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Horm Metab Res 2006; 38(5): 323-329
DOI: 10.1055/s-2006-925406
Original Clinical
© Georg Thieme Verlag KG Stuttgart · New York

The Effect of Oral Glucose Loads on Tissue Metabolism During Angiotensin II Receptor and Beta-receptor Blockade in Obese Hypertensive Subjects

M.  Boschmann1 , U.  Kreuzberg2 , S.  Engeli1 , F.  Adams1 , G.  Franke1 , S.  Klaua1 , J.  Scholze3 , G.  Weidinger2 , F.  C.  Luft1 , A.  M.  Sharma4 , J.  Jordan1
  • 1 Franz-Volhard Clinical Research Center, Charité Campus Buch and HELIOS Klinikum, Berlin, Berlin, Germany
  • 2 Clinical Research and Development, Novartis Pharma, Nürnberg, Germany
  • 3 Outpatient Department, Charité Campus Mitte, Berlin, Germany
  • 4 Canada Research Chair for Cardiovascular Obesity Research & Management, Department of Medicine, McMaster University, Hamilton General Hospital, 237 Barton Street East, Hamilton, Ontario L8L 2X2, Canada
Further Information

Publication History

Received 3 May 2005

Accepted after second revision 23 January 2006

Publication Date:
23 May 2006 (online)

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Abstract

AT1 receptor blockers and ACE inhibitors decrease the risk for new onset diabetes mellitus. The phenomenon could be related to a direct angiotensin II effect on tissue metabolism. To address the issue, we recruited eighteen obese hypertensive patients. Patients were randomized to double-blind treatment with either valsartan (n = 8) or atenolol (n = 10) for thirteen weeks. They underwent an oral glucose tolerance test before and during active treatment, while metabolism was monitored through subcutaneous and intramuscular microdialysis and indirect calorimetry. After glucose ingestion, venous glucose and insulin concentrations increased rapidly while systemic free fatty acid concentrations were suppressed. Dialysate glucose and lactate concentrations increased briskly in adipose tissue and in skeletal muscle. Dialysate glycerol decreased profoundly in both tissues. Respiratory quotient increased markedly after glucose ingestion. These responses were identical at baseline and during active treatment either drug. We conclude that AT1 receptor blockade in obese hypertensive patients has no effect on interstitial glucose supply, lipolysis, and substrate oxidation. One possible explanation is that angiotensin II levels in obese hypertensives are not sufficient to elicit the metabolic changes that have been observed after direct angiotensin II application. The exact mechanism by which inhibition of the renin-angiotensin-aldosterone system decreases the diabetes risk remains unresolved and requires further study.

Key words

Adipose tissue - angiotensin II - insulin - skeletal muscle

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Jens Jordan, M.D.

Franz Volhard Clinical Research Center

Haus 129 · Charité Campus Buch · Wiltbergstr. 50 · 13125 Berlin · Germany

Fax: +49 (30) 94 17 22 65

Email: jordan@fvk.charite-buch.de