Levels of betatrophin decrease during pregnancy despite increased insulin resistance, beta-cell function and triglyceride levels.

AIM: Evidence in support of an association between betatrophin and insulin resistance (IR) is mounting, with studies demonstrating that betatrophin is elevated in patients with type 2 diabetes, obesity and gestational diabetes. The aim of this study was to evaluate the role of betatrophin in IR and physiological proliferation of beta cells during pregnancy in healthy women. METHODS: Eighty healthy pregnant women were examined at each trimester [T1 (first), T2 (second), T3 (third)], with a subgroup (n=45) that was also examined at 3 months postpartum (3MPP). The controls comprised 30 non-pregnant healthy women (HW) of reproductive age. Also measured were levels of betatrophin (ELISA), glucose (enzymatic method with hexokinase), insulin (IRMA), C-peptide (EASIA) and HbA1c (HPLC), while HOMA-IR and HOMA-ß scores were calculated. RESULTS: Betatrophin concentration was highest at T1, and differed significantly from T2 and T3 (1.84 [Q1=1.16, Q3=2.67]ng/mL vs 1.46 [Q1=0.96, Q3=2.21]ng/mL; P<0.05 and 1.23 [Q1=0.85, Q3=2.14]ng/mL; P<0.01, respectively). The T3 median concentration of betatrophin was the lowest of all trimesters, and significantly lower than at 3MPP (1.23 [Q1=0.85, Q3=2.14]ng/mL vs 1.49 [Q1=1.06, Q3=2.60]ng/mL; P<0.01, respectively). At 3MPP, the level of betatrophin was similar to that of HW (1.47 [Q1=0.89, Q3=2.67]ng/mL). HOMA-IR and HOMA-%ß index scores increased during gestation, peaking at T3 (2.3 [Q1=1.66, Q3=2.72] and 227.7 [Q1=185.49, Q3=326.31], respectively) and returning to levels similar to those of HW at 3MPP (1.53 [Q1=1.12, Q3=2.41] and 88.86 [Q1=62.73, Q3=130.45] vs 1.35 [Q1=1.02, Q3=1.62] and 92.5 [Q1=74.20, Q3=111.47], respectively). CONCLUSION: Concentrations of betatrophin decrease during pregnancy, suggesting that the hormone does not play a significant role in the expansion of beta-cell mass and IR during pregnancy.

Endothelial dysfunction in Graves' disease.

PURPOSE: Graves' disease (GD) is an organ-specific autoimmune thyroid disease, characterized by hyperthyroidism due to excessive production of thyroid hormone induced by thyrotropin receptor-specific stimulatory autoantibodies. In this study, we determined serum levels of the soluble forms of ICAM-1, VCAM-1, vWF, IL-6, IL-12, IL-18, fibrinogen and CRP in patients with subclinical (SH) and overt hyperthyroidism (OH) caused by GD to elucidate a possible role of those parameters as markers of endothelium dysfunction (ED). MATERIAL/METHODS: The study included 96 patients: 52 with GD and 44 euthyroid controls, divided into 3 groups according to their thyroid function tests: SH, OH and controls (CG). RESULTS: The values of IL-6, IL-12 and IL-18 were significantly higher in GD than in CG patients (p < 0.0001, p < 0.0001; p < 0.00001, respectively). Significant difference of sVCAM-1 values were found in the patients with GD compared to CG (p < 0.0001). Patients with GD had significantly higher levels of PAI-1 (p < 0.00001), vWF (p < 0.0001), fibrinogen (p < 0.0001) in comparison to CG. In patients with OH, we observed statistically higher values of fibrinogen compared to SH group (p < 0.05). There were no significant differences in serum concentration of other study parameters in patients with SH compared to the OH. CONCLUSIONS: ED occurs during subclinical and overt hyperthyroidism causing decreased fibrinolytic activity, hypercoagulability and increased levels of IL-6, Il-12 and IL-18. These results support the notion that serum cytokines could be used as a marker of GD activity. Results of this study support the opinion that GD might require treatment as early as in the phase of SH.