No abstract

We determined that there are no differences in either surface area or volume estimations made using VUR sections and direct vertical sections. We have performed an exhaustive series analysis with a variety of objects.

The present study investigated whether diabetes worsened the onset of liver injury/damage during the ovariectomized (OVX)-induced postmenopausal period in rats. Diabetes results in severe complications in humans, such as liver failure. Estrogen and its derivatives are medically acceptable, powerful antioxidant agents that can enable liver and other important organs to defend themselves against oxidative related injury. Estrogen deficiency, which occurs in the postmenopausal period and in individuals with diabetes, may play a significant role in the progression of liver failure. In the present study, rats were divided into four groups: control (Group I), diabetic (Group II), ovariectomy (Group III) and ovariectomy plus diabetes (Group IV). After the experiments, quantitative histopathological and immunohistochemical changes in liver were detected using light microscopy and modern stereological systems. Histopathological examinations showed that there were many necrotic and apoptotic hepatocytes in the lobules of Group II. In addition, there were a larger number of necrotic cells in Group III than Group II. In contrast to Group II, there were also apoptotic cells in the portal areas in Group III. Moreover, evidence of liver injury was higher in the sections of Group IV compared with all other groups. In biochemical findings, there were statistically significant differences between all the groups (P < 0.001) for catalase (CAT), glutathione peroxidase (GSH) and myeloperoxidase (MPx) activity. In addition, the amount of lipid peroxidation (LPO) was significantly different between groups. In stereological results, there were significant differences between Groups I and II and Groups II and IV. The present study provided novel insight into the pernicious effects of ovariectomy on liver injury following the onset of diabetes. Indeed, the present study found that increases in liver oxidative activity in OVX rats following the onset of diabetes correlates with elevated MPx, LPO and histopathological changes in rat liver.

Oxidative stress is one of the main reasons of both menopause and diabetes. So, it plays crucial role in the pathogeneses of that condition and disease. Therefore, the objective of the present study was to investigate the effects of menopause and diabetes upon the hippocampus using a rat model. Adult female Sprague Dawley rats (n = 24) were allocated randomly as follows; control (C group) ovariectomized (O group), diabetic (D group) and ovariectomy plus diabetic groups (DO group) (n = 6; in each group), respectively. For evaluating the results, tissue biochemistry and stereological analysis were made. Biochemistry results (lipid peroxidase (LPO); catalase (CAT); superoxide dismutase (SOD); total glutatyon (GSH); and myeloperoxidase (MPO) values) in Group C-DO were determined as 12.27, 21.88, 23.08 and 29.90 nmol/gr tissue; 59.3, 70.06, 69.7 and 78.1 mmol/min/mg tissue; 174.2, 156.4, 159.7 and 154.6 mmol/min/mg tissue; 3.63, 3.61, 4.21 and 3.97 nmol/mg tissue; and 5.05, 5.68, 5.58 and 6.19 µmol/min/mg tissue, respectively. Moreover, both menopause and diabetes led to change of lipid profiles. There were significant differences between the control and other groups (Group C and D-DO) (p < 0.01) and among experimental groups (p < 0.01) in terms of neuron number. When the volumes of the hippocampus were compared, there were no significant differences between the all groups (P > 0.05). At this point, we suggested that diabetes could aggravate deleterious effects of ovariectomy.

The presence of liver disease in patients with progressively worsening insulin resistance may not be recognized until patients develop manifestations of the metabolic syndrome such as diabetes, hypertension, hyperlipidemia, and vascular disease. It was aimed to investigate whether three angiotensin II type 1 receptor antagonists (ARBs) (olmesartan, losartan, and valsartan) had preventive effect against hepatic fibrosis and this was a common characteristic among ARBs. In current study, 25 adult male rats were used and divided into five groups: the non-diabetic healthy group, alloxan induced diabetic (AID) control group, AID losartan group, AID valsartan group and AID olmesartan group. According to numerical density of hepatocytes, significant difference was found between the non-diabetic healthy group and diabetic control group. All treatments groups were significant when compared to diabetic control group. In diabetic control group it was examined swelling, irregular cristae arrangement in some of mitochondria. It was also determined mitochondria membrane degeneration in some areas of section profiles. In diabetic rats treated with losartan group, there were necrotic hepatocytes. In diabetic rats treated with valsartan group, predominantly, findings were similar to losartan group. In diabetic rats treated with olmesertan group, plates of hepatocytes were quite regular. There were hardly necrotic cells. Not only other organelles such as RER, SER and lysosom but also mitochondrial structures had normal appearance. In the diabetic control group electron microscopy revealed edema in both the cytoplasm and perinuclear area and the nuclear membranes appeared damaged. In conclusion, it was established that the most protective ARB the liver in diabetic rats was olmesartan, followed by losartan.