Chujo Daisuke, Yagi Kunimasa, Asano Akimichi, Muramoto Hiroaki, Sakai Satoko, Ohnishi Akitsu, Shintaku-Kubota Miyuki, Mabuchi Hiroshi, Yamagishi Masakazu, Kobayashi Junji
Department of Internal Medicine, Graduate School of Medical Science, Kanazawa University, Kanazawa, Japan.
Hypertens Res. 2007 Dec;30(12):1205-10. doi: 10.1291/hypres.30.1205.
Hypertension contributes to the occurrence and progression of cardiovascular diseases. The angiotensin II type 1 receptor blocker telmisartan is reported to activate the peroxisome proliferator-activated receptor gamma and improve insulin sensitivity. We investigated the effects of telmisartan treatment on visceral fat, serum adiponectin and vascular inflammation markers in Japanese hypertensive patients. This was an open-label, non-controlled study. Twenty-eight essential hypertensive patients (22 men and 6 women; age 60.6+/-1.9 years; body mass index [BMI] 25.5+/-0.6 kg/m(2)) participated. Fat area was assessed with computerized tomography. All the subjects were started on telmisartan 40 mg/day, which was increased to 80 mg/day to achieve the blood pressure target of less than 130/80 mmHg. We assessed the visceral and subcutaneous fat areas, serum adiponectin levels, and vascular inflammation markers at baseline and 24 weeks of telmisartan treatment. There were significant reductions in visceral fat area (from 103.1+/-7.9 to 93.3+/-8.4 cm(2), p<0.01) and pulse wave velocity (from 1,706+/-52 to 1,587+/-51 cm/s, p<0.01) at 24 weeks. In contrast, significant increases in serum high-density lipoprotein cholesterol (from 5.06+/-0.15 to 5.32+/-0.13 mmol/L, p<0.05) and adiponectin levels (from 8.27+/-0.76 to 9.13+/-0.81 microg/mL, p<0.05) were observed. Also, there were reductions in the interleukin-6 level (from 2.26+/-0.27 to 1.60+/-0.14 pg/mL, p<0.01). We also conducted these investigations in male subjects alone and similar findings were obtained for all of these parameters. In conclusion, telmisartan treatment was associated with an improvement of vascular inflammation, reductions in visceral fat and increases in serum adiponectin.
高血压会促使心血管疾病的发生与发展。据报道,血管紧张素II 1型受体阻滞剂替米沙坦可激活过氧化物酶体增殖物激活受体γ并改善胰岛素敏感性。我们研究了替米沙坦治疗对日本高血压患者内脏脂肪、血清脂联素及血管炎症标志物的影响。这是一项开放标签、非对照研究。28例原发性高血压患者(22例男性和6例女性;年龄60.6±1.9岁;体重指数[BMI]25.5±0.6kg/m²)参与了研究。采用计算机断层扫描评估脂肪面积。所有受试者均开始服用替米沙坦40mg/天,之后增至80mg/天,以实现血压目标低于130/80mmHg。我们在替米沙坦治疗的基线期及24周时评估了内脏和皮下脂肪面积、血清脂联素水平及血管炎症标志物。24周时,内脏脂肪面积显著减少(从103.1±7.9降至93.3±8.4cm²,p<0.01),脉搏波速度也显著降低(从1706±52降至1587±51cm/s,p<0.01)。相反,血清高密度脂蛋白胆固醇显著升高(从5.06±0.15升至5.32±0.13mmol/L,p<0.05),脂联素水平也显著升高(从8.27±0.76升至9.13±0.81μg/mL,p<0.05)。此外,白细胞介素-6水平降低(从2.26±0.27降至1.60±0.14pg/mL,p<0.01)。我们还仅在男性受试者中进行了这些研究,所有这些参数均获得了类似结果。总之,替米沙坦治疗与血管炎症改善、内脏脂肪减少及血清脂联素增加有关。