Recent studies have introduced serum uric acid (UA) as a potential risk factor for developing diabetes, hypertension, stroke, and cardiovascular diseases. The value of elevated levels of UA in serum as a risk factor for diabetes development is still under scrutiny. Recent data suggest that clearance of UA is being reduced with increase in insulin resistance and UA as a marker of prediabetes period. However, conflicting data related to UA in serum of patients with Type 2 diabetes prompted us to study the urine/serum ratio of UA levels (USRUA) in these patients and healthy controls. All subjects included in the study were free of evidence of hepatitis B or C viral infection or active liver and kidney damage. Patients receiving drugs known to influence UA levels were also excluded from this study. Analysis of glucose and uric acid were performed on Dade Behring analyzer using standard IFCC protocols. Interestingly, our data demonstrated about 2.5 fold higher USRUA values in diabetic patients as compared to control subjects. Furthermore, there was a trend of correlation of USRUA value with the blood glucose levels in diabetic patients, which was more prominent in diabetic men than in women. With aging, levels of uric acid increased in serum of diabetic patients, and this effect was also more profound in male than in female diabetics. In conclusion, this study showed significantly elevated USRUA levels in patients with Type 2 diabetes, a negative USRUA correlation with the blood glucose levels in diabetic patients, and an effect of sex and age on the uric acid levels. Since literature data suggest a strong genetic effect on UA levels, it would be pertinent to perform further, possibly genetic studies, in order to clarify gender and ethnic differences in UA concentrations.

Th is is the fi rst study performed in population from Bosnia & Herzegovina (BH), in which we analysed a signifi cance of genetic variations in drug-metabolising enzyme, cytochrome P (CYP), in pathogenesis of Type  diabetes. We have determined allele frequencies for CYPC*, CYPC*, and CYPD* in diabetic patients and nondiabetic controls. Genomic DNA was extracted from blood samples collected from  diabetic and  nondiabetic subjects. A real-time polymerase chain reaction was used for the detection of specifi c CYP polymorphisms, with the application of the specifi c TaqMan® SNP genotyping tests (Applied Biosystems). Interestingly, results from this study have demonstrated that frequencies of CYPC* and CYPD* variants were in line, while frequency of CYPC* polymorphism seemed to be lower in this sample of BH population as compared to the Caucasians genotype data. Furthermore, no signifi cant diff erence in allele frequencies for CYPC*, CYPC*, and CYPD* was demonstrated between diabetic and nondiabetic subjects. Th us, results form this study seem to indicate no relationship between CYPC, CYPC, and CYPD genotype and diabetes susceptibility in Bosnian population. Th is in part may refl ect a limited study population included in our study and would require larger cohorts to reveal potential relationships between analysed CYP genetic variants and diabetes risk. In addition, it would be pertinent to further explore possible eff ects of CYP genetic variations on therapeutic and adverse outcomes of oral antidiabetics, which might be the key in optimising therapy for individual patient with Type  diabetes. ©  Association of Basic Medical Sciences of FBIH. All rights reserved

Numerous studies conducted on acetylsalicylic acid (ASA, aspirin) confirmed that ASA inhibits proliferation and induces apoptosis in various types of human cells. Therefore, it was of interest to examine possible effects of different concentrations of ASA on viability and proliferation of lymphocytes in the cell culture. After separation from blood, lymphocytes were suspended in RPMI 1640 medium and cultured at 37 degrees C. Solution of ASA was added to cultures after 24 h, in final concentrations of 1, 3 and 5 mmol/l. After 48 h, proliferative response was evaluated by WST-1 assay. Significant difference in viability between controls and cell cultures treated with ASA in three different concentrations was observed (p<0.01). Percents of viable cells in cultures after application of 1, 3 and 5 mmol/l ASA were 9.9%, 2.5% and 16.9% (compared to controls), respectively. To determine whether this cytotoxic effect was result of induction of apoptosis, DNA from cell cultures was isolated and subjected to agarose gel electrophoresis. Fragmentation of DNA was not detected, excluding apoptosis as possible cause of cytotoxic effects. Addition of ASA caused change of initial extracellular pH value for each treated culture. After addition of 1 mmol/l ASA, pH of culture was 7.19, after 3 mmol/L, 6.99 and after addition of 5 mmol/l solution, pH was 6.75. Decreased lymphocyte viability could be attributed to either the effects of the added substance or possible further acidification of cell cultures during three days of incubation.

Diabetes mellitus can be looked upon as an array of diseases, all of which exhibit common symptoms. While pathogenesis of IDDM (insulin dependant diabetes mellitus) is well understood, the same is not true for diabetes mellitus type II. In the latter case, relative contribution of the two factors (insulin resistance or decreased insulin secretion) varies individually, being highly increased in peripheral tissues and strictly dependant on insulin for glucose uptake. Moreover, in patients with diabetes mellitus type II, disbalance at the level of regulation of glucose metabolism as well as lipid metabolism has been noted in skeletal muscles. It is normal to assume that in this type of diabetes, these changes are reflected at the level of total activity of enzyme creatine kinase. This experimental work was performed on a group of 80 regular patients of Sarajevo General Hospital. Forty of those patients were classified as patients with diabetes type I and forty as patients with diabetes type II. Each group of patients was carefully chosen and constituted of equal number of males and females. The same was applied for adequate controls. Concentration of glucose was determined for each patient with GOD method, while activity of creatine kinase was determined with CK-NAC activated kit. Statistical analysis of the results was performed with SPSS software for Windows. Obtained results point out highly expressed differences in enzyme activity between two populations examined. Changes in enzyme activity are more expressed in patients with diabetes type II. Positive correlation between concentration of glucose and serum activity of the enzyme is seen in both categories of diabetic patients which is not the case for the patients in control group. At the same time, correlation between age and type of diabetes does exist . This is not followed at the level of enzyme activity or concentration of glucose.