Insulin treatment decreases the antioxidant defense mechanism in experimental diabetes.
BACKGROUND
Hyperglycemia-induced oxidative stress and left ventricular hypertrophy is an independent risk factor for cardiovascular disease. Our aim was to determine the relationship between left ventricular hypertrophy and the total scavenger capacity (TSC) in diabetic rats.


METHODS
Control animals (n=30) were compared to streptozotocin-induced diabetic rats (n=38) and diabe-tic rats receiving insulin treatment (n=30) for 22 days. Half of the animals received angiotensin II on day 21. The left ventricular mass, TSC and carbohydrate parameters were determined.


RESULTS
Diabetes did not alter left ventricular mass; however, diabetes with insulin treatment was associated with left ventricular hypertrophy. The extent of ventricular hypertrophy did not change significantly in this group after angiotensin II treatment. TSC increased very significantly in diabetic rats. These differences remained high when angiotensin II-treated control rats [CA] were compared with treated diabetic rats [DA] (p<0.005). TSC decreased significantly when diabetic rats were treated with insulin.


CONCLUSIONS
Diabetes results in oxidative stress, which in turn enhances the activity of antioxidant enzymes. This increase in enzyme activity inhibits the subcellular remodeling processes, thus also inhibiting concomitant cardiac hypertrophy. Insulin treatment decreases the activity of the antioxidant system and can enhance the function of other localized tissue-specific growth factors. These changes may contribute to the early onset of cardiovascular damage detected in diabetic patients.
Somogyi
Anikó
A
2nd Department of Medicine, Semmelweis University, Budapest, Hungary. somogyi@bel2.sote.hu
Ruzicska
Eva
E
Blázovics
Anna
A
Vér
Agota
A
Rosta
Klára
K
Tóth
Miklós
M
D000804:Angiotensin II / Q000008:administration & dosage / Q000494:pharmacology; D000818:Animals; D000975:Antioxidants / Q000378:metabolism*; D003921:Diabetes Mellitus, Experimental / Q000150:complications / Q000188:drug therapy*; D006352:Heart Ventricles / Q000187:drug effects / Q000473:pathology*; D017379:Hypertrophy, Left Ventricular / Q000209:etiology; D007004:Hypoglycemic Agents / Q000009:adverse effects / Q000627:therapeutic use*; D007328:Insulin / Q000009:adverse effects / Q000627:therapeutic use*; D008297:Male; D018384:Oxidative Stress; D051381:Rats; D017208:Rats, Wistar
D000975:Antioxidants; D007004:Hypoglycemic Agents; D007328:Insulin; D000804:Angiotensin II