Adiponectin and tumor necrosis factor-alpha (TNF-alpha) have been implicated in insulin resistance and diabetes mellitus (DM). In the present study we investigated levels of adiponectin and TNF-alpha and their relationships with each other and metabolic factors in women with gestational DM (GDM). Thirty-four pregnant women with GDM and 31 pregnant women with normal glucose tolerance (NGT) were included in the study. Plasma adiponectin levels were lower in GDM than in NGT (36.9 +/- 6.7 vs. 61.3 +/- 13.0 ng/ml, p = 0.028). Serum TNF-alpha levels were increased in GDM compared with NGT (20.5 +/- 2.4 vs. 14.0 +/- 1.5 pg/ml, p = 0.042). After adjustment for pre-pregnancy and current body mass index (BMI), adiponectin levels correlated negatively with insulin resistance by homeostasis model assessment-insulin resistance (HOMA-IR) and 0-h and 1-h glucose both at glucose challenge test and oral glucose tolerance test in GDM. Adiponectin levels were correlated only with very low-density lipoprotein cholesterol and triglyceride levels in NGT. TNF-alpha levels were correlated with glycated hemoglobin in GDM. There was a significant positive correlation between TNF-alpha levels and pre-pregnancy and current BMI in GDM as well as NGT. HOMA-IR for adiponectin and pre-pregnancy BMI for TNF-alpha remained as significant determinants in multiple regression analyses. In conclusion, these data suggest that reduced adiponectin and increased TNF-alpha may be involved in the pathogenesis of GDM.
Increased levels of small, dense LDL are common in Mediterranean women with gestational diabetes. Whether these findings affect the atherogenic process and clinical end-points in these women remains to be determined by future prospective studies.
Our results suggest that SCH is associated with some lipid and lipoprotein abnormalities. Our results also suggest that this association does not depend on the subject's TSH level.
Abstract. The purpose of this study was to investigate plasma adiponectin concentration and its relation with metabolic parameters in overweight and normal weight subjects. The study was carried out in 46 overweight subjects (20 male, 26 female; mean age 39.4 ± 10.2 years) and 48 (19 male, 29 female; mean age 36.1 ± 10.6 years) sex-and age-matched normal weight subjects. Anthropometric measurements were recorded and adiponectin, glucose, insulin, lipid profile, total homocysteine (tHcy) and fibrinogen levels were measured. The insulin resistance index was assessed by homeostasis model assessment for insulin resistance (HOMA-IR). Plasma mean adiponectin concentrations of the overweight subjects were significantly lower than those of normal weight subjects (15.0 ± 4.2 vs 17.3 ± 5.6 ng/ml) (P<0.05). In overweight subjects, adiponectin levels negatively correlated with body weight (r = -0.35, P<0.001), body mass index (BMI) (r = -0.28, P<0.006), systolic blood pressure (r = -0.21, P<0.04), fasting insulin (r = -0.19, P<0.01) and HOMA-IR (r = -0.20, P<0.01) and positively with high-density lipoprotein cholesterol (HDL-C) (r = 0.27, P<0.009). Overweight subjects with low HDL-C levels had significantly decreased plasma adiponectin levels compared to those with high HDL-C levels (P<0.05). Multiple regression analysis revealed that BMI, HOMA-IR and HDL-C explained 12%, 20% and 15% variance of the adiponectin concentrations. These findings may suggest that circulating adiponectin is associated with insulin resistance and HDL-C levels independent from BMI in overweight subjects.
ABSTRACT. Our aim is to investigate visfatin concentration and its relationship to glycated hemoglobin (HbA 1c ), insulin resistance, lipid parameters, and neonatal birth weight in women with gestational diabetes mellitus (GDM). In our study group, there were 47 women with GDM and 31 women with normal glucose tolerance (NGT) between 33-39 weeks of gestation. Plasma visfatin levels were significantly decreased in pregnant women with GDM compared to those with NGT (p=0.001). Homeostasis model assessmentinsulin resistance (HOMA-IR) levels were higher in the GDM group than in the NGT group (p=0.006). In all subjects, plasma visfatin levels were negatively correlated with HOMA-IR, post-prandial blood glucose, triglycerides, and VLDL cholesterol (p<0.05). We did not observe any statistically significant correlation between the plasma visfatin levels and the selected parameters in the GDM group, but in the NGT group plasma visfatin levels were negatively correlated with HOMA-IR (r=-0.36, p=0.04). There was no correlation between visfatin concentrations and fetal birth weight in either group (p>0.05). By regression analysis, having GDM was found to be the only significant determinant (t=3.5, p=0.001) of visfatin concentration (R=0.39, r 2 =0.15). We conclude that women with GDM have significantly decreased visfatin concentrations in the third trimester. Future studies are required to establish the exact role of visfatin in the pathogenesis of GDM. (J. Endocrinol. Invest. 31: 610-613, 2008)
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