短期胰岛素泵强化治疗对2 型糖尿病患者脂糖代谢及胰岛β细胞功能的影响

目的:探讨短期胰岛素泵强化治疗对2型糖尿病患者脂糖代谢及胰岛β细胞功能的影响。方法:选择2013年10月到2015年10月我院收治的2型糖尿病患者86例,随机分为对照组(n=43)和实验组(n=43)。对照组患者给予门冬胰岛素常规治疗,实验组患者给予胰岛素泵强化治疗,两组疗程均为2周。检测并比较两组患者治疗前后血糖、血脂、糖化血红蛋白(Hb A1c)及口服葡萄糖刺激后胰岛β细胞功能指标。结果:治疗后两组患者空腹血糖(FPG)、Hb A1c、总胆固醇(TC)、甘油三酯(TG)及低密度脂蛋白胆固醇(LDL-C)、稳态模型评价-胰岛素抵抗(HOMA-IR)较治疗前均明显下降(P0.05),高密度脂蛋白胆固醇(HDL-C)、胰岛素曲线下面积(AUC)、稳态模型评价-胰岛β细胞功能(HOMA-β)及0.5h胰岛素浓度/血糖浓度(I30/G30)较治疗前明显升高(P0.05),且实验组患者以上各指标变化均优于对照组(P0.05)。结论:短期胰岛素泵强化治疗能明显纠正2型糖尿病患者血糖、血脂水平,改善胰岛β细胞功能,值得在临床上推广应用。     

32例初诊2型糖尿病胰岛素短期强化治疗的临床观察

目的:探讨短期胰岛素强化治疗对改善2型糖尿病患者的胰岛β细胞功能和血糖控制的影响。方法:采用自身前后对照,观察32例初诊2型糖尿病患者接受2周胰岛素强化治疗前后胰岛β细胞对血糖刺激的胰岛素分泌的变化及血糖控制的影响。结果:治疗2周前后患者胰岛素分泌曲线发生显著改善,血糖控制良好。结论:短期强化胰岛素治疗可以快速稳定控制血糖和显著改善胰岛β细胞功能,部分患者甚至不用任何降糖药物,仅通过饮食、运动就可获得良好的血糖水平。     

替米沙坦联合叶酸对老年H型高血压合并2型糖尿病患者凝血功能及肾功的影响

目的:观察替米沙坦联合叶酸治疗对老年H型高血压合并2型糖尿病患者凝血功能及肾功的影响.为老年H型高血压合并2型糖尿病患者的临床治疗以及延缓病程提供理论依据.方法:选择66例符合标准的老年H型高血压合并2型糖尿病患者,测定血压,胰岛素敏感指数,糖化血红蛋白,同型半胱氨酸,凝血指标及尿白蛋白排泄率(UAE)等基线数据.上述患者随机分为对照组及实验组,分别接受替米沙坦80 mg/d及替米沙坦80 mg/d+叶酸片0.8 mg/d治疗后,于24周后复查上述指标,并与用药前进行对比研究.结果:对照组及实验组患者均较治疗前血压下降,糖化血红蛋白、纤维蛋白原、尿白蛋白排泄率明显下降(P＜0.05),胰岛素敏感指数较治疗前升高(P＜0.05).经治疗后,实验组患者较对照组血压、糖化血红蛋白、同型半胱氨酸、纤维蛋白原、尿白蛋白排泄率下降均低于对照组(P＜0.05),胰岛素敏感指数较对照组升高(P＜0.05).结论:对于老年H型高血压合并2型糖尿病患者替米沙坦联合叶酸治疗较单纯替米沙坦治疗具有更良好的降压作用,增加胰岛素敏感性,改善高凝状态,改善肾功.     

2型糖尿病视网膜病变与胰岛素抵抗及β细胞功能的关系

目的:探讨新疆汉族2型糖尿病视网膜病变(DR)与胰岛素抵抗(IR)及β细胞功能的关系.方法:免散瞳眼底照相行眼底筛查我院内分泌科住院病人及体检正常人群258例,正常人(NC)83例、糖尿痛无视网膜病变(NDR)60例、糖尿病视网膜病变(DR)115例.测定其空腹血糖(FBG)、空腹胰岛素(FINS),计算胰岛素抵抗指数(HOMA-IR指数)、β细胞功能指数(HOMA-β指数),并测定其临床一般资料,记录身高、体重等.结果:NDR组、DR组HOMA-IR指数、HOMA-β指数明显高于NC组,差异有统计学意义(p<0.05),但NDR组与DR组相比,HOMA-IR指数、HOMA-β指数差异无统计学意义(p>0.05).2型糖尿病视网膜病变与FBG、FINS、HOMA.IR、HOMA-β呈正相关(p<0.01).多元Logistie回归分析显示病程、吸烟史、TG、Tc、尿微量白蛋白(UAE)、糖化血红蛋白(HbAlc)、血尿酸(SUA)、收缩压(SBP)HOMA-IR、HOMA-β为DR的危险因素.校正这些因素后DR仍与UAE、SUA、SBP、HOMA-IR、HOMA-β相关.结论:DR的发生与发展除了与病程、脂代谢紊乱、吸烟有关外,还与IR、β细胞功能、UAE及SUA等有关.     

α-硫辛酸联合胰岛素强化治疗对初诊2型糖尿病患者胰岛细胞功能的影响

目的:比较应用α-硫辛酸抗氧化应激治疗联合胰岛素强化降糖对初诊2型糖尿病患者胰岛β细胞功能的影响。方法:将104例初诊2型糖尿病患者随机分为联合组、单药组两组,分别给予α-硫辛酸联合胰岛素强化治疗及单独胰岛素强化治疗12周,比较两组患者治疗前后口服葡萄糖耐量试验(OGTT)、C肽释放试验各时间点血浆葡萄糖、C肽及胰岛功能相关指标的变化。结果:联合组OGTT试验1小时血糖(1 h PG)、2小时血糖(2 h PG)、3小时血糖(3 h PG)较单药组明显下降,空腹C肽(FCP)、0.5小时C肽(0.5 h CP)、2小时C肽(2 h CP)水平较单药组明显升高,胰岛β细胞功能指数[HOMA-β(CP)]、糖负荷0.5 h时净增C肽与净增血糖比值(△CP30/△Glu30)、C肽曲线下面积(AUCC)与血糖曲线下面积(AUCG)比值(AUCG/AUCC)较单药组明显升高,差异均有统计学意义(P0.05)。结论:α-硫辛酸联合胰岛素强化治疗较单独胰岛素强化治疗能够更好的恢复胰岛β细胞功能。     

厄贝沙坦联合氨氯地平治疗2 型糖尿病合并高血压的疗效及对糖代谢和 血压的影响

目的：探索厄贝沙坦联合氨氯地平治疗2型糖尿病合并高血压的疗效及对糖代谢和血压的影响。方法：选择2013年7 月至 2014 年8月期间我院收治的2 型糖尿病合并高血压患者50 例,根据随机数字表法,将患者分成联合用药组和美托洛尔组。联合 用药组口服厄贝沙坦和氨氯地平;美托洛尔组口服美托洛尔,疗程为3个月。分析比较治疗前后两组患者的空腹血糖（FBG）、空腹 胰岛素（FINS）、胰岛素敏感指数（HOMA-IR）、收缩压（SBP）和舒张压（DBP）水平之间的差异,观察临床疗效。结果：治疗后,两组 患者FBG、FINS、HOMA-IR、SBP和DBP 水平较治疗前均有所下降,其中联合用药组下降得更明显（P<0.05）,且治疗后联合用药 组上述指标均显著低于美托洛尔组,差异均有统计学意义（P<0.05）。治疗后,联合用药组的治疗有效率为88.00%,显著高于美托 洛尔组的48.00%,且差异具有统计学意义（P<0.05）。结论：厄贝沙坦联合氨氯地平治疗2 型糖尿病合并高血压患者具有良好的疗 效,可以改善血糖和血压情况,对于指导临床用药具有重要意义。     

西北地区初发2 型糖尿病人口胰岛功能的现状调查

目的:通过对榆林市初发2型糖尿病患者的胰岛功能进行跟踪观察,探讨初发2型糖尿病患者胰岛功能的变化特点。方法:选取榆林市1220例初发2型糖尿病患者作为观察对象,跟踪随访12个月,在就诊后的3个月、6个月及12个月时,检测全部患者的血糖水平、C-肽释放量,计算胰岛素分泌指数(HOMA-β)及胰岛素抵抗指数(HOMA-IR),观察总结患者的胰岛功能变化特点。结果:随访期间,糖尿病患者C-肽释放量持续降低,且在就诊后3个月内,C-肽释放量下降明显(P0.05),与就诊后6个月时及12个月时比较,糖尿病患者胰岛素放量持续降低,就诊后3个月内下降最明显(P0.05);患者胰岛素分泌指数持续降低(P0.05),胰岛素抵抗指数持续升高(P0.05),且与6个月时和12个月时比较,3个月时变化幅度最为显著(P0.05)。结论:随着病程的延长,初发2型糖尿病患者胰岛功能逐渐降低,二者具有显著相关性,且3个月内患者的胰岛功能下降最为显著。     

胰岛β细胞"质"、"量"的辩证关系——"质"的三要素

高血糖是糖尿病典型的病理特征,血糖的波动是决定糖尿病患者是否出现并发症的重要因素,而由胰岛β细胞合成分泌的胰岛素,是体内唯一可以降低血糖的多肽类激素.胰岛β细胞"质"与"量"决定着体内胰岛素分泌情况和血糖的调控.围绕"促进β细胞损伤修复,提升胰岛β细胞质量是治疗糖尿病的核心"之理念,提出构成胰岛β细胞"质"的三要素:细胞结构、"真""假"胰岛素和胰岛素调节型分泌.旨在为β细胞质量评价和糖尿病机制研究提供一定的理论参考.     

达格列净联合二甲双胍治疗2型糖尿病的疗效及对糖脂代谢的影响

目的:探讨达格列净联合二甲双胍治疗2型糖尿病的疗效及对糖脂代谢的影响。方法:选择2018年1月-2020年1月在我院接受治疗的120例2型糖尿病患者,采用抽签法分为观察组(n=61)和对照组(n=59)。对照组给予二甲双胍治疗,观察组在对照组的基础上给予达格列净治疗。比较两组患者的临床疗效、治疗前后血清空腹血糖(FBG)、空腹胰岛素(FINS)、糖化血红蛋白(Hb Alc)、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、胰岛素β细胞功能指数(HOMA-β)、胰岛素抵抗指数(HOMA-IR)的变化情况及不良反应的发生情况。结果:治疗后,观察组和对照组总有效率分别为93.62%,74.47%,观察组显著高于对照组(P0.05);两组FBG、FINS、HbAlc、TC、TG、LDL-C水平及HOMA-IR均较治疗前显著降低,且观察组上述指标均明显低于对照组(P0.05),两组HDL-C水平和HOMA-β均较治疗前显著升高,且观察组显著高于对照组(P0.05);两组不良反应总发生率为6.56%、8.47%,组间比较差异无统计学意义(P0.05)。结论:达格列净联合二甲双胍治疗2型糖尿病的效果显著优于单用二甲双胍治疗,其可有效改善患者糖脂代谢水平,且不会增加不良反应。     

利拉鲁肽联合利格列汀治疗2型糖尿病肥胖患者的临床研究

目的:探讨利拉鲁肽联合利格列汀治疗2型糖尿病肥胖患者的临床疗效。方法:选取2016年1月至2018年1月本院收治的104例2型糖尿病肥胖患者,按照随机数字表法将患者分为对照组(n=52)和治疗组(n=52)。对照组给予利格列汀治疗,治疗组给予利拉鲁肽联合利格列汀治疗,两组疗程均为3个月。比较两组治疗前后体质量指数(BMI)、血糖指标[糖化血红蛋白(HbA1c)、空腹血糖(FPG)、餐后2小时血糖(2hPG)]、血压指标[收缩压(SBP)、舒张压(DBP)]、胰岛功能指标[胰岛素抵抗指数(HOMA-IR)、胰岛β细胞功能(HOMA-β)]、骨代谢指标[N端中段骨钙素(N-MID-OT)、β胶联降解产物(β-CTX)]、氧化应激指标[丙二醛(MDA)、脂质过氧化氢(LHP)、谷胱甘肽过氧化物酶(GSH-Px)]和炎症指标[肿瘤坏死因子-α(TNF-α)、白细胞介素-6(IL-6)、C反应蛋白(CRP)]水平,记录两组治疗过程中不良反应的发生情况。结果:治疗后,两组的BMI、血糖指标、血压指标、HOMA-IR、β-CTX、MDA、LHP、炎症指标水平均低于治疗前,HOMA-β、N-MID-OT、GSH-Px水平均高于治疗前(P0.05),且治疗组以上指标的改善程度明显优于对照组。治疗组不良反应发生率为15.38%(8/52),与对照组的11.54%(6/52)比较差异无统计学意义(P0.05)。结论:利拉鲁肽联合利格列汀治疗2型糖尿病肥胖患者安全有效,能够明显降低患者体重、血糖、血压水平,改善胰岛功能和骨代谢,减轻氧化应激和炎症反应。     

miR-335-5p induces insulin resistance and pancreatic islet β-cell secretion in gestational diabetes mellitus mice through VASH1-mediated TGF-β signaling pathway

Multiple studies have reported different methods in treating gestational diabetes mellitus (GDM); however, the relationship between miR-335-5p and GDM still remains unclear. Here, this study explores the effect of miR-335-5p on insulin resistance and pancreatic islet β-cell secretion via activation of the TGFβ signaling pathway by downregulating VASH1 expression in GDM mice. The GDM mouse model was established and mainly treated with miR-335-5p mimic, miR-335-5p inhibitor, si-VASH1, and miR-335-5p inhibitor + si-VASH1. Oral glucose tolerance test (OGTT) was conducted to detect fasting blood glucose (FBG) fasting insulin (FINS). The OGTT was also used to calculate a homeostasis model assessment of insulin resistance (HOMA-IR). A hyperglycemic clamp was performed to measure the glucose infusion rate (GIR), which estimated β-cell function. Expressions of miR-335-5p, VASH1, TGF-β1, and c-Myc in pancreatic islet β-cells were determined by RT-qPCR, western blot analysis, and insulin release by ELISA. The miR-335-5p mimic and si-VASH1 groups showed elevated blood glucose levels, glucose area under the curve (GAUC), and HOMA-IR, but a reduced GIR and positive expression of VASH1. Overexpression of miR-335-5p and inhibition of VASH1 contributed to activated TGFβ1 pathway, higher c-Myc, and lower VASH1 expressions, in addition to downregulated insulin and insulin release levels. These findings provided evidence that miR-335-5p enhanced insulin resistance and suppressed pancreatic islet β-cell secretion by inhibiting VASH1, eventually activating the TGF-β pathway in GDM mice, which provides more clinical insight on the GDM treatment.     

Islet NADPH oxidase activity modulates β-cell mass and endocrine function in rats with fructose-induced oxidative stress

BackgroundIslet NADPH oxidase activity is modulated by glucose and other insulin secretagogues and it might be part of the regulatory mechanism of insulin secretion. We studied its modulatory role of islet NADPH oxidase upon β-cell function in rats with fructose-induced oxidative stress.MethodsNormal rats were fed for 3 weeks with a standard diet, a fructose-rich diet or both diets plus apocynin. We measured plasma glucose, insulin, triacylglycerol and lipid peroxidation levels and the homeostasis model assessment-insulin resistance (HOMA-IR) and HOMA-β indexes, and performed an oral glucose tolerance test. β-cell volume density and the number of islets per mm² were determined by immunomorphometric analysis of the pancreas. Insulin secretion, glucose metabolism, glucokinase and NADPH oxidase activities were studied in islets isolated from each experimental group.ResultsFructose-fed rats had increased plasma triacylglycerol, insulin and lipid peroxidation levels associated with an insulin resistance state; the reactive higher secretion was unable to cope with the increased demand of insulin, leading to an impaired glucose tolerance. They also have a lower number of islets per area unit with a decreased β-cell volume density. All these alterations were prevented by blocking NADPH oxidase activity with apocynin.ConclusionFructose-induced changes are partly mediated by modulation of NADPH oxidase activity.General significanceThe metabolic dysfunctions and enhanced oxidative stress measured in fructose-fed rats resemble those recorded in human prediabetes; thus, successful strategies employed in this model could be later used to prevent the progression of this state towards type 2 diabetes in human beings.     

糖尿病不同发展阶段胰岛功能的变化趋势*

目的:研究糖尿病不同发展阶段胰岛素敏感性及胰岛素分泌功能的改变,指导2型糖尿病的早期诊断。方法:57例行OGTT体检者,分为NGT、IGT、IFG+IGT、新诊断T2DM四组,并行IVGTT,采用HOMA-IR评估胰岛素敏感性,采用葡萄糖处置指数[DI1=HOMA-β/HOMA-IR,DI2=ΔI30/ΔG30/HOMA-IR,DI3=MBCI×IAI,DI4=AIR0-10/HOMA-IR]及AUCINS/HOMA-IR评估胰岛素分泌功能。结果:IGT、IFG+IGT、新诊断T2DM组HOMA-IR无统计学差异(P>0.05),均显著高于NGT组(P<0.05)。IGT、IFG+IGT、新诊断T2DM组DI1逐步降低(P<0.05);NGT、IGT组DI1无统计学差异(P>0.05)。NGT、IGT、IFG+IGT、新诊断T2DM组DI2、DI3、DI4逐步降低(P<0.05)。IFG+IGT、新诊断T2DM组OGTTAUCINS/HOMA-IR逐步降低(P<0.05),且显著低于NGT组(P<0.05);NGT、IGT组OGTTAUCINS/HOMA-IR无统计学差异(P>0.05)。结论:(1)IGT阶段胰岛素抵抗及胰岛素1相、早期相分泌功能的下降同时存在。IFG+IGT阶段胰岛素1相、早期相分泌进一步下降,并出现基础相、2相分泌的减少,胰岛素抵抗加重不明显。新诊断T2DM阶段胰岛素各相分泌进一步减少,胰岛素抵抗加重不明显。(2)在T2DM发生过程中,胰岛素分泌功能下降较胰岛素敏感性下降更为明显。(3)胰岛素抵抗及胰岛素1相、早期相分泌功能的下降是T2DM的预测因子。(4)IFG+IGT阶段应积极干预。     

糖尿病前期与糖尿病相关因素的研究

目的：探讨糖尿病前期与糖尿病的相关因素。方法：选取我院2009年1月到2011年12月之间ADA糖尿病诊断标准纳入的200例患者为研究对象,正常血糖患者60例,糖尿病前期患者80例,糖尿病患者60例,并对糖尿病前期与糖尿病的相关因素进行Logistic回归分析。结果：三种类型的患者FPG、2hPG、TG、HOMA-IR、HOMA．B、IgE、CRP比较具有显著地的差异（P〈0．05）。并且以上指标除了HOMA—β外,其余的指标数值均是糖尿病〉糖尿病前期〉正常血糖的情况,差异有统计学意义（P〈0．05）;HOMA-IR、HOMA-β是糖尿病前期和糖尿病的危险因子,并且随着HOMA—IR的不断增加,患者发生糖尿病前期和糖尿病的几率将大大增加,并且随着HOMA-β的不断增加,发生发生糖尿病前期和糖尿病的几率将大大降低。结论：临床中胰岛素抵抗指数和胰岛素分泌指数均是糖尿病的危险因素。     

姜黄素对db/db小鼠基因组DNA甲基化的影响

目的:观察姜黄素对2型糖尿病模型db/db小鼠糖尿病症状的改善作用,并从表观遗传角度分析其对小鼠外周血DNA甲基化水平的影响。方法:2型糖尿病模型db/db小鼠随机分为糖尿病组和姜黄素干预组(给予250 mg/kg姜黄素溶液),连续灌胃8周。OGTT检测葡萄糖耐量,ELISA法测定空腹胰岛素并计算HOMA-IR和HOMA-β,RRBS技术检测外周血基因组DNA甲基化水平。结果:与糖尿病组相比,姜黄素干预小鼠的血糖、空腹胰岛素和HOMA-IR显著降低,葡萄糖耐量显著改善(P<0.05);且小鼠外周血基因组启动子区、CGI岸和5’-非编码区CpG甲基化水平显著降低(P<0.05);对两组间差异甲基化基因进行功能富集分析,筛选出前10位显著富集的可能与2型糖尿病相关的差异基因包括Hdac7、Micall1、Vangl2、Dhcr24、Kcnj8、Gnas、Tcf7l2、Dgkh、Dlgap1和Plekhg4。结论:姜黄素能够改善db/db小鼠的葡萄糖耐量及胰岛素抵抗,并且其外周血中存在显著低甲基化改变,提示姜黄素可能是通过抑制糖尿病小鼠中某些基因的异常甲基化修饰而发挥抗糖尿病作用。     

Shiftwork and Higher Pancreatic Secretion: Early Detection of an Intermediate State of Insulin Resistance?

Previous studies have suggested that shiftwork can affect the prevalence of metabolic syndrome. This is thought to be related to disturbance of lipid parameters rather than their effects on glucose metabolism. Several complex mechanisms are suspected to be involved and notably insulin resistance, though the available data are limited. The objective of the present study was to provide further evidence for the effects of shiftwork on glucose and lipid metabolism with a specific focus on insulin resistance. A cross-sectional study has recruited 97 shiftworkers (SWs) (three shifts, 8 h) and 95 strictly day workers (DWs) from the same plant for 2001–2002. Several indices of insulin sensitivity or resistance were calculated, based on formulas of the homeostasis model assessment for insulin resistance (HOMA-IR), the Revised-Quicki, McAuley and Disse indices. The HOMA-β-cell index was used as a reflection of pancreatic secretion. Characteristics of the occupation, habitual diet and lifestyles were recorded. Logistic regression analysis in which pancreatic function or insulin sensitivity was the dependent variable was used to compare alternative models. Results: SWs were characterized as having significantly higher triglycerides and free fatty acids and normal but lower blood glucose. The risk of a high β-cell activity was increased almost three-fold in SWs. By adjusting for many confounding factors, SWs had significantly lower insulin sensitivity according to several indices, whereas HOMA-IR was not meaningfully different between shift and DWs. Lower insulin sensitivity and a compensatory pancreas response to maintain a normal glucose tolerance may suggest an intermediate state before development of frank insulin resistance in SWs. Early detection of these moderate alterations of the insulin/glucose balance could be important in the prevention of diabetes.     

Voluntary running exercise prevents β-cell failure in susceptible islets of the Zucker diabetic fatty rat

Physical activity improves glycemic control in type 2 diabetes (T2D), but its contribution to preserving β-cell function is uncertain. We evaluated the role of physical activity on β-cell secretory function and glycerolipid/fatty acid (GL/FA) cycling in male Zucker diabetic fatty (ZDF) rats. Six-week-old ZDF rats engaged in voluntary running for 6 wk (ZDF-A). Inactive Zucker lean and ZDF (ZDF-I) rats served as controls. ZDF-I rats displayed progressive hyperglycemia with β-cell failure evidenced by falling insulinemia and reduced insulin secretion to oral glucose. Isolated ZDF-I rat islets showed reduced glucose-stimulated insulin secretion expressed per islet and per islet protein. They were also characterized by loss of the glucose regulation of fatty acid oxidation and GL/FA cycling, reduced mRNA expression of key β-cell genes, and severe reduction of insulin stores. Physical activity prevented diabetes in ZDF rats through sustaining β-cell compensation to insulin resistance shown in vivo and in vitro. Surprisingly, ZDF-A islets had persistent defects in fatty acid oxidation, GL/FA cycling, and β-cell gene expression. ZDF-A islets, however, had preserved islet insulin mRNA and insulin stores compared with ZDF-I rats. Physical activity did not prevent hyperphagia, dyslipidemia, or obesity in ZDF rats. In conclusion, islets of ZDF rats have a susceptibility to failure that is possibly due to altered β-cell fatty acid metabolism. Depletion of pancreatic islet insulin stores is a major contributor to islet failure in this T2D model, preventable by physical activity.     

Long-term use of angiotensin II receptor antagonists and calcium-channel antagonists in Algerian hypertensive patients: Effects on metabolic and oxidative parameters

The effects of calcium antagonists (amlodipine) and angiotensin II receptor antagonists (telmisartan) on lipid profile and oxidative markers were investigated in Algerian hypertensive patients. At the beginning and after 1 year of antihypertensive therapy, blood samples are collected for determination of biochemical parameters (glucose, cholesterol, triglycerides, urea, creatinine) and oxidative markers (malondialdehyde, carbonyl proteins, nitric oxide, superoxide anion, vitamin C, glutathione, catalase, superoxide dismutase). The results of this study indicate that telmisartan and amlodipine are effective antihypertensive agents in the treatment of hypertension because a significant reduction in systolic and diastolic blood pressure was observed in all hypertensive patients after 1 year of treatment. Our results show also that telmisartan and amlodipine treatments counteracted hypertension-dependent lipid abnormalities and oxidative stress. Telmisartan treatment appears to be more efficient than amlodipine treatment. In addition, telmisartan, which reversed all lipid and redox changes associated with hypertension, should be prescribed, especially in hypertensive patients with hypertriglyceridemia and with severe oxidative stress.