ABSTRACT
Objective To assess the effects of gonadotropin-releasing hormone analog on glucose and lipid metabolism in girls with idiopathic central precocious puberty(ICPP).Methods A total of 26 girls (aged 6-8 years,breast stage B2) with ICPP were followed up in Department of Endocrinology,Shenzhen Children's Hospital from Jan.2008 to Jun.2011.Those girls received triptorelin therapy for 12 months.Before and the end of the 6th month,the 12th month of the treatment,body mass index(BMI) was calculated,fasting plasma glucose(FPG),fasting plasma insulin(FPI),total cholesterol,triacylglycerols,high density lipoprotein cholesterol,low density lipoprotein cholesterol,apolipoprotein A,apolipoprotein B and estradiol(E2) were measured.Insulin sensitivity was estimated by homeostasis model assessment of insulin resistance(HOMA-IR).Twenty age-matched prepuberty girls were set as controls.Results 1.Before treatment,BMI,FPG,FPI and HOMA-IR in ICPP girls had no significant difference compared with the controls.2.After 6 months treatment of triptrolin,serum E2 concentration in ICPP girls declined from(30.5 ± 9.8) ng/L at the beginning of treatment to (11.2 ± 4.6) ng/L at the end of 6th month (P ＜ 0.01) ; The end of 12 th month of the treatment,FPG and FPI had no significant difference compared with that before of the treatment,but BMI increased from(16.46 ± 1.10) kg/m2 to(18.35 ± 1.30) kg/m2,the difference was significant(P ＜0.05),HOMA-IR increased from 1.24 ±0.30 to 2.08 ±0.40,the difference was significant(P ＜0.05).3.Lipid metabolism parameters remained unchangeable after 12 months of triptrolin treatment.Conclusion Triptorelin may lead to raise of BMI and HOMA-IR in girls with ICPP at 12 months after treatment.
ABSTRACT
SW872 preadipocytes were cultured and induced to differentiate by oleic acid in vitro.The levels of adiponectin and its receptors (AdipoR1 and AdipoR2) mRNA were measured by semiquantitative RT- PCR.The concentration of adiponectin in the culture medium was assayed by ELISA.The results showed that rhIL- 6 could inhibit adiponectin,AdipoR1 mRNA expressions and adiponectin secretion in SW872 adipocytes in a time- and dose-dependent manner,but did not influence adipoR2 mRNA expression.