Background:We examined the possible association of adiponectin gene polymorphisms with polycystic ovary syndrome (PCOS) and their influence on serum adiponectin and insulin resistance indexes in Greek women with PCOS. Methods: We genotyped samples from 100 women with PCOS characterized with respect to body mass index (BMI), glucose and insulin concentrations during an oral glucose tolerance test (OGTT), lipid profile, and serum adiponectin concentrations and from 140 healthy controls for the 45T>G and 276G>T polymorphisms in the adiponectin gene. Results: The distributions of genotypes and alleles of both polymorphisms were no different in women with PCOS and controls, indicating that the individual polymorphisms are not associated with increased risk for PCOS. However, the two polymorphisms were found to be associated with insulin resistance indexes among women with PCOS and to influence adiponectin production. In particular, carriers of the TG genotype at position ؉45 had greater hyperinsulinemia, as estimated by the area under the curve for insulin (AUC insulin ) during the OGTT, than those with the TT genotype

Objective: To determine circulating levels of adiponectin in preterm infants and examine possible associations with anthropometric measurements, weight gain, and leptin and insulin levels. Design: Prospective study. Setting: A university hospital neonatal care unit. Study population: 62 preterm (mean (SD) gestational age 32.0 (2.1) weeks) and 15 full-term infants (reference group). Interventions: Blood samples taken at discharge (40.9 (14.8) days of life) from the preterm infants and at a comparable postnatal age in full-term infants. All infants were fed the same commercial formula, but in nine preterms the formula contained long-chain polyunsaturated fatty acids (LCPUFAs). Main outcome measures: Serum levels of adiponectin, leptin and insulin. Associations of adiponectin levels were tested only in the preterm group. Results: Serum levels of adiponectin were lower in preterm (40.9 (14.8) mg/ml) than full-term infants (53.1 (16.0) mg/ml, p,0.01). However, after adjustment for body weight, the influence of prematurity on adiponectin levels was no longer significant. In preterm infants, adiponectin levels independently correlated with being born small for gestational age (SGA) (b = 20.35, p = 0.01), weight gain (b = 0.28, p = 0.03) and LCPUFA-supplemented formula (b = 0.34, p = 0.009). Serum adiponectin levels did not correlate with insulin or leptin levels. However, insulin levels were higher in preterm than in full-term infants after adjustment for body weight. Conclusions: Adiponectin levels are lower in preterm infants at discharge than full-term infants probably due to decreased adiposity. The levels are influenced by being born SGA, weight gain and, possibly, by dietary LCPUFAs. The importance of these findings in the development of insulin or leptin resistance in children born prematurely needs to be further studied. N utrition and growth during fetal life and early infancy have been linked to health and disease in later life.