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Endogenous Insulin Modulates Circulating Endothelin-1 Concentrations in Humans

  1. Claudio Ferri, MD,
  2. Cesare Bellini, MD,
  3. Giovambattista Desideri, MD,
  4. Giancarlo De Mattia, MD and
  5. Anna Santucci, MD
  1. University “La Sapienza” Institute of 1 Clinica Medica, Andrea Cesalpino Foundation Rome
  2. Department of Internal Medicine, University of L'Aquila L'Aquila, Italy
  3. Experimental Medicine, University of L'Aquila L'Aquila, Italy
  1. Address correspondence and reprint requests to Claudio Ferri, MD, Universitá “La Sapienza,” Istituto di 1 Clinica Medica, Fondazione Andrea Cesalpino, 00161 Rome, Italy

Abstract

OBJECTIVE To assess the effect of oral glucose loading on plasma endothelin-1 (ET-1) levels in humans.

RESEARCH DESIGN AND METHODS A total of 75 g D-glucose was given orally to 14 nonobese nondiabetic essential hypertensive subjects (eight men and six women, mean age 43.1 ± 3.0 years) and eight normotensive subjects (four men and four women, mean age 45.2 ± 4.1 years). Blood samples for plasma ET-1 measurement were drawn every 30 min for 2 h and then at 180 and 240 min.

RESULTS After glucose load, insulin increased more significantly in hypertensive subjects than in normotensive subjects at times 60 (P = 0.004) and 90 (P = 0.001) min. Glucose loading was followed by a mild but significant increase in circulating ET-1 levels in both groups (hypertensive subjects, from 0.87 ± 0.25 pg/ml at time 0 to 1.64 ± 0.33 pg/ml at 120 min and 1.74 ± 0.38 pg/ml at 180 min, P < 0.05; normotensive subjects, from 0.82 ± 0.38 pg/ml at time 0 to 1.42 ± 0.18 pg/ml at 180 min, P < 0.05). Whereas baseline ET-1 levels were similar between the two groups, postload ET-1 levels were higher in hypertensive subjects than in normotensive subjects (P = 0.003 at 120 min; P = 0.04 at 180 min).

CONCLUSIONS This study indicates that significant changes in circulating ET-1 levels occur after oral glucose loading, probably due to a glucose-induced increment in endogenous insulin concentration.

  • Received May 16, 1995.
  • Accepted December 21, 1995.
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