Comparative effects of telmisartan and eprosartan on insulin sensitivity in the treatment of overweight hypertensive patients.
The aim of this study was to compare the effect of telmisartan and eprosartan on insulin sensitivity in overweight hypertensive patients. Fifty overweight (BMI > or = 25 and <30 kg/m (2)) outpatients, aged 41-65 years, with mild to moderate hypertension [systolic blood pressure (SBP) >140 and diastolic blood pressure (DBP) > or = 90 and < or = 110 mmHg], after a 4-week placebo period, were randomized to receive telmisartan 80 mg or eprosartan 600 mg for 8 weeks. Following another 4-week placebo period, patients were crossed to the alternative regimen for further 8 weeks. At the end of each placebo and active treatment period, blood pressure (BP), insulin sensitivity (by euglycemic hyperinsulinemic clamp), fasting plasma glucose (FPG), insulin (FPI), total cholesterol (TC), LDL-C, HDL-C, and triglycerides (Tg) were evaluated. Insulin sensitivity was expressed as the amount of glucose infused during the last 30 min (glucose infusion rate, GIR) in micromol/min/kg. Both telmisartan and eprosartan significantly reduced SBP/DBP values (by a mean of 19.4/13.3 mmHg and 17.9/12.1 mmHg respectively, all p<0.001 vs. placebo), with no significant difference between the two treatments. GIR was significantly increased by telmisartan (2.25+/-0.61 micromol/min/kg, p<0.05 vs. placebo) but not by eprosartan (0.25+/-0.14 micromol/min/kg, p=ns), the difference between the two drugs being statistically significant (p<0.02). No change in FPG, FPI, HDL-C, and Tg was observed with either treatment. Telmisartan significantly reduced TC (-9.9 mg/dl, -5%, p<0.04 vs. placebo) and LDL-C (-8.8 mg/dl, -7%, p<0.03 vs. placebo), whereas eprosartan did not influence them. These findings indicate a superiority regarding an improvement of insulin sensitivity and plasma lipid profile in overweight hypertensives by telmisartan as compared to eprosartan, possibly related to the selective stimulating PPAR-gamma property of telmisartan.
Fogari
R
R
Department of Internal Medicine and Therapeutics, Centro Ipertensione e Fisiopatologia Cardiovascolare, University of Pavia, 27100 Pavia, Italy. r.fogari@unipv.it
Zoppi
A
A
Ferrari
I
I
Mugellini
A
A
Preti
P
P
Lazzari
P
P
Derosa
G
G
D000179:Acrylates / Q000627:therapeutic use*; D000328:Adult; D000368:Aged; D047228:Angiotensin II Type 1 Receptor Blockers / Q000627:therapeutic use; D001562:Benzimidazoles / Q000627:therapeutic use*; D001565:Benzoates / Q000627:therapeutic use*; D001786:Blood Glucose; D005260:Female; D006801:Humans; D006973:Hypertension / Q000097:blood / Q000150:complications* / Q000188:drug therapy* / Q000503:physiopathology; D007093:Imidazoles / Q000627:therapeutic use*; D007328:Insulin / Q000378:metabolism*; D008297:Male; D008875:Middle Aged; D050177:Overweight / Q000097:blood / Q000150:complications* / Q000188:drug therapy* / Q000503:physiopathology; D000077333:Telmisartan; D013876:Thiophenes / Q000627:therapeutic use*
D000179:Acrylates; D047228:Angiotensin II Type 1 Receptor Blockers; D001562:Benzimidazoles; D001565:Benzoates; D001786:Blood Glucose; D007093:Imidazoles; D007328:Insulin; D013876:Thiophenes; C068373:eprosartan; D000077333:Telmisartan