## 4 Discussion  
The aim of the present study was to investigate the alterations caused by oxidative stress in routinely used clinical parameters measured from blood and urine, and on the morphology of RBCs, in a widely used STZ-diabetic rat model. These alterations may contribute to the pathophysiology of diabetes mellitus and its complications, such as microvascular disturbances. A single dose of STZ led to body weight loss, extremely high levels of blood and urine glucose, and elevated HbA1c value and percentage. Interestingly, in some cases, diabetic rats became spontaneously normoglycemic and their blood glucose level decreased below 18 mmol/L during the ten-week experimental period; these rats were grouped as reverted diabetics. The representative double-labeled fluorescent micrographs against insulin and glucagon showed the lack of insulin-producing pancreatic beta cells in diabetics and insulin-treated diabetics. In the case of reverted diabetics, we detected insulin-positive cells in Langerhans islets surrounded by a major mass of glucagon-immunoreactive cells. Further studies are required to elucidate the underlying mechanisms. In the past decade, some effort has been dedicated to replace the lost beta cells in the therapy of diabetes mellitus. Recently, researchers found that alpha cells, as a replacement for beta cells, may be a potential target for the production of insulin. One of the most important reasons for this new therapeutic strategy is the ability of alpha cells to be spontaneously converted into insulin-producing cells [22; 23; 24]. The routinely used metabolic panel measurements from blood or urine showed the most remarkable changes in diabetic groups. The urine carbamide level was increased in acute as well as in chronic diabetics; however, blood carbamide levels were similar to those of the control. These blood results indicate normal renal function [25], and the urine results highlight increased protein catabolism consistent with the reduced weight gain of diabetic rats and the elevated blood ALP level of chronic diabetics [26; 27]. Elevated serum GPT and ALP levels, and decreased serum albumin and TP levels, of diabetics are in line with earlier studies [28; 29]. These results raise the possibility of liver damage because ALP and GPT levels in the blood are the most important indicators of hepatic injury [28]. On the other hand, low albumin and TP levels not only reflect hepatic failure, but also oxidative status, since they are antioxidant marker proteins. Moreover, albumin is the most abundant extracellular protein and plays an important role in buffering serum redox status [30]. The effects of insulin on metabolic parameters were revealed in insulin-treated diabetic and reverted diabetic groups. Both spontaneously recovered, and endogenously and exogenously administered insulins were effective, with the measured parameters being similar to those of controls, except for the TP level. These results are consistent with the findings of [PERSON] et al. [31], where the effectiveness of insulin in inhibiting hepatic injury was shown using biochemical and histological parameter monitoring. The routinely used complete blood count revealed changes only in the chronic diabetic group when compared to controls. We measured increased levels in RBC indices, namely RBC count, hematocrit, and Hb concentration, but a decreased level of HDW. Our observations correlate with the findings of others [5; 32]. These findings could result from the extremely high glucose concentration causing blood thickening, or the lack of insulin. Moreover, insulin may stimulate the proliferation of erythroid progenitor cells [33]. The complete blood count of insulin-treated diabetics and reverted diabetics was similar to that of control data. The complete blood count test showed alteration in RBC count and in RBC-derived parameters.