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The renin-angiotensin-aldosterone system, glucose metabolism and diabetes

Gilberta Giacchetti1, Leonardo A Sechi, Silvia Rilli

  • 1The Division of Endocrinology, Department of Internal Medicine, Universita Politecnica della Marche, 60020 Ancona, Italy.

Trends in Endocrinology and Metabolism: TEM
|April 6, 2005
PubMed

Insights

In diabetes mellitus, activated renal renin-angiotensin system (RAS) causes tissue damage. Blocking the Angiotensin II type 1 receptor (AT(1)) improves endothelial function and protects against diabetic complications.

Area of Science:

  • Endocrinology
  • Cardiovascular Research
  • Nephrology

Background:

  • Diabetes mellitus (DM) involves suppressed circulating renin-angiotensin system (RAS) but activated renal RAS.
  • Hyperglycemia in DM elevates tissue angiotensin II (Ang II), leading to oxidative stress and endothelial damage.
  • Early DM shows AT(1) receptor upregulation and AT(2) receptor downregulation, contributing to tissue injury.

Purpose of the Study:

  • To investigate the role of the tissue renin-angiotensin-aldosterone system (RAAS) in diabetic tissue damage.
  • To understand the impact of hyperglycemia on Ang II levels and receptor expression in DM.
  • To evaluate the therapeutic potential of AT(1) receptor blockers in mitigating DM-related tissue pathology.

Main Methods:

  • Analysis of circulating and tissue RAS components in diabetic models.
  • Assessment of Ang II, aldosterone, and oxidative stress markers.
  • Evaluation of AT(1) and AT(2) receptor expression patterns.
  • Investigating the effects of AT(1) receptor blockers on endothelial function and NAD(P)H oxidase activity.

Main Results:

  • Hyperglycemia-induced Ang II activation of AT(1) receptors drives oxidative stress and endothelial damage.
  • Imbalance in AT(1)/AT(2) receptor expression is linked to diabetic tissue pathology.
  • Insulin resistance exacerbates endothelial dysfunction via NAD(P)H oxidase activation.
  • AT(1) receptor blockade normalizes oxidase activity and enhances endothelial function.

Conclusions:

  • The tissue RAAS is a critical mediator of diabetic tissue damage.
  • Targeting the AT(1) receptor offers a promising strategy for protecting against diabetic complications.
  • Understanding the RAAS in DM is essential for developing effective therapeutic interventions.

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