Abstract
Clinical evidence suggests that type 2 diabetes mellitus can increase the risk of intracerebral hemorrhage and provocation of neurodegeneration. This study was aimed at evaluating biomarkers of glycemic control, lipid profile, oxidative modification of proteins, as well as the functional state of endothelium in Wistar rats with type 2 diabetes mellitus complicated by intracerebral hemorrhage. Experimental type 2 diabetes mellitus was induced by intraperitoneal injection of streptozotocin (65 mg/kg) and nicotinamide (230 mg/kg). The intracerebral hemorrhage was induced by microinjection of sterile saline containing 0.2 IU bacterial collagenase into the striatum. Assessed biomarkers included the area under glycemic curve, glycated hemoglobin, total cholesterol, triglyceride, high-density lipoprotein, advanced glycation end products, markers of oxidative modification of proteins – aldehyde- and ketonephenylhydrazones, and markers of endothelial dysfunction – homocysteine, endothelin-1, von Willebrand factor and asymmetric dimethylarginine in blood serum. Both rats with type 2 diabetes mellitus and rats with intracerebral hemorrhage and diabetes had a significant elevated glycemic control as compared to intact animals. But combined pathology was additionally characterized by an impairment of lipid profile (increased triglyceride level and decreased as total cholesterol and high-density lipoprotein) resulting in a rise in the atherogenic index of plasma. A significant increase in the content of the markers of oxidative modification of proteins was observed in both experimental groups. But the rats with intracerebral hemorrhage and diabetes only had higher levels of advanced glycation end products in comparison with intact animals. The highest levels of endothelin-1, as a biomarker of endothelial dysfunction, were observed in animals with intracerebral hemorrhage and diabetes. Homocysteine and von Willebrand factor were elevated in rats with type 2 diabetes mellitus, while acute intracerebral hemorrhage did not potentiate the further growth in its levels. Such effect was not accompanied by a marked increase of asymmetric dimethylarginine level in blood serum, although there was a clear trend. In conclusion, the development of intracerebral hemorrhage in rats with type 2 diabetes mellitus can intensify the manifestations of oxidative stress, worsen lipid profile, and aggravate endothelial dysfunction. In this case, the pathological process may have the character of a “vicious circle”.
Highlights
Diabetes mellitus (DM) is one of the fastest growing global health challenges of the 21st century
The results of the study showed that the development of type 2 diabetes mellitus in rats led to a significant increase in basal glycemia, but intracerebral hemorrhage did not affect its severity (Fig. 1a)
Modeling intracerebral hemorrhage under diabetes did not affect glucose tolerance in this test significantly, and area under the glycemic curve (AUC) value was higher by 75.3% (P = 0.0007) as compared to the negative control group
Summary
Diabetes mellitus (DM) is one of the fastest growing global health challenges of the 21st century. Type 2 diabetes mellitus belongs to a group of chronic metabolic diseases that is caused by insulin resistance or deficiency, resulting in increased blood glucose levels. This form of diabetes is the most common, as it accounts for 90–95% of patients with diabetes mellitus. Insulin resistance in type 2 diabetes mellitus is associated with many risk factors that usually precede the development of hyperglycemia. These typically include obesity, dyslipidemia, which is characterized by high triglycerides, elevated blood pressure, oxidative stress, and endothelial dysfunction (ED) (Su, 2015). Endothelial cells, as well as their main products – nitric oxide (NO), prostacyclin, endothelin-1
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