浓度含氟水 1个月 ,来复制慢性氟中毒动物模型。用改良 Falch方法提取和分离动物肝、肾组织磷脂 ,用气相色谱法分离和测定磷脂各类脂肪酸构成。结果　所有饲以高浓度氟水的动物均有不同程度的氟斑牙形成 ,尿氟含量增高 ,肝和肾组织蛋白质含量降低等慢性氟中毒的表现 ;氟中毒动物肝、肾组织磷脂脂肪酸组成发生异常改变 ,表现为多不饱和脂肪酸减少 ,饱和脂肪酸组成增加 ,减少的多不饱和脂肪酸种类是花生四稀酸和二十二碳六烯酸。结论　表明长期摄入过量氟可导致肝、肾组织磷脂脂肪酸组成改变 ,磷脂多不饱和脂肪酸减少可能与自由基水平升高所造成的脂质过氧化增强有关     

Special stain and X‐ray probe microanalysis of livers with Wilson disease

Aim: Primary copper toxicosis due to Wilson disease is clinically complex, often leading to delayed diagnosis. Because the metabolic disorder is frequently complicated by iron overload due to hypoceruloplasminemia, either a special stain or microanalysis has been recommended for liver biopsy specimens. Methods: Liver biopsy was performed in three patients in whom Wilson disease was highly suspected. Light microscopic study included rubeanic acid stain for copper and Berlin blue stain for iron. To improve the resolution of ultra‐structures and preservation of toxic metals, short‐term fixation with a 0.1% osmic acid solution was applied for X‐ray probe microanalysis. Their diagnosis was confirmed by genetic study and copper chelation therapy. Results: Two patients at the age of 17 and 23 years, respectively, demonstrated cirrhotic livers surrounded by fibrous septa, while a 7‐year‐old patient demonstrated fatty liver with mildly expanded portal tracts. Both copper grains stained with rubeanic acid and cuprothionein by microanalysis were found in the cirrhotic livers of aged patients. However, either morphological method failed to detect copper deposition in fatty liver tissues from the young patient. Iron deposits were also found in the cirrhotic livers of aged patients. The molecular basis of Wilson disease was confirmed by gene analysis. All patients responded to copper chelation therapy. Conclusion: A morphological method of special staining or microanalysis improved with a new fixative may be unreliable for detecting diffusely distributed copper in the early stage of Wilson liver disease.     

Adipose differentiation-related protein is a reliable lipid droplet marker in alcoholic fatty liver of rats

Background: Adipose differentiation‐related protein (ADRP) is a lipid droplet‐associated protein that coats cytoplasmic lipid droplets. The present study evaluated whether alcohol feeding enhances ADRP expression and whether ADRP is a lipid droplet marker in alcoholic fatty liver of rats. Because medium‐chain triglycerides (MCT) reduce alcoholic hepatosteatosis, their effects on ADRP were also evaluated. Methods: Fatty liver was induced in rats by the consumption of the Lieber‐DeCarli alcohol liquid diet with or without replacement of long‐chain triglycerides (LCT) by MCT (32% of calories). Immunohistochemical staining for ADRP was performed in formalin‐fixed, paraffin‐embedded liver sections. ADRP immunostaining was quantified by image analysis. Triacylglycerol was measured chemically. ADRP mRNA and protein were analyzed by real‐time polymerase chain reaction and western blot, respectively. Double staining technique was performed to distinguish ADRP from glycogen in hepatocytes. Results: Alcohol feeding for 21 days increased ADRP staining in the centrilobular and mid zonal regions of the liver lobules coincident with fat deposition in the liver. Replacing LCT in the alcohol diet with MCT diminished ADRP immunostaining in parallel with reduced steatosis. MCT also attenuated the up‐regulation of ADRP mRNA and protein after alcohol. In steatotic hepatocytes ADRP selectively stained the surface of macrovesicular and microvesicular lipid droplets. ADRP immunostaining quantitatively correlated with hepatic triacylglycerol levels, validating ADRP as a reliable lipid droplet marker. Compared with hematoxylin and eosin stains, ADRP was more sensitive in detecting microvesicular lipid droplets. ADRP immunostaining also distinguished lipid droplets from glycogen, as demonstrated by double staining for ADRP and glycogen. Conclusions: Alcohol induction of fatty liver enhances ADRP expression and MCT oppose the alcohol effects. ADRP is a reliable and sensitive marker for lipid droplets in alcoholic fatty liver. ADRP immunostaining permits quantification of fatty change in hepatocytes and can be used as an ancillary technique in assessing the efficacy of diets or drugs against hepatosteatosis.     

酒精性脂肪肝患者血脂水平与肝组织病理改变相关性的实验研究

目的:研究大鼠酒精性脂肪肝模型血脂水平同肝组织病理改变的相关性,并探讨降血脂及护肝治疗对酒精性脂肪肝的治疗作用。方法:建立酒精性脂肪肝大鼠模型,并分为模型组、治疗组和对照组,3周后处死,分别测定肝功能、血清甘油三酯(TG)、胆固醇(TC)、高密度脂蛋白(HDL)及肝脏病理变化。结果: 酒精性脂肪肝组与必需磷脂治疗组比较,治疗组血清TG、TC、HDL、肝功能均有明显改善,同时肝脏病理明显改善(P<0．05)。结论:脂质代谢紊乱在酒精性脂肪肝的发病中占有重要位置,经必需磷脂治疗降低血脂及保护肝脏功能后,可以明显减轻酒精性脂肪肝肝内脂质含量,改善肝脏病理变化。     

体内外高脂对肝脏NLRP3炎性小体相关基因表达的影响

背景:炎症-免疫系统活化是非酒精性脂肪性肝病(NAFLD)发生、发展的重要机制。炎性小体介导的促炎细胞因子活化在NAFLD中的作用日益受到重视。目的:探讨体内外高脂处理对肝脏NLRP3炎性小体相关基因表达的影响。方法:30只C57BL/6J小鼠随机分为高脂饮食组和正常饮食组(对照组),喂饲16周后处死小鼠,光学显微镜下观察肝组织病理学表现。以胶原酶原位灌注法分离正常饮食组小鼠肝细胞,分别以含饱和脂肪酸[棕榈酸(PA)]、单不饱和脂肪酸[油酸(OA)]、多不饱和脂肪酸[二十二碳六烯酸(DHA)]的培养液培养,以油红O染色检测肝细胞内脂质沉积。以real-time PCR法和蛋白质印迹法检测肝组织和肝细胞中的NLRP3、caspase-1、白细胞介素(IL)-1βmRNA和NLRF3蛋白表达。结果:高脂饮食组小鼠肝组织内可见空泡样脂肪变性。PA、OA和DHA组肝细胞内可见中-大量脂质沉积。与对照组相比,高脂饮食组小鼠肝组织内NLRF3、caspase-1、IL-1βmRNA表达显著升高(P0.05)。PA组肝细胞NLRP3和IL-IβmRNA表达显著高于对照组(P0.05),DHA组NLRP3和IL-1βmRNA表达显著低于对照组(P0.05),PA、OA、DHA组caspase-1 mRNA表达与对照组相比差异无统计学意义(P0.05)。PA、OA组NLRP3蛋白表达较脂多糖(LPS)组升高,DHA组NLRP3蛋白表达较LPS组降低。结论:肝内脂质尤其是饱和脂肪酸沉积可引起NLRP3炎性小体相关基因表达升高,促进肝脏局部炎症反应和NAFLD进展,而多不饱和脂肪酸可降低NLRP3炎性小体相关基因表达,可能具有抗炎、保护肝细胞的作用。     

Effects of n-3 polyunsaturated fatty acids in subjects with nonalcoholic fatty liver disease

BACKGROUND: Long-chain polyunsaturated fatty acid omega-3 levels are decreased in the hepatic tissue of patients with nonalcoholic fatty liver disease. Polyunsaturated fatty acids are negative regulators of hepatic lipogenesis and attenuate the inflammatory response in mice. AIM: To investigate whether polyunsaturated fatty acid may be effective in the treatment of nonalcoholic fatty liver disease. METHODS: Forty patients with nonalcoholic fatty liver disease were randomized into two groups for treatment of 6 months duration. Group DP (n=20) received an AHA recommended diet and polyunsaturated fatty acid 2g/day; Group D (n=20) received only the AHA regular diet. Outcome measurements were fatty liver assessed by abdominal ultrasound, liver aminotransferase and tumour necrosis factor-alpha serum levels, and insulin resistance assessed by HOMA(IR). RESULTS: After 6 months of treatment, the DP group displayed a decrease in alanine aminotransferase levels (p<0.01), as well as in triglyceride levels (p<0.01), serum tumour necrosis factor-alpha levels (p<0.05) and in HOMA(IR) (p<0.05). In the D group, no significant modification was observed. In the DP group, complete fatty liver regression was observed in 33.4% of the patients, and an overall reduction in 50%. In contrast, no patient achieved complete regression in the D group, whereas some amount of reduction occurred in 27.7% of the patients; the remaining 72.2% did not change. CONCLUSION: Our results indicate that alanine aminotransferase, triglyceride and serum tumour necrosis factor-alpha levels, as well as fatty liver improved after polyunsaturated fatty acid administration.     

Experimental study of osthole on treatment of hyperlipidemic and alcoholic fatty liver in animals

AIM: To evaluate the effects of osthole on fatty liver, and investigate the possible mechanism. METHODS: A quail model with hyperlipidemic fatty liver and rat model with alcoholic fatty liver were set up by feeding high fat diet and alcohol, respectively. These experimental animals were then treated with osthole 5-20 mg/kg for 6 wk, respectively. Whereafter, the lipid in serum and hepatic tissue, and coefficient of hepatic weight were measured. RESULTS: After treatment with osthole the levels of serum total cholesterol (TC), triglyceride (TG), lower density lipoprotein-cholesterol (LDL-C), coefficient of hepatic weight, and the hepatic tissue contents of TC and TG were significantly decreased. The activity of superoxide dismutase (SOD) in liver was improved. In alcohol-induced fatty liver rats, the level of malondialdehyde (MDA) in liver was decreased. In high fat-induced fatty liver quails, glutathione peroxidase (GSH-PX) in liver was significantly improved. The histological evaluation of liver specimens demonstrated that the osthole dramatically decreased lipid accumulation. CONCLUSION: These results suggested that osthole had therapeutic effects on both alcohol and high fat-induced fatty liver. The mechanism might be associated with its antioxidation.     

肝宝胶囊治疗脂肪肝的临床研究

目的:观察肝宝胶囊治疗脂肪肝的临床疗效和安全性.方法:选择100例脂肪肝患者,随机分为治疗组和对照组各50例.治疗组患者口服肝宝胶囊,对照组患者口服东宝肝泰,两组治疗12周后,观察比较其症状积分、肝功能、血脂及肝脏B超影像的变化.结果:治疗组改善临床症状总有效率为84%,肝脏B超影像总改善率76%,治疗后肝功能及血脂水平较治疗前明显降低(均为P＜0.01);与对照组比较,差异有统计学意义(P＜0.05).两组的不良反应发生率比较,差异无统计学意义(P＞0.05),均未见严重的不良反应.结论:肝宝胶囊治疗脂肪肝有较好的临床疗效,无明显的副作用.     

高脂高糖、饮酒建立家兔脂肪肝模型及超声量化诊断

目的:模拟人类不良饮食结构建立家兔不同程度脂肪肝模型,进行肝脏背向散射积分 (integrated backscatter,IBS)和图像灰阶平均强度(gray scale,GS)测定,并结合临床研究,探讨具有病理基础的脂肪肝无创性超声量化诊断标准．方法:选用纯种新西兰家兔40只,采用高脂高糖饲料及乙醇饮料建立不同程度脂肪肝模型三组(每组n=10),设立对照组(n=10):临床病例同步进行肝组织病理学及超声检测．病理组织学检测采用苏丹Ⅳ,HE和Masson三色染色:应用HP Sonos 5500超声诊断仪实时检测肝脏IBS,包括图像平均强度(average image intensity,AII)、峰-峰强度及图像强度标准差; 采用Photo shop 7．0直方图分析超声图像GS．所得数据采用SAS8．2进行统计学分析．结果:肝脏AII随脂肪变加重呈递增趋势,正常肝<轻度脂肪肝<中度脂肪肝<重度脂肪肝,尤以近区各组间差异显著(P<0．0001);同等程度肝脂肪变AII随炎症的发生而增大．临床研究显示,IBS对脂肪肝诊断率及与病理组织学符合率(85．7％)较常规超声检测(57．1％) 明显增高,重度脂肪肝AII显著高于轻度脂肪肝(P<0．0001,0．001或0．05)．肝脏GS与AII相关,于肝左、右叶近区二者随病变加重呈一致性增高趋势(r1=0．442 21,P1=0．0012:r2= 0．335 73,P2=0．0160)．中重度脂肪肝伴炎症 GS显著高于正常肝及轻度脂肪肝(P<0．05)．结论:高营养及乙醇联合喂养家兔可快速建立不同程度脂肪性肝病模型;肝脏超声IBS及 GS强度可反映肝脂肪变、炎症和纤维化的病变程度,为脂肪肝无创性量化诊断提供可靠依据．     

Study of the Liver Changes Occurring in Preeclampsia and Their Possible Pathogenetic Connection with Acute Fatty Liver of Pregnancy

Objective: The objective of the present study was to investigate liver involvement in preeclampsia on the basis of clinical, laboratory, and histological data and to detect a possible connection with fatty liver of pregnancy by the determination of microvesicular fatty infiltration of the liver. Methods: The authors studied the liver changes in 10 patients with preeclampsia, observing the clinical and laboratory alterations, the macroscopic liver surface features by laparoscopy, and the presence of microvesicular fatty infiltration by specific lipid staining of hepatic tissue collected by needle biopsy. Results: Macroscopy of the liver surface disclosed some degree of subcapsular liver hemorrhage in all cases; however, the hemorrhage was not related to the clinical and histological severity of the disease. Microvesicular fat droplets were observed in all patients, and the intensity of the fat deposition was not related to pressor levels, laboratory alterations, or the evolution of preeclampsia. Conclusions: The presence of fatty liver infiltration in all patients studied supports the idea that preeclampsia and acute fatty liver of pregnancy could be components of the same pathologic spectrum, with a probable, but still unproved, pathogenetic connection. The deficiency of the long chain 3-hydroxyacyl-coenzyme A dehydrogenase activity may be the determining factor in the evolution of the disease.