Mori Yutaka, Itoh Yohta, Tajima Naoko
Department of Internal Medicine, National Hospital Organization, Utsunomiya National Hospital, Kawachi, Tochigi, Japan.
Adv Ther. 2007 Jan-Feb;24(1):146-53. doi: 10.1007/BF02850002.
Angiotensin II receptor blockers as a class are reported to act as insulin sensitizers. Of these, telmisartan has been shown to have additional unique peroxisome proliferator-activated receptor-gamma-mediated, insulin-sensitizing properties. In this study, investigators explored the effects of telmisartan on glycemic control and lipid metabolism in hypertensive patients with type 2 diabetes who had switched to telmisartan from another angiotensin II receptor blocker. The study subjects were 42 hypertensive outpatients with type 2 diabetes who were being treated with candesartan 8 mg/d and who agreed to switch to treatment with telmisartan 40 mg/d. Relevant laboratory variables were measured 6 mo before treatment switching, at the time of switching, and 6 mo after switching. No significant differences were noted in blood pressure, body mass index, or glycosylated hemoglobin among subjects before and after therapy was switched. No adverse reactions such as edema or hepatic toxicity were noted. No significant changes in fasting plasma glucose, fasting insulin, HOMA-R (insulin resistance as measured by the homeostasis model), preheparin lipoprotein lipase mass, high-density lipoprotein cholesterol, and free fatty acids were noted. Triglyceride levels were significantly decreased, however, and adiponectin levels were significantly increased (8.1+/-3.1 microg/mL at switching; 8.6+/-3.0 microg/mL 6 mo after switching; P<.01) after the switch to telmisartan therapy. Study results show that telmisartan did not affect glycemic control, but it improved lipid metabolism and adiponectin production in patients with type 2 diabetes, suggesting that AT(1)-receptor antagonism and selective peroxisome proliferator-activated receptor-gamma activation by telmisartan combine to account for observed effects on lipid metabolism and adiponectin production.
据报道,血管紧张素II受体阻滞剂作为一类药物可起到胰岛素增敏剂的作用。其中,替米沙坦已被证明具有额外独特的过氧化物酶体增殖物激活受体γ介导的胰岛素增敏特性。在本研究中,研究人员探讨了替米沙坦对从另一种血管紧张素II受体阻滞剂转换为替米沙坦治疗的2型糖尿病高血压患者血糖控制和脂质代谢的影响。研究对象为42例2型糖尿病高血压门诊患者,他们正在接受8mg/d坎地沙坦治疗,并且同意转换为40mg/d替米沙坦治疗。在治疗转换前6个月、转换时以及转换后6个月测量相关实验室变量。治疗转换前后受试者的血压、体重指数或糖化血红蛋白无显著差异。未观察到水肿或肝毒性等不良反应。空腹血糖、空腹胰岛素、HOMA-R(通过稳态模型测量的胰岛素抵抗)、肝素前脂蛋白脂肪酶质量、高密度脂蛋白胆固醇和游离脂肪酸均无显著变化。然而,转换为替米沙坦治疗后,甘油三酯水平显著降低,脂联素水平显著升高(转换时为8.1±3.1μg/mL;转换后6个月为8.6±3.0μg/mL;P<0.01)。研究结果表明,替米沙坦不影响血糖控制,但可改善2型糖尿病患者的脂质代谢和脂联素生成,提示替米沙坦的AT(1)受体拮抗作用和选择性过氧化物酶体增殖物激活受体γ激活共同导致了对脂质代谢和脂联素生成的观察到的影响。