The effect of angiotensin II receptor antagonism with losartan on glucose metabolism and insulin sensitivity

Moan, Andreas; Høieggen, Aud; Seljeflot, Ingebjørg; Risanger, Terje; Arnesen, Harald; Kjeldsen, Sverre E.

doi:10.1097/00004872-199609000-00008

Cited by 65 publications

(49 citation statements)

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“…The present study confirms the findings and hypothesis in our early studies, which suggested that losartan improves insulin sensitivity, 12,24 particularly in patients with severe hypertension 24 or insulin resistance. 12 In the Insulin Carotids US Scandinavia (ICARUS)-study, 25 a Losartan Intervention For Endpoint-Reduction in Hypertension (LIFE) substudy, long-term treatment with losartan for 3 years maintained insulin sensitivity in hypertensive patients with electrocardiographic left ventricular hypertrophy, whereas on treatment with atenolol insulin sensitivity decreased.…”

Section: Discussionsupporting

confidence: 93%

“…The sample size needed was calculated based on earlier studies of Moan et al 12 of the effect of losartan on glucose metabolism and insulin sensitivity in hypertensive patients. They had standard errors of mean (s.e.m.)…”

Section: Discussionmentioning

confidence: 99%

“…12 In the Insulin Carotids US Scandinavia (ICARUS)-study, 25 a Losartan Intervention For Endpoint-Reduction in Hypertension (LIFE) substudy, long-term treatment with losartan for 3 years maintained insulin sensitivity in hypertensive patients with electrocardiographic left ventricular hypertrophy, whereas on treatment with atenolol insulin sensitivity decreased. Atenolol and other bblockers are known to increase the risk of diabetes mellitus.…”

Section: Discussionmentioning

confidence: 99%

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Improved insulin sensitivity with the angiotensin II-receptor blocker losartan in patients with hypertension and other cardiovascular risk factors

et al. 2006

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We aimed to compare the effects of two different vasodilating principles, angiotensin II-receptor blockade and calcium channel blockade, on peripheral insulinmediated glucose uptake in patients with hypertension and other cardiovascular risk factors. Twenty-one hypertensive patients (11 women and 10 men) with mean age 58.6 years (range 46-75 years), body mass index 29.271.0 kg/m 2 and blood pressure 16073/ 9672 mm Hg entered a 4-week run-in period with open-label amlodipine 5 mg. Thereafter they were randomized double-blindly to additional treatment with amlodipine 5 mg or losartan 100 mg. After 8 weeks of treatment, all patients underwent clinical examination and laboratory testing, and 17 of them underwent a hyperinsulinaemic isoglycaemic glucose clamp. After a 4-week open-label wash-out phase, the participants crossed over to the opposite treatment regimen and final examinations with hyperinsulinaemic isoglycaemic glucose clamp after another 8 weeks. Blood pressure was lowered to the same level in both treatment periods. The glucose disposal rate was significantly higher after treatment with losartan 100 mg þ amlodipine 5 mg compared to amlodipine 10 mg (4.970.4 vs 4.270.5 mg/kg/ min, P ¼ 0.039). Thus our data suggest that angiotensin II-receptor blockade with losartan improves glucose metabolism at the cellular level beyond what can be expected by the vasodilatation and blood pressure reduction alone.

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Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Improved insulin sensitivity with the angiotensin II-receptor blocker losartan in patients with hypertension and other cardiovascular risk factors

et al. 2006

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“…45,46,54 In the present study, imidapril significantly increased insulin sensitivity, as assessed by euglycemic-hyperinsulinemic clamp, whereas candesartan did not. These findings, which are in agreement with previous observations by ourselves and other authors, 35,[55][56][57] besides providing another possible explanation for the different effects of the two drugs on the fibrinolytic balance, also suggest that mechanisms other than Ang II inhibition, such as the increase in endogenous kinins because of ACE inhibition, might be responsible for the observed different influences of imidapril and candesartan on insulin sensitivity.…”

Section: Discussionsupporting

confidence: 93%

Fibrinolysis and insulin sensitivity in imidapril and candesartan (FISIC study) recipients with hypertension

et al. 2010

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The aim of this study was to evaluate the effects of imidapril and candesartan on fibrinolysis and insulin sensitivity in normoweight hypertensive patients. After a 2-week wash-out period, 61 patients with mild-to-moderate hypertension were randomized to imidapril or candesartan for 12 weeks. Blood pressure (BP), plasma tissue plasminogen activator (t-PA) and plasminogen activator inhibitor-1 (PAI-1) antigen activities were evaluated at baseline and during treatment. The patients underwent a euglycemic-hyperinsulinemic clamp (insulin sensitivity was evaluated as glucose infusion rate during the last 30 min) and a desmopressin test (with desmopressin infusion in the brachial artery) to evaluate endothelial ability to release t-PA. Imidapril and candesartan induced similar systolic/diastolic BP reductions (À16/12.6 and À16.1/12.2 mm Hg, respectively, Po0.001 vs. baseline). Imidapril increased glucose infusion rate (+1.1 mg min À1 per kg, Po0.02), whereas candesartan did not change it. Both drugs decreased PAI-1 antigen activity after 4 weeks of treatment; subsequently, only the decreasing effect of imidapril was sustained throughout the 12 weeks, whereas candesartan increased PAI-1 activity at week 12 (Po0.05 vs. baseline, Po0.01 vs. imidapril). Activity of t-PA decreased with candesartan (from 0.48 ± 0.16 to 0.43 ± 0.14 IU ml À1 , Po0.05) but not with imidapril. Activity of t-PA in response to desmopressin was increased more by imidapril (+4.45 IU ml À1 ) than by candesartan (+2.73 IU ml À1 , Po0.01 vs. imidapril). These results indicate that in normoweight hypertensive patients, despite similar BP reduction, imidapril but not candesartan improved the fibrinolytic balance, suggesting that mechanisms other than Ang II inhibition, possibly including bradykinin-mediated effects on insulin sensitivity and endothelial function, may be responsible for these different effects.

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“…In addition, the beneficial effects of a low dose of an ARB in the prevention of target organ damage have been demonstrated in mildly hypertensive patients with type 2 diabetes, with prevention of early kidney damage being independent of the antihypertensive activity (34). To date, the ARBs valsartan, losartan, and candesartan cilexetil given for periods of up to 12 weeks have been shown not to affect glucose homeostasis (16,35,36) and, when given for a (16,36). Only one study has evaluated the longer-term impact on lipid profiles in diabetic patients (17).…”

Section: Discussionmentioning

confidence: 99%

Effects of Telmisartan Compared with Eprosartan on Blood Pressure Control, Glucose Metabolism and Lipid Profile in Hypertensive, Type 2 Diabetic Patients: a Randomized, Double-Blind, Placebo-Controlled 12-Month Study

et al. 2004

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The effect of angiotensin II receptor antagonism with losartan on glucose metabolism and insulin sensitivity

Cited by 65 publications

References 0 publications

Improved insulin sensitivity with the angiotensin II-receptor blocker losartan in patients with hypertension and other cardiovascular risk factors

Improved insulin sensitivity with the angiotensin II-receptor blocker losartan in patients with hypertension and other cardiovascular risk factors

Fibrinolysis and insulin sensitivity in imidapril and candesartan (FISIC study) recipients with hypertension

Effects of Telmisartan Compared with Eprosartan on Blood Pressure Control, Glucose Metabolism and Lipid Profile in Hypertensive, Type 2 Diabetic Patients: a Randomized, Double-Blind, Placebo-Controlled 12-Month Study

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