title: The role of adipocytokines in insulin resistance in normal pregnancy: visfatin concentrations in early pregnancy predict insulin sensitivity.
abstract: BACKGROUND
  Throughout pregnancy maternal adipose tissue is metabolically active, producing adipocytokines involved in the process of insulin resistance. We explored the role of serum adipocytokines, including the newly identified adipocytokine visfatin, in the process of insulin resistance in normal pregnancy.
  
  
  METHODS
  We examined 80 pregnant nonobese, nondiabetic white women during the 3 trimesters of pregnancy. All study participants underwent anthropometric measurements, adipocytokine evaluation, and a 75-g oral glucose tolerance test. Homeostasis mathematical model assessment (HOMA-R), insulin sensitivity index (ISI), and indices of beta-cell secretion were calculated.
  
  
  RESULTS
  Maternal weight, percentage total body fat, hip circumference, and indices of beta-cell secretion increased significantly during the 3 trimesters, and HOMA-R and ISI increased and decreased, respectively, in the 3rd trimester. During early pregnancy, insulin resistance, beta-cell secretion, and weight correlated positively with leptin. During the 1st trimester, visfatin correlated negatively with percentage body fat and was the best positive predictor of 2nd trimester ISI. In the 2nd trimester, serum visfatin was the best negative predictor of percentage body fat.
  
  
  CONCLUSIONS
  During normal pregnancy of nonobese, nondiabetic women, adipose tissue increases, accompanied by a significant progressive increase of insulin resistance. Visfatin concentrations in the 1st trimester positively predict insulin sensitivity during the 2nd trimester. Body fat mass during 1st trimester of pregnancy is negatively associated with insulin sensitivity during the 2nd trimester and perhaps should be kept under control.
authors.affiliation: Endocrine Unit, 2nd Department of Obstetrics and Gynecology, Aretaieion University Hospital, Athens Medical School, Athens, Greece.
authors.forename: George
authors.initials: G
authors.lastname: Mastorakos
authors.forename: Georgios
authors.initials: G
authors.lastname: Valsamakis
authors.forename: Dimitrios C
authors.initials: DC
authors.lastname: Papatheodorou
authors.forename: Ioannis
authors.initials: I
authors.lastname: Barlas
authors.forename: Alexandra
authors.initials: A
authors.lastname: Margeli
authors.forename: Anastasios
authors.initials: A
authors.lastname: Boutsiadis
authors.forename: Evangelia
authors.initials: E
authors.lastname: Kouskouni
authors.forename: Nikolaos
authors.initials: N
authors.lastname: Vitoratos
authors.forename: Apostolos
authors.initials: A
authors.lastname: Papadimitriou
authors.forename: Ioannis
authors.initials: I
authors.lastname: Papassotiriou
authors.forename: George
authors.initials: G
authors.lastname: Creatsas
mesh_terms: D000273:Adipose Tissue / Q000502:physiology*; D000328:Adult; D000886:Anthropometry; D050260:Carbohydrate Metabolism; D016207:Cytokines / Q000378:metabolism*; D005260:Female; D006801:Humans; D007333:Insulin Resistance; D054409:Nicotinamide Phosphoribosyltransferase; D011247:Pregnancy / Q000378:metabolism / Q000502:physiology*; D011264:Pregnancy Trimesters; D012016:Reference Values
chemical_list: D016207:Cytokines; D054409:Nicotinamide Phosphoribosyltransferase; C085455:nicotinamide phosphoribosyltransferase, human