INTRODUCTION: Gonadotropins are released under the control of gonadotropin-releasing hormone (GnRH) from thearcuate nucleus and preoptic area of the hypothalamus. The gonads — testes and ovaries — are the primary targetorgans for LH and FSH. The gonadotropins affect multiple cell types and elicit multiple responses from the targetorgans. As a simplified generalization, LH stimulates the Leydig cells of the testes and the theca cells of the ovaries to produce testosterone (and indirectly estradiol), while FSH stimulates the spermatogenic tissue of the testes andthe granulosa cells of ovarian follicles.Reproductive aging is endocrinologically characterized by a progressive rise in serum FSH levels associated with adecrease in serum estradiol (E2) and testosterone (T) levels. The rise in FSH is associated with reduced levels of sexsteroid and peptide negative feedback regulators of FSH secretion.The aim of study is: determination of serum FSH level changes in relation to aging and sex.MATERIALS AND METHODS: In this study were involved 169 healthy Mongolian adults aged above 45 years old. Subjectswere randomly selected and undergone physical examination by geriatrician. People, who are receiving hormonereplacement therapy, using inproper use of alcohol, injured and had surgery were excluded from our surgery. Bloodsamples were collected in the early morning (8.30–10.30 AM) after an all night fast and plasma was separatedimmediately by centrifugation; then sera obtained were stored at -20°C until assayed by ELISA kit from United BiotechCoLTD, USA, which sensitivity is 1mIU/ml. Statistical analyses have been performed by statistical software SPSS 16,using ANOVA, Pearson correlation, T-test.RESULT: Mean level of FSH for both sexes was 21.19±16.2 mIU/ml, which is in comparison with males (12.33±10.58mIU/ml) it was comparatively higher (p<0.001) in women (29.61±16.15 mIU/ml). FSH has no correlation with aging inman (r=0.084, p>0.05), but in women it was stronger correlation (r=0.203, p<0.05). in 51-60 years age group FSH wasincreased by 56%, in 61-65 years group by 91%, in 66-70 years group it was increased 100% in comparison with until50 years age group. In older age (above 70 years) it decreased to 70% from reached concentration. ANOVA analysishas not showed significant difference between age groups.CONCLUSIONS: Average mean of FSH in old age are: 29.61±16.15 mIU/ml in women and 12.33±10.58 mIU/ml in men.Correlation with aging was observed stronger in women than in man (r=0.203, p<0.05). FSH increases with aging untilround 70 and decreases after 70 years old.

Background:In females reproductive system aging is very important. Females spend the last 1/3 period of their life in insufficiency of sex hormone of late menopause. Due to decrease of ovary function noticeable change is detected in nervous endocrine system. Although menstrual cycle hasn’t been lost amount of FSH increased. It shows decrease of reproductive function females. Therefore recently researchers define that amount of FSH increase is an important biomarker which detects in an early period of menopause. But amount of estradiol hormone is almost in normal level until the late post menopause. Goal: to study the dynamic feature of age related changes and dependence of serum FSH and estradiol level in female aging.Materials and Methods:In this study were involved 177 healthy Mongolian women aged above 35 years old. We drained 5 ml fasting vein blood at 8.00-10.00 am. Sera were separated and kept frozen until assayed by ELISA. Results:Аaverage mean of FSH was 19.84±22.6 IU/l, at the age of 35-45 1.62±3.29 IU/l, at the age of 46-55 16.39±15.39 IU/l, at the age of 56-65 31.38±33.69IU/l, at the age of 66-75 28.83±17.31 IU/l, over 75 34.52±13.94 IU/l and there was positive correlation between age and FSH levels (r=0.647, p<0.001).Average mean of estradiol of participants: at the age of 35-45 37.03±22.09 pg/ml, at the age of 46-55 21.1±16.65pg/ml, at the age of 56-65 13.7±20.07 pg/ml, at the age of 66-75 9.11±15.1pg/ml, over 75 age 1.8±1.53 pg/ml and there was inverse correlation between age and estradiol levels (r= -0.453, р<0.001).There was an inverse correlation between log E2 and FSH levels (r= -0.434, p<0.001). Multiple regression analysis shows that age (β= -0.350, p<0.001) and FSH (β=-0.222, p=0.016) had significant inverse correlation with serum estradiol level. Conclusion: For females over 35 average mean of FSH is 19.84±2.26 IU/l, average mean of estradiol hormone is 19.6±2.0pg/ml. between the mid age (35–45 years) and oldest (>75 years) groups, mean estradiol level declined by 20.6 times, whereas FSH increased by 21.3 times. It shows that this is an important marker of menopause. Multiple regression analysis shows that age (β= -0.350, p<0.001) and FSH (β= -0.222, p=0.016) had had significant inverse correlation with serum estradiol level.

BackgroundLeptin is a mediator of long-term regulation of energy balance, suppressing food intake and therebyinducing weight loss.GoalThe main goal of our study was the analyzing of serum leptin level in correlation with some influencingfactors in adults with metabolic syndrome.Materials and MethodsWe included 260 randomly selected people aged 18-72 years old; among them 105 had metabolicsyndrome which was identified by the criteria of the International Diabetes Federation. All participantsunderwent general medical examinations and signed a written consent paper. Fasting blood glucose,triglyceride, HDL-C, insulin, adiponectin, leptin level were measured in fasting blood serum and insulinresistance was calculated as a HOMA-IR model.ResultsAverage level of leptin for participants with MS was 16.44±14.21ng/ml, in participants without MS was9.59±12.69ng/ml. MS exposed group had much higher level of leptin than the control group (p<0.001).Leptin level was correlated with waist circumference (β=-0.253±0.1; p=0.013), and body mass index(β=1.778±0.274; p<0.001).ConclusionLeptin level in the MS exposed group were higher than in the control group. The level of leptin had aconsistent and significant correlation with body mass index and waist circumference in compare to otherinfluencing factors.

Introduction. The metabolic syndrome is related to increased risk of developing cardiovascular disease andtype 2 diabetes. Adiponectin is an adipose tissue-specific collagen-like factor, which is abundant in plasma, anda decrease of adiponectin is associated with obesity and type-2 diabetes.Goal. This study aimed to determine the ADIPOQ gene -11377 polymorphism in association with plasmaadiponectin level and risk factors of metabolic syndrome.Materials and Methods. We investigated adiponectin gene -11377C>G polymorphism in 156 subjects withmetabolic syndrome and 142 healthy control subjects. The -11377C>G polymorphic locus was amplified using theforward primer 5’-ACTTGCCCTGCCTCTGTCTG-3’ and the reverse primer, 5-CCTGGAGAACTGGAAGCTG-3’.A p value <0.05 was considered statistically significant.Results. Adiponectin level positively correlated with age, but correlated negatively with TG, waist circumference,waist hip ratio, diastolic blood pressure, weight and BMI (p < 0.05). With genotype CG and GG (6.57±3.09ng/ml) of -11377C>G had lower levels of serum adiponectin than those with the genotype CC (7.38±3.68ng/ml) butno significant difference in people with MS (p=0.157). Therefore with genotype CG and GG (168.56±113.31mg/dl) of -11377C>G had higher levels of serum triglycerides than those with the genotype CC (132.94±74.78mg/dl) significant difference in people with MS (OR=1.006, p=0.015). With CG and GG (75.04±12.49mg/dl) of-11377C>G had significantly higher glucose level compared to with the genotype CC (68.85±11.76mg/dl) inwithout MS (OR=1.071, p=0.017).Сonclusions.1. ADIPOQ gene -11377>G polymorphism of the adiponectin gene was found not to be related to adiponectinlevel (p=0.157).2. -11377C>G polymorphism was related to the metabolic syndrome susceptibility, and this polymorphismimpacted on circulating triglyceride and glucose concentrations.

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).

IntroductionThe metabolic syndrome is a cluster of the most dangerous heart attack risk factors: diabetes andprediabetes, abdominal obesity, high cholesterol and high blood pressure. Also it is known as acluster of changes associated with resistance to insulin.There is a convincing evidence of important ethnic differences in the prevalence of metabolic syndrome,its components and sequelae. Estimates vary by country, but generally they show higher prevalenceof metabolic syndrome in non-European groups. Based on these findings, we were convinced inthe importance of studying the prevalence of metabolic syndrome and insulin resistance among thepopulation of Mongolia.Materials and MethodsThe main goal of our study was the determination of insulin level and insulin resistance in metabolicsyndrome exposed and non-exposed groups. We included 194 randomly selected people aged 20-60 years old; among them 51 had metabolic syndrome which was identified by the criteria of theInternational Diabetes Federation. All participants underwent general medical examinations andsigned a written consent paper. Fasting blood glucose, triglyceride, HDL, insulin levels were measuredin fasting blood serum and insulin resistance was calculated as a HOMA-IR model.ResultsAverage age of participants was 44,26±8,66 years, of whom 46,4% (n=90) were male, 53,6%(n=104)were female. By IDF criteria, 26,2% (n=51) of the participants had metabolic syndrome. Insulin levelwas 17,23±14,91μIu/mL in MS exposed group which was much higher than in the control group.Insulin, HOMA-IR, had direct correlation with the body mass, BMI and waist circumference andinverse correlation between HDL.Conclusions26.2% of the study participants had metabolic syndrome which was defined by IDF criteria. Insulin levelin the MS exposed group was 17,23±14,91μIu/mL, higher than in the control group by 7,53±2,21μIU/mL. Insulin, HOMA-IR, showed a direct correlation with the body mass, BMI and waist circumferenceand inverse correlation between HDL.

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.