OBJECTIVE: Severe energy restriction in the treatment of obesity is limited by catabolism of body protein stores and, consequently, loss of lean as well as fat tissue. Growth hormone (GH), whose secretion is markedly impaired in obesity, is endowed with both lipolytic and protein anabolic properties. The aim of this study was to verify the effects of GH administration on body composition, plasma leptin levels and energy metabolism in obese patients undergoing severe dietary restriction. DESIGN: Single-blind placebo-controlled study. Twenty obese women were fed a diet of 41.86 kJ/kg ideal body weight (IBW) daily for 4 weeks: 10 of them were randomly assigned to a 4 week treatment with biosynthetic GH (rhGH, Saizen, Serono, Rome, Italy), 1 U/kg IBW/week in daily subcutaneous injections; the other 10 patients, matched for age and BMI, received vehicle only. SUBJECTS: Twenty women with simple obesity (age: 25.4 AE 1.07 y, BMI: 35.9 AE 0.35 kg/m 2 ). MEASUREMENTS: Plasma IGF-I and leptin, serum markers of bone turnover (serum bone isoenzyme of alkaline phosphatase, osteocalcin and urinary hydroxyproline), nitrogen balance, body composition (by DEXA), and resting energy expenditure (REE, by indirect calorimetry) were evaluated at baseline and after 4 weeks. RESULTS: Mean IGF-I plasma levels, not in¯uenced by energy restriction in patients receiving placebo, displayed a signi®cant increase in the group treated with rhGH. The mean weight reduction and fat mass loss were not signi®cantly different in the two groups (6.0 AE 0.51 vs 7.2 AE 0.30 kg, NS, and 5.36 AE 0.460 vs 4.28 AE 0.572 kg, NS, with rhGH and placebo, respectively). Likewise, plasma leptin levels decreased signi®cantly in weight-reduced subjects receiving either rhGH (from 16.2 AE 2.37 to 6.4 AE 0.39 ng/ml, P`0.05) or placebo (from 14.3 AE 2.55 to 7.7 AE 3.77 ng/ml, P`0.05). On the contrary, the mean decrease of lean body mass (LBM) was signi®cantly lower in the GH-treated patients than in those receiving vehicle (1.52 AE 0.60 vs 3.79 AE 0.45 kg, P`0.05). In keeping with these ®ndings, the mean daily nitrogen balance was signi®cantly less negative in the GH-treated subjects than in the vehicle-injected patients (mean of the 4 week daily urine collections 7185.7 AE 40.33 vs 7363.9 AE 55.47 mmol/d, P`0.05, respectively). Further, a signi®cant reduction of mean REE was recorded in the energy-restricted placebo-treated patients (from 8807 AE 498 to 7580 AE 321 kJ/24 h, P`0.05), but not in the patients receiving rhGH (from 8367 AE 580 to 8903 AE 478 kJ/ 24 h, NS). Actually, when corrected for LBM, REE was even increased by GH administration (from 197.9 AE 11.76 to 219.3 AE 9.87 kJ/kg LBM/24 h, P`0.05), whereas it was unchanged in the placebo group (from 201.7 AE 13.85 to 190.0 AE 9.87 kJ/kg LBM/24 h, NS). A tendency of serum markers of bone turnover to increase was observed in the patients treated with rhGH, however with no changes in bone mineral content and density. CONCLUSION: rhGH treatment, though unable to enhance diet-induced weight and fat mass reduction...
To evaluate whether histamine exerts a direct effect on coronary hemodynamics in humans, and to investigate the role played by H1 and H2 receptors in this response, intracoronary saline solution or histamine (4 micrograms) was administered in 10 patients with normal coronary arteries during diagnostic cardiac catheterization. Histamine injection was repeated after intravenous cimetidine (400 mg) and diphenhydramine (10 mg). The electrocardiogram, arterial pressure and thermodilution coronary blood flow were continuously monitored during and for 40 seconds after each injection. Immediately after histamine injection there was a significant increase in coronary blood flow (65 +/- 6%) and a decrease in coronary vascular resistance (-40 +/- 3%) (both p less than 0.001), with minor changes in the RR interval and the mean arterial pressure. H2 receptor blockade with cimetidine did not affect these changes, while H1 receptor blockade with diphenhydramine significantly reduced the histamine-induced increase in coronary blood flow and the decrease in coronary vascular resistance (26 +/- 6%, p less than 0.005 and -18 +/- 5%, p less than 0.001, respectively). Twenty to 30 seconds after histamine injection, a significant decrease in mean arterial pressure (-17 +/- 2%, p less than 0.001) and in the RR interval (-4 +/- 1%, p less than 0.01) was observed. These changes persisted after H2 receptor blockade with cimetidine, but were completely abolished after H1 receptor blockade with diphenhydramine. In each case coronary and systemic hemodynamics returned to normal within 40 seconds of the injection.(ABSTRACT TRUNCATED AT 250 WORDS)
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