Introduction: The metabolic syndrome (MS) is characterized by central obesity, hypertriglyceridemia,low high-density lipoprotein (HDL), increase blood pressure and raise fasting plasma glucose. ThePGC-1α gene is located on chromosome 4 p.15.1 in humans and encodes a protein containing 798amino acids. The protein encoded by this gene is a transcriptional coactivator that regulates thegenes involved in energy metabolism. PPARγ, a coactivator molecule recently identified based on itsability to interact with PPARγ, is involved in many important metabolic processes, including adaptivethermogenesis, mitochondrial biogenesis and fatty acid β–oxidation.Goal: To study the frequency of PGC-1α Gly482Ser polymorphism in people with MS in relation to therisk factors of the MS.Materials and methods: The study population comprised 302 unrelated Mongolian subjects (158 withmetabolic syndrome and 144 controls). The genotypes for polymorphism of candidate gene related toMS were determined using a RFLP analysis of the MspI digest of the PCR product.Result: From the control group, 33.4% (48) had GG, 47.2% (68) had GS and 19.4% (28) had SSgenotypes. 51.9% (82) of people with MS had GG, 35.4% (56) had GS and 12.7% (20) had SSgenotypes. The prevalence of G allele in people with MS was 69.6%, which is much higher than healthygroup. Comparing PGC-1α Gly482Ser GG, GS and SS genotypes with systolic arterial blood pressurerevealed statistically significant difference which was higher among subjects with GG genotype. Theblood pressure of people with MS and carrying GG genotype of PGC-1α Gly482Ser polymorphismwas significantly increased 2.35 times than people without MS.Conclusions:1. 69.6 percentages of the people with MS had G allele and 2.2 times more than those withoutmetabolic syndrome.2. We determined that the odds ratio for the high blood pressure and it was 2.35 times higher inpeople with GG allele of Gly482Ser carriers than GS and SS alleles carriers (OR = 2.35, p =0.012).

INTRODUCTION: The PGC-1 gene is located on chromosome 4 p.15.1 in humans and encodes a protein containing 798 amino acids. As PGC-1a regulates multiple aspects of energy metabolism, it is not surprising that PGC-1a has been found to be deregulated in several pathological conditions. Might be associated with type 2 diabetes because PGC-1, besides being a coactivator of PPAR a and b, has a critical role in glucose uptake and adaptive thermogenesis. Addition, a common polymorphism of the PGC-1 gene Gly482Ser, which apparently reduces PGC-1 activity, has been linked to increased risk of type 2 diabetes. Association has also been reported between the Gly482Ser substitution and insulin resistance in Japanese subjects. Similar reduction of PGC-1 expression was also observed in the adipose tissue of insulin-resistant and morbidly obese individuals. Previous studies have reported significant association between the Gly482Ser missense mutation of the PGC-1 gene and reduced insulin sensitivity in obese subjects. This association resulted independent from all other known modulators of insulin resistance, and suggests a primary role for the PGC-1 gene on the genetic susceptibility to insulin resistance in obesity.GOAL: To study the presence of PGC-1 gene Gly482Ser polymorphism in people with Metabolic syndrome and study the relation to serum insulin level and insulin resistance.MATERIALS AND METHODS: The study population comprised 302 unrelated Mongolian subjects (158 with metabolic syndrome and 144 controls). MS was determined by IDF (International Diabetes Federation) criteria. The genotypes for polymorphism of candidate gene related to MS were determined using a RFLP analysis of the MspI digest of the PCR product. We determined serum insulin by ELISA, using Eucardio Company’s kit and insulin resistance was defined by the HOMA-IR formula.RESULT: 33.4% (48) of control group had GG, 47.2% (68) had GS and 19.4% (28) had SS genotypes of PGC-1 gene. 51.9% (82) of people with MS had GG, 35.4% (56) had GS and 12.7% (20) had SS genotypes. The prevalence of G allele in people with MS was 69.6%, which is much higher than healthy group. Insulin and HOMA-IR of MS group were higher than compared to healthy group (p<0.05). HOMA-IR was lower in people with GS genotype comparing to GG and SS in people with metabolic syndrome. CONCLUTIONS: 1. People with MS had higher levels of serum insulin (p<0.013) and insulin resistance (p<0.004) in compare to healthy people. 2. 69.6 percentages of the people with MS had G allele, which was 2.2 times more than those without metabolic syndrome.3. People with MS who carry SS genotype had higher levels of serum insulin (p=0.02) and insulin resistance (p=0.008) than people without MS. Insulin resistance was significantly correlated (r=0.302, p<0.001) with hypertension in people with G allele.

BACKGROUND. Regular blood donation can lead to pre-clinical iron deficiency as well as iron deficiency anemia. With Each donation donors lose 220-250 mg of iron. Early detection of iron deficiency is important for the blood donors and even useful for blood and blood product safety and supply. The research work we studied present Ret-HE to be used to detect the occurrence of iron deficiency eritrony level. Purpose: The aim of this study was to determine Ret-He to have sensitivity and specificity for diagnosing iron deficiency than traditional iron measurements. Materials and methods: We performed a cross sectional and case control study of 156 blood donors who served National Center for Transfusion Medicine. Ret-He, hemoglobin, plasma iron and ferritin were measured using XN2000 Sysmex, and CobasE600 Roche. The statistical analysis was done using One way Anova, Rock curve, Kruskal Wallis test. Results: We examined 64(41.02%) male donors, 92(58.9%) female donors by measurements of Ret-He,hemoglobin, serum, iron and ferritin. Survey participants were 8.33%(n=13) with anemia, 91.67% (n=143) without anemia. In donors with anemia the results were: RBC 4.9*106 u/l, HGB 10.8 g/dl (10;11), serum ferritin 5.2 (4.3; 6.3) mmol, serum iron 4.5 (3.7; 5.8) mmol and Ret-He 25.5 (22; 26) pg. Donors were divided into 3 age groups: group I age was up to 25years, group II was between 26-35 years, group III age criteria was above 35. Group I had serum iron 13.5 (10.; 18.), serum ferritin 41.8 (14; 78), Ret-He 32.2 (30; 33.) RBC 5×106 u/l (4.6;5), HGB14.2g/dl (13.3;14. 2). Group II had serum iron 14.6 (11; 19), serum ferritin 54.1 μg/l (29; 138), Ret-He 32.2pg (31; 33), RBC 5.1×106 u/l(4.7;5.1), HGB14.8 g/dl (13.5;14.8),Group III had serum iron 15.1 umol/l (9; 20), serum ferritin 95.7 μg/l (39; 141), Ret-He 32.7pg (31; 34) , RBC4.9×106 u/l(4.6;4.9), HGB 14.5g/dl(13.8;14.5), respectively. According to a curve (Roc) analysis, AUC of serum iron was 0.0963, serum ferritin 0.909, Ret-He 0.975. The mean Ret-He was 32.3pg (31.3;33.4). The optimal cut off value for the Ret-He was 29,25pg by ROC analysis and are presented along with sensitivity 92.3% and specificity 95.1%. Conclusion: 1. Determining the amount of Ret-He has a better sensitivity and specificity for diagnosing iron deficiency compared to traditional iron measurements. 2. Ret-He has diagnostic indicators that are able to detect the depletion of iron reserves, erythron level. And it need to be used in further clinical practices, as well as doctors should be required to use it for diagnosis and treatment.