健脾消浊颗粒治疗痰湿质代谢综合征43例临床研究

目的观察健脾消浊颗粒治疗痰湿质代谢综合征的临床疗效。方法将85例痰湿质代谢综合征患者随机分为2组。治疗组43例予健脾消浊颗粒治疗,对照组42例予阿卡波糖片治疗。2组均治疗12周后统计临床疗效,并观察2组血清总胆固醇(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)、空腹血糖(FPG)及体质量指数(BMI)变化。结果治疗组总有效率93.0%,对照组总有效率66.7%,2组比较差异有统计学意义(P0.05),治疗组疗效优于对照组。2组治疗后BMI、FPG、TC、TG、LDL-C均降低(P0.05),HDL-C均升高(P0.05),且治疗组BMI、FPG、TC、TG、LDL-C、HDL-C改善优于对照组(P0.05)。结论健脾消浊颗粒治疗痰湿质代谢综合征疗效确切,可显著改善患者血脂、血糖。     

代谢和免疫相互作用稳态——复杂性科学视角下的营卫解读

免疫炎症和代谢调节高度统一,功能上相互依赖,这种免疫和代谢之间的相互作用可以被看作机体稳态调节的核心机制.只有把免疫炎症和营养代谢的非线性相互作用作为一个整体来研究,刻画其状态的变化,才能有效的调控它.可是由于非线性防御系统的超级复杂性,系统生物学从下向上的研究在这方面存在着几乎不可克服的困难.中医营卫学说从整体出发,对免疫和代谢相互作用的状态变化进行了有效的刻画,这中间研究的思路、方法以及记载在历代文献中的丰富经验是弥足珍贵的.     

化瘀温胆汤对代谢综合征大鼠血脂、血压及脂肪细胞因子的干预作用

目的：探讨化瘀温胆汤对代谢综合征大鼠血压、血脂异常的治疗作用及部分机制。方法：健康雄性SD大鼠高温高湿环境下喂饲高脂高糖高盐饮食12周,复制大鼠代谢综合征模型。通过检测血压、血清胆固醇（TC）、甘油三酯（TG）、低密度脂蛋白（LDL-C）、高密度脂蛋白（HDL-C）,探讨化瘀温胆汤灌胃给药4周后对模型大鼠血压、血脂异常的改善作用。检测脂联素、瘦素、肿瘤坏死因子-α（TNF-α）、白介素-6（IL-6）变化情况,探讨该方治疗代谢综合征的部分机制。结果：化瘀温胆汤可明显降低模型大鼠的血清TC、TG、LDL-C水平,升高HDL-C,与模型对照组比较有显著性差异（P〈0.01）;可降低模型大鼠血压,与模型对照组比较有显著性差异（P〈0.01）。化瘀温胆汤可使脂联素水平明显升高,与模型对照组比较有显著性差异（P〈0.01）;瘦素水平、TNF-α、IL-6水平均有不同程度的降低,与模型对照组比较均具有显著性差异（P〈0.01）。结论：化瘀温胆汤对代谢综合征模型大鼠血压、血脂异常有较好的疗效,其机制可能与其调节脂联素、瘦素、TNF-α、IL-6水平有关。     

Protective potential of epigallocatechin-3-gallate against benign prostatic hyperplasia in metabolic syndrome rats

Epigallocatechin-3-gallate (EGCG) is a major catechin in green tea with functions of antioxidant, anti-proliferative, anti-inflammatory and attenuating metabolic syndrome. In this study, rat model of benign prostatic hyperplasia (BPH) accompanied with metabolic syndrome was induced by fed on high-fat diet for 12 weeks combined with testosterone injection (10 mg/kg/d) from 9th to 12th weeks. EGCG was orally given from 9th to 12th weeks. Finally, the levels of glucose, total cholesterol, triglyceride, prostate weight, insulin-like growth factors (IGFs), inflammatory cytokines, antioxidant enzymes, and prostatic expression of IGF binding protein-3 (IGFBP-3) and peroxisome proliferator activated receptors (PPARs) were evaluated. It was found that EGCG significantly decreased the levels of glucose, total cholesterol, triglyceride, IGFs, and inflammatory cytokines, normalized the activities of antioxidant enzymes, as well as increased the prostatic expression of IGFBP-3 and PPARs. These results indicated that EGCG was able to exert anti-BPH activities in metabolic syndrome rats.     

Metabolic phenotype of bladder cancer

Metabolism of bladder cancer represents a key issue for cancer research. Several metabolic altered pathways are involved in bladder tumorigenesis, representing therefore interesting targets for therapy.Tumor cells, including urothelial cancer cells, rely on a peculiar shift to aerobic glycolysis-dependent metabolism (the Warburg-effect) as the main energy source to sustain their uncontrolled growth and proliferation. Therefore, the high glycolytic flux depends on the overexpression of glycolysis-related genes (SRC-3, glucose transporter type 1 [GLUT1], GLUT3, lactic dehydrogenase A [LDHA], LDHB, hexokinase 1 [HK1], HK2, pyruvate kinase type M [PKM], and hypoxia-inducible factor 1-alpha [HIF-1α]), resulting in an overproduction of pyruvate, alanine and lactate. Concurrently, bladder cancer metabolism displays an increased expression of genes favoring the pentose phosphate pathway (glucose-6-phosphate dehydrogenase [G6PD]) and the fatty-acid synthesis (fatty acid synthase [FASN]), along with a decrease of AMP-activated protein kinase (AMPK) and Krebs cycle activities. Moreover, the PTEN/PI3K/AKT/mTOR pathway, hyper-activated in bladder cancer, acts as central regulator of aerobic glycolysis, hence contributing to cancer metabolic switch and tumor cell proliferation.Besides glycolysis, glycogen metabolism pathway plays a robust role in bladder cancer development. In particular, the overexpression of GLUT-1, the loss of the tumor suppressor glycogen debranching enzyme amylo-α-1,6-glucosidase, 4-α-glucanotransferase (AGL), and the increased activity of the tumor promoter enzyme glycogen phosphorylase impair glycogen metabolism. An increase in glucose uptake, decrease in normal cellular glycogen storage, and overproduction of lactate are consequences of decreased oxidative phosphorylation and inability to reuse glucose into the pentose phosphate and de novo fatty acid synthesis pathways. Moreover, AGL loss determines augmented levels of the serine-to-glycine enzyme serine hydroxymethyltransferase-2 (SHMT2), resulting in an increased glycine and purine ring of nucleotides synthesis, thus supporting cells proliferation.A deep understanding of the metabolic phenotype of bladder cancer will provide novel opportunities for targeted therapeutic strategies.     

高脂血症长爪沙鼠模型的转录组检测和代谢性炎症通路的初步研究

目的研究饮食诱发的高脂血症长爪沙鼠模型的关键基因及代谢性炎症通路调控网络。方法利用RNA-Seq测序技术及生物信息学技术对正常组与模型组两个RNA池进行测序和分析。结果 De novo拼接后获得有效长爪沙鼠基因47 522个(即≥100 bp的unigene),大小26.9 Mb,与GenBank中现有的基因比对结果表明,约82.53%的序列与基因组上的外显子序列同源;诱发高脂血症动物与正常动物之间共获得21 125个差异基因,其中16 087个下调,5 038个上调,模型组相对于正常组存在显著的下调关系(P0.01)。其中与长爪沙鼠高脂血症代谢性炎症密切相关的通路有8个(P0.01),这8个通路所表达的基因中有15个与免疫和炎症相关的基因显著下调(P0.01)。结论 RNA-Seq测序和生物信息技术可作为研究高脂血症动物模型的整体基因转录的工具,筛选出的关键基因和通路可作为研究的候选基因或操作靶点。     

高糖高脂饮食诱导大鼠代谢综合征模型并发阿尔茨海默样变

目的 通过长期高糖高脂饮食导致动物出现代谢综合征合并阿尔茨海默(AD)样改变动物模型的研究。方法 将48只SD大鼠随机分为2组, 正常对照组(用普通饲料饲喂) 24只, 高糖高脂组(饲以高糖高脂饲料)24只, 连续喂养12 个月。于实验第 6、9、12月末观察动物体重、肾周和附睾或子宫周围脂肪重量并计算Lee指数; 检测血液中代谢综合征相关生化指标的变化;Western blotting测定海马Tau蛋白含量及其磷酸化水平;ELISA法检测海马Aβ的含量;HE染色观察脑组织病理改变。结果 与正常对照组相比, 各阶段高糖高脂组大鼠体重、内脏脂肪重量明显增加; 血清中FPG、TG、LDL等明显升高, HDL显著下降;海马Aβ、P-tau较对照组明显升高, 其差异有统计学意义;病理组织学显示模型组脑组织有明显的炎性浸润、小胶质细胞活化明显。结论 高糖高脂饮食诱导大鼠代谢综合征动物模型可并发AD样变, 可为老年痴呆动物模型的构建提供一个新的思路。     

An association between diet,metabolic syndrome and lower urinary tract symptoms

Diet is a key factor in the aetiology of many diseases, including metabolic syndrome and lower urinary tract disorders. Metabolic syndrome is a growing and increasingly expensive health problem in both the developed and the developing world, with an associated rise in morbidity and mortality. On the other hand, lower urinary tract symptoms affect millions of individuals worldwide, lowering their quality of life. Associations have been established between both conditions in existing literature and the various components of the metabolic syndrome have been linked with the onset and aggravation of symptoms in various forms of LUTS. This current review explores the relationships between these in detail, focusing on their inter-relationships particularly vis-a-vis dietary macronutrient and micronutrient intake.