Adiponectin/leptin ratio and insulin resistance in pregnancy.

OBJECTIVE: Pregnancy is characterized by progressive insulin resistance. The present study evaluated whether the adiponectin/leptin ratio is associated with insulin resistance in pregnancy, since this ratio has been shown to be associated with insulin resistance in obesity, type 2 diabetes mellitus, metabolic syndrome and polycystic ovary syndrome. METHODS: In this cross-sectional study, adiponectin and leptin concentrations were measured in pregnant women using enzyme-linked immunosorbent assays. Insulin resistance was assessed using the homeostasis model assessment of insulin resistance (HOMA-IR). RESULTS: Mean ± SD age of the participants (n = 74) was 30.76 ± 4.27 years, mean ± SD gestational age was 26.81 ± 3.52 weeks and median body mass index (BMI) before pregnancy was 22.68 kg/m(2) (interquartile range 20.75-26.79 kg/m(2)). There was a significant correlation between the HOMA-IR and leptin concentration, but not between the HOMA-IR and adiponectin concentration. There was a significant inverse correlation between the HOMA-IR and adiponectin/leptin ratio. The adiponectin/leptin ratio was inversely correlated with BMI before pregnancy. CONCLUSION: The adiponection/leptin ratio inversely correlates with HOMA-IR in pregnancy.

Adipocytokines and insulin resistance across various degrees of glucose tolerance in pregnancy.

OBJECTIVE: Gestational diabetes mellitus is characterized by progressive insulin resistance. Adipocytokines are thought to be associated with insulin resistance. This cross-sectional study evaluated the associations between serum concentrations of several adipocytokines and insulin resistance at different stages of glucose tolerance in pregnancy, using the homeostasis model assessment of insulin resistance (HOMA-IR) as a reference. METHODS: According to oral glucose tolerance test results, 74 pregnant women were divided into three groups: normal glucose tolerance (n = 25); intermediate glucose tolerance (n = 19); gestational diabetes mellitus (n = 30). Adiponectin, leptin, resistin, visfatin and retinol-binding protein 4 (RBP4) concentrations were measured using enzyme-linked immuno sorbent assays. RESULTS: Groups were comparable regarding age, week of gestation and body mass index before gestation. There were statistically significant between-group differences in HOMA-IR, but no significant differences regarding serum adipocytokine concentrations. CONCLUSIONS: Adipo nectin, leptin, resistin, visfatin and RBP4 were not associated with the degree of glucose tolerance in pregnancy. Concentrations of these adipocytokines are not sufficiently sensitive to replace HOMA- IR in pregnancy.

Association of CT60 cytotoxic T lymphocyte antigen-4 gene polymorphism with thyroid autoantibody production in patients with Hashimoto's and postpartum thyroiditis.

Strong genetic contribution has been demonstrated to influence the development of autoimmune thyroid disease (AITD) as well as thyroid autoantibody production. In order to assess the relation between CT60 cytotoxic T lymphocyte antigen-4 (CTLA-4) gene polymorphism and thyroid autoantibody production, we investigated 180 consecutive newly diagnosed patients with two forms of AITD, 105 with Hashimoto's thyroiditis (HT) and 75 with postpartum thyroiditis (PPT). We evaluated thyroid function, measured antibodies against thyroid peroxidase (TPO) and thyroglobulin (Tg), and determined CT60 CTLA-4 gene polymorphism. In HT, TPO antibody median value was significantly lower in the AA compared to the AG and GG genotypes (65, 122 and 319 U/ml, P<0.005), while the Tg antibody median value was lower in the AA compared to the AG genotype (91 and 189 U/ml, P<0.02). In PPT, the frequency of thyroid autoantibody-positive patients was higher among G-allele-carrying genotypes (P<0.04). Similar to HT, the TPO antibody median value was lower in the AA compared to the AG and GG genotypes (12, 130 and 423 U/ml, P<0.006). Hypothyroid PPT patients were more often thyroid autoantibody-positive (P<0.005) and the TPO antibody median value was higher compared to hyperthyroid PPT patients (500 and 32 U/ml, P<0.0001). The frequency of the G-allele was significantly higher among hypothyroid patients (P<0.05). Our data suggest that in both HT and PPT, the CT60 CTLA-4 gene polymorphism contributes importantly to thyroid autoantibody production. In PPT, the genotype also seems to influence thyroid function, as patients with the polymorphous allele are more prone to develop hypothyroid form of PPT.

Thyroid autoantibody production is influenced by exon 1 and promoter CTLA-4 polymorphisms in patients with Hashimoto's thyroiditis.

Strong genetic susceptibility to thyroid autoantibody (TAb) diathesis has been shown and one of the major genes involved is probably CTLA-4 gene. Our recent study of patients with Graves' disease has demonstrated that exon 1 CTLA-4 gene polymorphism influences higher TAb production. Here, we evaluated the influence of exon 1 and promoter CTLA-4 polymorphisms on TAb production in 109 newly diagnosed patients with Hashimoto's thyroiditis (HT). Serum TSH, thyroid peroxidase antibodies (TPOAb) and thyroglobulin antibodies (TgAb) were measured. 49 A/G and -318 C/T polymorphisms were detected using polymerase chain reaction amplification of genomic DNA and restriction fragment length polymorphism analysis. Patients with AG and GG genotype had significantly higher TPOAb median values compared to patients with AA genotype (P < 0.003). Similarly, TgAb median value was significantly higher in AG patients and in the entire G-allele carrying group (P < 0.02). Compared to both T-allele carrying genotypes, CC genotype presented with significantly higher TPOAb median value (P < 0.02), whereas TgAb median values did not differ significantly between various genotypes. In conclusion, our results indicate that G allele influences higher TPOAb and TgAb production, whereas C allele affects especially TPOAb production in patients with HT. Therefore, our findings provide further evidence that CTLA-4 is a major TAb susceptibility gene.