title: Telmisartan improves lipid metabolism and adiponectin production but does not affect glycemic control in hypertensive patients with type 2 diabetes.
abstract: 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.
authors.affiliation: Department of Internal Medicine, National Hospital Organization, Utsunomiya National Hospital, Kawachi, Tochigi, Japan. moriyutakajp@yahoo.co.jp
authors.forename: Yutaka
authors.initials: Y
authors.lastname: Mori
authors.forename: Yohta
authors.initials: Y
authors.lastname: Itoh
authors.forename: Naoko
authors.initials: N
authors.lastname: Tajima
mesh_terms: D052242:Adiponectin / Q000096:biosynthesis*; D047228:Angiotensin II Type 1 Receptor Blockers / Q000627:therapeutic use*; D001562:Benzimidazoles / Q000627:therapeutic use*; D001565:Benzoates / Q000627:therapeutic use*; D001786:Blood Glucose / Q000187:drug effects*; D001835:Body Weight; D003924:Diabetes Mellitus, Type 2 / Q000150:complications / Q000378:metabolism / Q000517:prevention & control*; D005260:Female; D006442:Glycated Hemoglobin; D006801:Humans; D006973:Hypertension / Q000150:complications / Q000188:drug therapy*; D050356:Lipid Metabolism / Q000187:drug effects*; D008055:Lipids / Q000097:blood; D008297:Male; D008875:Middle Aged; D000077333:Telmisartan
chemical_list: D052242:Adiponectin; D047228:Angiotensin II Type 1 Receptor Blockers; D001562:Benzimidazoles; D001565:Benzoates; D001786:Blood Glucose; D006442:Glycated Hemoglobin; D008055:Lipids; D000077333:Telmisartan