[Study on the altered nitric oxide metabolism in experimental diabetes]

Tamási Tábi1, Zsuzsa Soltész, Kálmán Magyar

  • 1Semmelweis Egyetem Gyógyszerhatástani Intézet, Budapest.

Acta Pharmaceutica Hungarica
|November 11, 2006
PubMed

Insights

Diabetic angiopathy involves nitric oxide (NO) dysfunction. Insulin therapy reduces NO

Area of Science:

  • Biochemistry
  • Physiology
  • Endocrinology

Context:

  • Diabetic angiopathy is characterized by endothelial dysfunction, linked to reduced nitric oxide (NO) biological action and increased oxidative stress.
  • Early stages of diabetes mellitus can exhibit altered nitric oxide synthase (NOS) activity and heightened oxidative modification of NO.

Purpose:

  • To investigate the changes in nitric oxide synthase (NOS) activity and nitric oxide (NO) oxidative metabolism in the early phase of streptozotocin-induced diabetes in rats.
  • To evaluate the effect of insulin treatment on NO metabolism and oxidative stress in diabetic rats.

Summary:

  • Streptozotocin-induced diabetic rats showed increased NOS activity in the aorta and decreased activity in the kidney.
  • Oxidative transformation of NO was augmented in the kidney and heart of diabetic rats.
  • Insulin treatment effectively reduced NO oxidative metabolism without increasing NO production, suggesting oxidative inactivation contributes to NO's reduced biological effects in endothelial dysfunction.

Impact:

  • This study elucidates the role of oxidative inactivation in the reduced biological effects of NO during diabetic endothelial dysfunction.
  • Findings highlight potential therapeutic targets for managing diabetic complications by addressing NO metabolism and oxidative stress.

Related Concept Videos

Nitric Oxide Signaling Pathway01:28

Nitric Oxide Signaling Pathway

Nitric oxide (NO), an inorganic gas, acts as a potent second messenger in most animal and plant tissues. NO diffuses out of the cells that produce it and enters the neighboring cells to generate a downstream response. NO synthase (NOS) catalyzes NO production by the deamination of the amino acid arginine. There are three isoforms of NOS. Endothelial cells have endothelial NOS (eNOS), nerve and muscle cells have neuronal NOS (nNOS), and macrophages produce inducible NOS (iNOS) upon exposure to...
Type II Diabetes II: Pathophysiology01:24

Type II Diabetes II: Pathophysiology

PathophysiologyType 2 diabetes mellitus (T2DM ) is a chronic metabolic disorder characterized by insulin resistance and progressive pancreatic β-cell dysfunction, leading to impaired glucose homeostasis. It results from interactions among genetic predisposition, environmental factors, and metabolic stressors, such as overnutrition and a sedentary lifestyle.Insulin Resistance and Glucose DysregulationEarly T2DM involves insulin resistance in skeletal muscle, adipose tissue, and the liver.
Type I Diabetes II: Pathophysiology01:26

Type I Diabetes II: Pathophysiology

Type 1 diabetes mellitus arises from an immune-mediated destruction of pancreatic β-cells, resulting in an absolute deficiency of insulin. This process develops in genetically susceptible individuals when autoimmunity, environmental exposures, and immunologic dysregulation converge to trigger a targeted attack on the insulin-producing cells of the pancreas. The β-cells are located within the islets of Langerhans and are essential for regulating blood glucose by facilitating cellular uptake of...
Pathophysiology of Diabetes01:20

Pathophysiology of Diabetes

Diabetes mellitus is a chronic metabolic disorder characterized by hyperglycemia. The four categories of diabetes are type 1 diabetes, type 2 diabetes, other specific types of diabetes, and gestational diabetes.
Type 1 diabetes is characterized by autoimmune-mediated destruction of pancreatic β cells, with environmental factors potentially triggering this process in genetically susceptible individuals. Despite many not having a family history, certain genes increase susceptibility, suggesting a...
Coronary Artery Disease II: Pathophysiology01:26

Coronary Artery Disease II: Pathophysiology

Coronary Artery Disease (CAD) originates from a series of events that impair the function of coronary arteries, the blood vessels responsible for delivering oxygen-rich blood to the heart muscle. The pathophysiology of CAD is closely linked to atherosclerosis, a chronic inflammatory and lipid-driven condition affecting the vascular endothelium.1. Endothelial DamageThe process begins with damage to the vascular endothelium, which serves as a protective barrier between the blood and the vessel...