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Induction of Insulin Resistance by Beta- Blockade but Not ACE-Inhibition: Long- Term Treatment with Atenolol Or Trandolapril

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Induction of Insulin Resistance by Beta- Blockade but Not ACE-Inhibition: Long- Term Treatment with Atenolol Or Trandolapril Journal of Human Hypertension (2000) 14, 175–180 2000 Macmillan Publishers Ltd All rights reserved 0950-9240/00 $15.00 www.nature.com/jhh ORIGINAL ARTICLE Induction of insulin resistance by beta- blockade but not ACE-inhibition: long- term treatment with atenolol or trandolapril R Reneland, E Alvarez, P-E Andersson, A Haenni, L Byberg and H Lithell Uppsala University, Uppsala, Sweden The effects on glucose metabolism by the beta-blocker and high-density lipoprotein cholesterol (؊13% vs atenolol and the angiotensin-converting enzyme (ACE)- ؉0.7%) also differed significantly between atenolol and inhibitor trandolapril were investigated in a randomised trandolapril. Results after 8 weeks were similar. Glucose double-blind parallel group study of patients with pri- tolerance was not affected by either drug. Atenolol mary hypertension. Twenty-six patients were treated reduced diastolic blood pressure (DBP) better than tran- with 50–100 mg atenolol and 27 patients with 2–4 mg dolapril (؊15.3 mm Hg vs ؊6.6 mm Hg for supine DBP The difference in effect on .(0.012 ؍ trandolapril o.d. Intravenous glucose tolerance tests, after 48 weeks, P euglycaemic hyperinsulinaemic clamps and serum lipid insulin sensitivity between the drugs corresponded to measurements were performed after 8 and 48 weeks of 25% of the baseline values of insulin sensitivity, and active treatment. After 48 weeks insulin sensitivity was persisted over 48 weeks of treatment. The choice of anti- reduced by 23% by atenolol while it remained hypertensive treatment could influence the risk of dia- unchanged during trandolapril treatment (؉0.5%, betes associated with treated hypertension. Journal of .for difference between treatments, Human Hypertension (2000) 14, 175–180 0.0010 ؍ P (ANCOVA). The effect on triglycerides (؉22% vs ؊8.5% Keywords: angiotensin-converting enzyme inhibitors; beta-blockers; human; insulin; randomised clinical trial Introduction duration of 6 months or less. Therefore, we wanted to study the metabolic effects of the ACE inhibitor It has been shown that antihypertensive treatment 1,2 trandolapril and the beta-blocker atenolol in a ran- increases the risk for diabetes mellitus. One poss- domised double-blind parallel group trial with end- ible mediator of that effect may be the impaired point assessment after 8 and у48 weeks to see insulin sensitivity associated with the use of beta- whether the effects differed between the long and blockers and diuretics, the dominating drug classes short term. in these epidemiological studies.3–5 Furthermore, recently a randomised intervention study showed that treatment based on the angiotensin-converting Patients and methods enzyme (ACE)-inhibitor, captopril, was associated Patients and protocol with a lower incidence of diabetes than conven- tional antihypertensive treatment.6 Patients with Patients were recruited through advertisements in primary hypertension are insulin resistant.7,8 Elev- the local newspapers. At the initial screening visit ated plasma insulin levels, an indirect marker of inclusion and exclusion criteria (Table 1) were insulin resistance, are associated with increased risk assessed, informed consent was obtained, and any of coronary heart disease.9–12 Therefore, metabolic ongoing antihypertensive medication was stopped. factors may contribute to the excess risk for coronary After that, blood pressure (BP) was monitored at reg- heart disease associated with even well-controlled ular visits at the clinic. When the diastolic BP (DBP) treated hypertension.13,14 However, there has been reached 95 mm Hg single-blind placebo adminis- some uncertainty as to whether the metabolic effects tration was initiated. As soon as a patient had met of antihypertensive drugs persist during continuing the BP criterion for inclusion in the active phase, treatment since most metabolic studies have had a randomisation was performed and baseline investi- gations were carried out. Intravenous glucose toler- ance tests and the euglycaemic, hyperinsulinaemic Correspondence: Richard Reneland, Department of Public Health clamps were performed on separate days, so that the and Caring Sciences/Geriatrics Unit, Uppsala University, P O Box 609, S-751 25 Uppsala, Sweden investigations were performed during a period of 4– Received 10 March 1999; revised and accepted 24 September 8 days. All metabolic investigations were performed 1999 in the morning after an overnight fast and before Metabolic effects of trandolapril and atenolol R Reneland et al 176 Table 1 Inclusion and selected exclusion criteria Insulin sensitivity measurements Inclusion Exclusion criteria Whole body sensitivity to insulin was measured by criteria the euglycaemic hyperinsulinaemic clamp pro- cedure according to DeFronzo et al,15 with minor Age 18–75 years Diabetes mellitus modifications. Insulin (Actrapid Human, Novo, DBP 95–115 mm Hg Lipid-lowering drugs, hormones, etc Copenhagen, Denmark) was infused at a rate of Stable weight Secondary hypertension 2 (Ͻ2.5 kgs change Recent cardiovascular event 56 mU/(min/m body surface area). The amount of during run-in Cardiac arrhythmias glucose infused to maintain the target glucose level period) Unstable angina/congestive heart failure during the period of assumed steady-state was Informed consent Mitral/aortic valve stenosis; defined as glucose uptake (M; mg/kg/min). Adjust- cardiomyopathy ment for the steady-state insulin concentration Renal or hepatic dysfunction Hereditary angioneurotic edema defined the insulin sensitivity index (M/I; Haematologic or electrolyte disturbances mg/min/kg/(mU/l). The intra-individual coefficient Treatment with enzyme inducing agents of variation for the insulin sensitivity index in our Treatment with antihypertensive drugs laboratory was 14%. Pregnancy/lactation/child-bearing potential Hypersensitivity to any of the study drugs Intravenous glucose tolerance test (IVGTT) Each patient’s response to an intravenous glucose load was assessed by a 90-min intravenous glucose drug intake. The clinical characteristics of the two tolerance test. The glucose load was an intravenous treatment groups are reported in Table 2. After base- injection within 1.5 min of 300 mg glucose per kg of line investigations, active treatment was initiated body weight in a 50% glucose solution. The disap- with 2 mg trandolapril or 50 mg atenolol with reg- pearance rate of glucose was expressed as a k value = × ular BP follow-up visits every 4 weeks (weeks 0–16) calculated from the formula k ln2 100/t1/2 where or 8 weeks (weeks 16–48). At each of these visits t1/2 is the time required for the glucose concentration to be halved. Plasma glucose was measured by the adverse events and concomitant medication were monitored by a trained nurse. After 4 weeks, the glucose dehydrogenase method (Gluc-DH , Merck, dose was doubled if the DBP was Ͼ90 mm Hg. Eight Darmstadt, Germany). Insulin was assayed in EDTA weeks into the active phase, investigations were plasma in duplicate using an enzymatic-immuno- repeated and patients were dropped out if their DBP logical assay (Enzymmun , Boehringer Mannhein, was Ͼ95 mm Hg on two consecutive measurements. Germany) performed in a ES300 automatic analyser A third assessment of end-points was performed (Boehringer Mannheim). The mean fasting plasma after 48 weeks of active treatment. glucose and insulin values were calculated from three blood samples drawn 5 min apart prior to the injection of glucose. Peak insulin response was Office blood pressure defined as the mean of insulin values measured in Supine BP and heart rate were measured in tripli- the samples drawn at 4, 6, and 8 min and the insulin cate by trained personnel. Cuff sizes of 12 × 45 or increment is reported as the difference between the 15 × 45 cm were used depending on the arm circum- peak and mean fasting value. Area under the ference. The three measurements on each occasion incremental curve (AUC) for glucose and insulin were averaged and the mean value of the DBP was was calculated by a trapezoid method. the basis for treatment decisions. Normalisation was р defined as a DBP 90 mm Hg at the time-point at Lipid and lipoprotein measurement which efficacy was assessed (8 or 48 weeks). In addition, responders were defined as patients hav- Cholesterol and triglyceride concentrations in serum ing normalised or reduced their DBP у10 mm Hg were assayed by enzymatic techniques (Instru- during the observation period. mentation Laboratories, Lexington, MA, USA) in a Monarch 2000 centrifugal analyzer. High-density lipoproteins (HDL) were separated by precipitation Table 2 Baseline characteristics of the study participants accord- with magnesium cloride/phosphotungstate. Low- ing to treatment (means s.d.) density lipoprotein (LDL) cholesterol was calculated using Friedewald’s formula: LDL = serum choles- Atenolol Trandolapril terol-HDL-(0.45 serum triglycerides). (n = 26) (n = 27) Age (years) 56 (9) 53 (10) Plasminogen activator inhibtor-1 (PAI-1) activity Sex (f/m) 7/19 7/20 BMI (kg/m2) 28 (4) 27 (3) PAI-1 activity was analysed in 18 atenolol treated and 20 trandolapril treated patients with a two-step ء(17) 158 ء(Systolic BP (mm Hg) 169 (14 Diastolic BP (mm Hg) 104 (4.9) 100 (4.5) indirect enzymatic assay (Spectrolyse/pL PAI kits, Insulin sensitivity index 4.8 (3) 5.3 (3) (mg/kg/min/100 mU) Biopool AB, Umea˚, Sweden). The activity is given Fasting plasma glucose 5.7 (0.6) 5.5 (0.4) in U/mL, where one unit is the amount of PAI-1 that (mmol/l) inhibits one international unit of single chain tissue- type plasminogen activator.
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