Metabolism - Clinical and Experimental
Volume 47, Supplement 1 , Pages 7-11, December 1998

Role of angiotensin-converting enzyme inhibition in glucose metabolism and renal injury in diabetes

  • Manuel T. Velasquez

      Affiliations

    • Corresponding Author InformationAddress reprint requests to Manuel T. Velasquez, MD, Division of Renal Diseases and Hypertension, Department of Medicine, George Washington University Medical Center, 2150 Pennsylvania Avenue, NW, Washington, DC 20037.
    • Department of Medicine, George Washington University Medical Center, Washington, DC, USA
    • Beltsville Human Nutrition Research Center, Agricultural Research Service, US Department of Agriculture, Beltsville, MD, USA
    • University of Maryland, College Park, MD, USA
    • Institut De Recherches Internationales Servier and Compagnie-Developpement, Paris, France
  • ,
  • Sam J. Bhathena

      Affiliations

    • Department of Medicine, George Washington University Medical Center, Washington, DC, USA
    • Beltsville Human Nutrition Research Center, Agricultural Research Service, US Department of Agriculture, Beltsville, MD, USA
    • University of Maryland, College Park, MD, USA
    • Institut De Recherches Internationales Servier and Compagnie-Developpement, Paris, France
  • ,
  • John S. Striffler

      Affiliations

    • Department of Medicine, George Washington University Medical Center, Washington, DC, USA
    • Beltsville Human Nutrition Research Center, Agricultural Research Service, US Department of Agriculture, Beltsville, MD, USA
    • University of Maryland, College Park, MD, USA
    • Institut De Recherches Internationales Servier and Compagnie-Developpement, Paris, France
  • ,
  • Nancy Thibault

      Affiliations

    • Department of Medicine, George Washington University Medical Center, Washington, DC, USA
    • Beltsville Human Nutrition Research Center, Agricultural Research Service, US Department of Agriculture, Beltsville, MD, USA
    • University of Maryland, College Park, MD, USA
    • Institut De Recherches Internationales Servier and Compagnie-Developpement, Paris, France
  • ,
  • Elizabeth Scalbert

      Affiliations

    • Department of Medicine, George Washington University Medical Center, Washington, DC, USA
    • Beltsville Human Nutrition Research Center, Agricultural Research Service, US Department of Agriculture, Beltsville, MD, USA
    • University of Maryland, College Park, MD, USA
    • Institut De Recherches Internationales Servier and Compagnie-Developpement, Paris, France

Abstract 

The role of angiotensin-converting enzyme (ACE) inhibition in glucose metabolism and renal injury in diabetes has been extensively investigated in diabetic humans, as well as in animal models of diabetes. Accumulated data indicate that ACE inhibitors have either no adverse effect on glucose control or insulin sensitivity or may even improve them. ACE inhibitors also appear to have neutral or positive effects on lipid metabolism. The variability of results between studies may relate to differences in experimental design, the degree of glycemia or insulin resistance, potassium balance, and dose or duration of ACE inhibitor treatment, among others. In contrast, ACE inhibitors have proved effective in limiting proteinuria and retarding renal function loss in insulin-dependent diabetes mellitus (IDDM) or non—insulin-dependent diabetes mellitus (NIDDM) patients. In rats with experimental or spontaneous diabetes, ACE inhibitors also reduce proteinuria and limit glomerular as well as tubulointerstitial damage, independent of their effects on systemic arterial pressure. How ACE inhibitors limit renal injury in diabetes is not entirely clear, but hemodynamic and nonhemodynamic mechanisms may be involved. Increasing evidence suggests that the intrarenal renin-angiotensin system (RAS) may be altered or activated in the diabetic kidney. Such activation may be specifically inhibited by ACE inhibitors and may explain the superiority of this class of agents over other antihypertensive agents in reducing proteinuria and slowing the progression of diabetic nephropathy.

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PII: S0026-0495(98)90363-8

Metabolism - Clinical and Experimental
Volume 47, Supplement 1 , Pages 7-11, December 1998