中长链脂肪酸食用油可降低超重高甘油三酯血症患者体脂肪和血脂水平

T可以减少超重高甘油三酯血症患者体脂肪,降低血甘油三酯和低密度脂蛋白胆固醇水平.     

鹌鹑高血尿酸高甘油三酯血症模型塑造

目的和方法:建立一种与人类代谢途径相似的高血尿酸并高甘油三酯血症动物模型。鹌鹑随机分为3组, 除空白对照组外, 模型Ⅰ组以15g·kg^-1·d^-1的酵母食饵喂饲鹌鹑, Ⅱ组以10g·kg^-1·d^-1的酵母食饵喂饲鹌鹑, 动态检测血清尿酸(UA)、甘油三酯(TG)、胆固醇(TC)、尿素氮(BUN)、血糖(GLU)、黄嘌呤氧化酶(XOD)含量。结果:模型Ⅰ组7d后血尿酸水平开始升高, 第2、3、4、5周血UA水平显著高于空白对照组(P＜0.05, P＜0.05, P＜0.05, P＜0.01);第3周血TG水平显著高于空白对照组, 持续至5周, 血BUN含量与空白对照组比差异不显著;GLU及TC可见一过性升高。模型Ⅱ组动物血UA水平亦于第2周升高;TG于第4周显著高于空白对照组, 但持续时间短;血BUN于第2周和第3周显著高于空白组(P＜0.05)。结论:以15g/kg酵母喂饲鹌鹑, 可建立高血尿酸高甘油三酯模型, 以进行尿酸与血脂代谢交互紊乱的药理与病理研究。     

高脂血症患者血流剪切率的变化及对血管功能的影响

目的：观察高脂血症患者血流剪切率的变化特点及探讨非诺贝特提高血管舒张功能的机制。方法:以20例正常人、62例高甘油三酯血症病人(其中30例予以饮食治疗、32例予非诺贝特治疗)为观察对象，以肱动脉B超测量血流、血管弹性和舒张功能等指标，检测血浆一氧化氮(NO)、氧化型低密度脂蛋白(Ox-LDL)、血脂的变化。结果:高甘油三酯血症病人超声显示平均血流剪切率（MSR）、血流介导的扩张效应(FMD)和血管弹性指标Da、Dr显著小于正常对照组，而平均血管壁紧张度(MCWT)显著大于正常对照组；血Ox-LDL浓度高于、NO水平低于正常对照组，且NO与MSR、 FMD水平呈正相关，与甘油三酯(TG)、总胆固醇(TC)、低密度脂蛋白胆固醇(LDL-C)和Ox-LDL浓度呈负相关。8周的低脂饮食治疗可使TC、TG水平下降，但NO、Ox-LDL和血管超声指标未见显著改变；非诺贝特治疗组血管超声MSR 、FMD显著高于对照组，血TG、TC、LDL-C和Ox-LDL浓度低于、NO水平高于对照组。结论:高甘油三酯血症时MSR的下降和氧化因子Ox-LDL的升高共同参与内皮的损伤机制，导致NO水平下降，表现为血管舒张功能的下降和弹性下降，MSR的上升和Ox-LDL的下降有利于内皮功能的修复。     

中国9个长寿地区65岁及以上人群氧化应激水平与高甘油三酯血症的关联研究

目的探讨我国长寿地区65岁及以上老年人氧化应激水平与高甘油三酯血症的关系。方法研究对象来源于2017-2018年“老年健康生物标志物队列研究”,最终将我国9个长寿地区2393名65岁及以上老年人群纳入研究。通过问卷调查和体格检测,收集调查对象的人口学特征、生活方式及健康状况等信息,同时采集调查对象的静脉血以检测丙二醛(MDA)、超氧化物歧化酶(SOD)及甘油三酯水平。采用限制性立方样条拟合多重线性回归模型分析MDA、SOD与甘油三酯的关联,采用广义线性混合效应模型分析氧化应激与高甘油三酯血症的关联。结果2393例调查对象年龄为(84.6±11.3)岁,最小65岁,最大112岁;男性1145名(47.9%);甘油三酯水平为(1.4±0.8)mmol/L,高甘油三酯血症检出率为9.99%(239名)。限制性立方样条拟合多重线性回归模型分析结果显示,MDA水平与甘油三酯水平呈线性关联;SOD水平与与甘油三酯水平呈非线性关联。广义线性混合效应模型分析结果显示,调整相关混杂因素后,MDA每升高1 nmol/ml,高甘油三酯血症检出风险增加[OR(95%CI)值为1.063(1.046,1.081)];SOD每升高1 U/ml,高甘油三酯血症检出风险降低[OR(95%CI)值分别为0.986(0.983,0.989)]。结论我国9个长寿地区65岁及以上老年人MDA和SOD水平与高甘油三酯血症发生风险有关联。     

Phase I-II study: triciribine (tricyclic nucleoside phosphate) for metastatic breast cancer

Triciribine is a purine analogue which inhibits DNA and protein synthesis. We performed two studies to define its activity against metastatic breast cancer. The first study was a phase II study in 14 patients with metastatic breast cancer who had received two or fewer chemotherapy treatments. The treatment schedule was triciribine 20 mg/m² per day by 24-h infusion (CI) daily for 5 days every 6 weeks as recommended by a previous open phase I trial. When neither response nor toxicity was seen in the phase II trial, we assumed the starting dose was too low for this group of patients with good performance status and repeated the phase I trial in patients with metastatic breast cancer with good performance status. The starting dose was 35 mg/m² per day using the same 5-day CI schedule, and starting doses were increased in subsequent cohorts of three patients in increments of 5 mg/m² until toxicity occurred. In the initial (phase II) study, one patient had stable disease for 18 weeks (three courses), the remainder progressed. There were no significant toxic effects. In the subsequent phase I study, ten patients were treated until the study was closed The maximum dose was 40 mg/m². Two patients died, one each at the 35 and 40 mg/m² levels, respectively, 3 months and 6 weeks after their last course, one without interveing disease progression. Both had severe hypertriglyceridemia (18- and 21-fold elevation) and severe fatigue. At postmortem examination, one had congestive cardiomyopathy, and the other had severe pancreatitis and hypothyroidism. One patient had severe exacerbation of psoriasis which made her bedridden for more than 30 days. Four patients had hyperglycemia. Plasma pharmacology studies showed erratic drug levels, presumably related to enterohepatic circulation. Postmortem pharmacology studies showed residual drug present as long as 12 weeks after the last dose. We conclude that triciribine is ineffective at all doses tested and at doses of 35 mg/m² has unacceptable toxic effects.This work was performed under National Cancer Institute contract 1-CM-57739     

Systematic review of hypertriglyceridemia-induced acute pancreatitis: A more virulent etiology?

ObjectiveWe sought to define the severity and natural history of hypertriglyceridemia induced acute pancreatitis (HTG-AP), specifically whether HTG-AP causes more severe AP than that caused by other etiologies.MethodsSystematic review of the English literature.ResultsThirty-four studies (15 countries; 1972–2015) included 1340 HTG-AP patients (weighted mean prevalence of 9%). The median admission triglyceride concentration was 2622 mg/dl (range 1160–9769). Patients with HTG have a 14% weighted mean prevalence of AP. Plasmapheresis decreased circulating triglycerides, but did not conclusively affect AP mortality. Only 7 reports (n = 392 patients) compared severity of HTG-AP to that of AP from other etiologies. Of these, 2 studies found no difference in severity, while 5 suggested that HTG-AP patients may have increased severity compared to AP of other etiology.Conclusions1) hypertriglyceridemia is a relatively uncommon (9%) cause of acute pancreatitis; however, patients with hypertriglyceridemia have a high (14%) incidence of acute pancreatitis; 2) plasmapheresis may offer specific therapy unique to this patient population; and 3) data specifically comparing the severity of HTG-AP with AP caused by other etiologies are heterogeneous and scarce.