title: [The influence of metabolic parameters on fetal development weight in women with type 1 diabetes and homozygotic variant in -2548 G/A of leptin gene and its 668 A/G receptor polymorphism].
abstract: BACKGROUND
  Leptin, as many other hormones and metabolic factors, may play a role in fetal development in pregnancy complicated by type 1 diabetes. Different genetic variants in leptin gene and leptin gene receptor may have influence on leptin synthesis in the course of pregnancy and metabolic state of the mother.
  
  
  OBJECTIVE
  To assess the possible influence of metabolic factors on fetal weight in type 1 diabetic subjects with homozygotic variants in leptin gene (-2548 G/A) and leptin gene receptor (668 G/A).
  
  
  METHODS
  30 diabetic and homozygotic subjects (out of 100 diabetic subjects) were qualified to the study Genotyping was performed by PCR-RFLR The following factors were assessed: glycemia, leptin concentration, glycated hemoglobin, lipid profile (total cholesterol, LDL, HDL, triglycerides), maternal body weight. Multiple regression models were developed and ROC curves were used in the analysis.
  
  
  RESULTS
  Mean fetal weight in the analyzed group was 3600 g. The following parameters were found to have influence on fetal weight: I trimester leptin (R2-0.80741288, p < 0.05), I trimester glycemia (R2-0.80741288, p < 0.05), III trimester glycemia (R2-0.80741288, p < 0.05), I trimester HbA1C (R2-0.80741288, p < 0.05), III trimester LDL (R2 = 0.63192254, p < 0.05). Moreover the influence of LDL and maternal BMI (R2-0.81869348, p < 0.05) was found. ROC curve analysis revealed the influence of I trimester leptin--AUC 0.62; sensitivity 0.75; specificity 0.5; cut-off 28.127 ng/ml, III trimester HbA1C AUC 0.66; sensitivity 0.23; specificity 0.91; cut-off 7.9%, III trimester mothers weight AUC 0.63; sensitivity 0.25; specificity 0.93; cut-off 98 kg.
  
  
  CONCLUSIONS
  Apart from well-known metabolic factors influencing fetal weight, I trimester leptin concentration was found to have an impact on fetal growth.
authors.affiliation: Klinika Potoinictwa i Chorób Kobiecych, Uniwersytet Medyczny im. Karola Marcinkowskiego w Poznaniu. ralfiho@o2.pl
authors.forename: Rafał
authors.initials: R
authors.lastname: Iciek
authors.forename: Ewa
authors.initials: E
authors.lastname: Wender-Ozegowska
authors.forename: Agnieszka
authors.initials: A
authors.lastname: Zawiejska
authors.forename: Agnieszka
authors.initials: A
authors.lastname: Seremak-Mrozikiewicz
authors.forename: Krzysztof
authors.initials: K
authors.lastname: Drews
authors.forename: Jacek
authors.initials: J
authors.lastname: Brazert
mesh_terms: D000328:Adult; D015992:Body Mass Index; D001835:Body Weight / Q000235:genetics; D016022:Case-Control Studies; D003922:Diabetes Mellitus, Type 1 / Q000235:genetics* / Q000378:metabolism; D005260:Female; D020567:Fetal Weight / Q000235:genetics*; D005838:Genotype; D006801:Humans; D007231:Infant, Newborn; D020738:Leptin / Q000235:genetics*; D009765:Obesity / Q000235:genetics; D016133:Polymerase Chain Reaction / Q000379:methods; D011110:Polymorphism, Genetic; D011247:Pregnancy; D011254:Pregnancy in Diabetics / Q000235:genetics* / Q000378:metabolism; D054411:Receptors, Leptin / Q000235:genetics*
chemical_list: C515448:LEPR protein, human; D020738:Leptin; D054411:Receptors, Leptin