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      Does Bromocriptine Improve Glycemic Control of Obese Type-2 Diabetics?

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          Abstract

          Background: Various oral hypoglycemic agents have already been administered to type-2 diabetic patients to normalize their plasma glucose concentrations but they have not had complete and sustained success. In recent years, bromocriptine has been tried with controversial results. In present study, the effect of bromocriptine on glycemic control was evaluated in obese type-2 diabetic patients. Methods: In a double-blind placebo-controlled clinical trial, 40 obese patients with type-2 diabetes (aged 32–70 years) were randomly allocated to the two treatment groups. The first group received bromocriptine (2.5 mg daily) for a total of 3 months. The second group received placebo. They had been uncontrolled on fixed doses of glibenclamide or its combination with metformin in the 3 months before enrolling in the study. The fasting plasma glucose (FPG) level and glycosylated hemoglobin (HbA<sub>1</sub>) were measured and body mass index (BMI) was calculated before and 1, 2 and 3 months after treatment. Results: The FPG level decreased in the bromocriptine-treated group from 10.59 ± 0.42 to 9.06 ± 0.41 mmol/l (mean ± SEM; p < 0.01), whereas in the placebo group it was not changed, 10.69 ± 0.52 and 10.6 ± 0.57 mmol/l, respectively. The HbA<sub>1</sub> concentration was reduced in the bromocriptine-treated group from 9.9 ± 0.3 to 9.5 ±0.2% (p = 0.06), whereas it increased in the placebo-treated group from 10.2 ± 0.3 to 11.3 ± 0.6% (p < 0.05). The differences in HbA<sub>1</sub> (1.8%, p < 0.01) and FPG (1.55 mmol/l, p < 0.05) levels between the bromocriptine and placebo groups at 3 months were significant. No changes in body weight or BMI occurred during the study in either placebo- or bromocriptine-treated group. Conclusion: The data further support the contention that bromocriptine improves glycemic control in obese type-2 diabetic patients, although the mechanism of action remains to be determined.

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          Bromocriptine inhibits in vivo free fatty acid oxidation and hepatic glucose output in seasonally obese hamsters (Mesocricetus auratus).

          Seasonally obese hyperinsulinemic hamsters were treated for 5 weeks with bromocriptine (500 to 600 micrograms per animal) and tested for drug effects on energy balance, body fat stores, nocturnal whole-body free fatty acid (FFA) metabolism and hepatic glucose output, and diurnal glucose tolerance. After 5 weeks, bromocriptine treatment reduced retroperitoneal fat pad weight by 45% without altering either daily food consumption or end-treatment total daily energy expenditure. Also, 5 weeks of treatment improved the diurnal glucose tolerance, resulting in a 47% and 33% decrease in the area under glucose and insulin curves, respectively. After 4 weeks, bromocriptine treatment reduced nocturnal lipolysis by 28%, palmitate rate of appearance into plasma by 30%, palmitate oxidation by 33%, and hepatic glucose output by 28%. Moreover, these reductions were accompanied by a 75% reduction in plasma insulin concentration. The data suggest that bromocriptine may improve diurnal glucose tolerance in part by inhibiting the preceding nocturnal lipolysis and FFA oxidation. Reductions in nocturnal FFA oxidation and hepatic glucose production may result from bromocriptine's influences on circadian organization of hypothalamic centers known to regulate these activities. Available evidence suggests that bromocriptine may impact this neuroendocrine organization of metabolism by increasing the dopamine to noradrenaline activity ratio in central (hypothalamic) and peripheral (eg, liver and adipose) target tissues.
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            Author and article information

            Journal
            HRE
            Horm Res Paediatr
            10.1159/issn.1663-2818
            Hormone Research in Paediatrics
            S. Karger AG
            1663-2818
            1663-2826
            2004
            September 2004
            13 September 2004
            : 62
            : 2
            : 55-59
            Affiliations
            Isfahan Endocrinology and Metabolism Research Center, Isfahan University of Medical Sciences and Health Services, Isfahan, Iran
            Article
            78932 Horm Res 2004;62:55–59
            10.1159/000078932
            15205563
            © 2004 S. Karger AG, Basel

            Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

            Page count
            Tables: 3, References: 21, Pages: 5
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