超声背散射信息熵成像评价脂肪肝的新方法

提出超声背散射Tsallis信息熵成像评价脂肪肝的新方法。利用滑动窗口法,估算窗口内局部背散射包络信号的Tsallis信息熵参数值,对信息熵参数值矩阵进行扫描变换、颜色映射及感兴趣区域设置,叠加到超声B模式图像,实现Tsallis信息熵成像。分析72名肝脏捐献者和204名患者的超声背散射信号,参考标准分别为磁共振波谱测得的肝脏脂肪分数(Hepatic Fat Fraction, HFF)和肝活检组织学检查测得的脂肪肝程度。对于72名肝脏捐献者,Tsallis信息熵与lg(HFF)的相关系数r=0.67(P<0.000 1)。对于204名患者,受试者工作特征曲线下面积分别为0.82、0.88、0.89(≥轻度、≥中度、≥重度),而超声背散射零差K成像分别为0.76、0.82、0.82。超声背散射Tsallis信息熵成像可以直观定征并定量评价脂肪肝的严重程度,其诊断性能优于超声背散射零差K成像,可作为一种超声评价脂肪肝的新方法。     

Long-Term Measures of Dyslipidemia,Inflammation, and Oxidative Stress in Rats Fed a High-Fat/High-Fructose Diet

Inflammation and oxidative stress are thought to be involved in, or associated with, the development of obesity, dyslipidemia, hepatic steatosis, and insulin resistance. This work was designed to determine the evolution of inflammation and oxidative stress during onset and progression of hepatic steatosis and glucose intolerance. Seventy-five male Wistar rats were divided to control and high-fat high-fructose (HFHFr) groups. A subgroup of each group was sacrificed at 4, 8, 12, 16, and 20 weeks. HFHFr-fed rats exhibited overweight, glucose intolerance, and hepatic steatosis with increased contents of hepatic diacylglycerols and ceramides. The HFHFr diet increased hepatic interleukin 6 (IL-6) protein and adipose tissue CCL5 gene expression and hepatic nicotinamide adenine dinucleotide phosphate (NADPH) oxidase activity but not mitochondrial reactive oxygen species (ROS) production. The HFHFr diet decreased plasma and liver levels of isoprostanoid metabolites as well as plasma thiobarbituric acid-reactive substance (TBARS) levels. Hepatic glutathione content was decreased with a moderate decrease in superoxide dismutase (SOD) and glutathione peroxidase (GPx) with the HFHFr diet. Overall, HFHFr diet led to hepatic lipid accumulation and glucose intolerance, which were accompanied by only moderate inflammation and oxidative stress. Most of these changes occurred at the same time and as early as 8 or 12 weeks of diet treatment. This implies that oxidative stress may be the result, not the cause, of these metabolic alterations, and suggests that marked hepatic oxidative stress should probably occur at the end of the steatotic stage to result in frank insulin resistance and steatohepatitis. These findings need to be further evaluated in other animal species as well as in human studies.     

乙型肝炎病毒X蛋白表达与肝细胞脂肪变性的关系及其机制

目的探讨乙型肝炎病毒X蛋白(Hepatitis Bvirus X protein,HBx)在肝组织中的表达与慢性乙型肝炎(Chronic hepatitis B,CHB)合并肝脂肪变性的关系及其可能的机制。方法对经病理证实的18例CHB及18例CHB合并肝脂肪变性的病例标本进行血脂、肝功能、血清病毒学及病理组织学指标分析,免疫组化法检测肝组织HBx、肝X受体(Liver X receptorα,LXRα)和脂肪酸合成酶(Fatty acid synthase,FAS)的表达。结果两组病例生化指标、HBV血清标志物及HBV-DNA载量、肝组织炎症活动度分级及纤维化程度分期的构成比差异均无统计学意义(P>0.05);HBx、LXRα和FAS表达的阳性率差异也无统计学意义(P>0.05);但CHB合并肝脂肪变性组HBx、LXRα和FAS的表达强度明显高于CHB组,且差异有统计学意义(P<0.05);在CHB合并肝脂肪变性组中,HBx与LXRα、LXRα与FAS及HBx与FAS的表达呈正相关。结论 HBx在CHB肝组织中广泛表达,在CHB合并肝脂肪变性组的表达明显增强,提示HBx可能通过诱导LXRα进而刺激FAS表达上调,参与CHB合并肝细胞脂肪变性的发生。     

Cholesterol‐Lowering Properties of Whole Cowpea Seed and Its Protein Isolate in Hamsters

ABSTRACT: Hypercholesterolemic hamsters were fed for 4 wk on diets rich in saturated fatty acids and cholesterol, differing only in protein source (20 %): casein (control group, HC), whole cowpea seed (HWS), and cowpea protein isolate (HPI). Hamsters fed on HWS and HPI presented significant reductions in plasma total cholesterol and non‐HDL cholesterol. HPI and HC presented similar protein digestibility, which were significantly higher than that of HWS. Animals fed on HWS presented significantly higher levels of bile acids and cholesterol in feces than did the animals fed on casein or HPI diets. Histological analyses of the liver showed that HC diet resulted in steatosis widely distributed throughout the hepatic lobule, while HWS and HPI diets promoted reductions in liver steatosis. The effectiveness of HWS for modulating lipid metabolism was greater than that of HPI, as measured by plasma cholesterol reduction and liver steatosis.     

Postnatal High-Fat Diet Increases Liver Steatosis and Apoptosis Threatened by Prenatal Dexamethasone through the Oxidative Effect

The objective of this study was to investigate cellular apoptosis in prenatal glucocorticoid overexposure and a postnatal high fat diet in rats. Pregnant Sprague-Dawley rats at gestational days 14 to 21 were administered saline (vehicle) or dexamethasone and weaned onto either a normal fat diet or a high fat diet for 180 days; in total four experimental groups were designated, i.e., vehicle treated group (VEH), dexamethasone treated group (DEX), vehicle treated plus high-fat diet (VHF), and dexamethasone treated plus high-fat diet (DHF). Chronic effects of prenatal liver programming were assessed at postnatal day 180. The apoptotic pathways involved proteins were analyzed by Western blotting for their expressions. Apoptosis and liver steatosis were also examined by histology. We found that liver steatosis and apoptosis were increased in the DHF, DEX, and VHF treated groups, and that the DHF treated group was increased at higher levels than the DEX and VHF treated groups. The expression of leptin was decreased more in the DHF treated group than in the DEX and VHF treated groups. Decreased peroxisome proliferator-activated receptor-gamma coactivator 1α, phosphoinositide-3-kinase, manganese superoxide dismutase and increased malondialdehyde expression levels were seen in DHF treated group relative to the DEX treated group. The DHF treated group exhibited higher levels of oxidative stress, apoptosis and liver steatosis than the DEX treated group. These results indicate that the environment of high-fat diet plays an important role in the development of liver injury after prenatal stress.