title: Low adiponectin concentration during pregnancy predicts postpartum insulin resistance, beta cell dysfunction and fasting glycaemia.
abstract: OBJECTIVE
  The postpartum phase following gestational diabetes (GDM) is characterised by subtle metabolic defects, including the beta cell dysfunction that is believed to mediate the increased future risk of type 2 diabetes in this patient population. Low circulating levels of adiponectin and increased leptin and C-reactive protein (CRP) have recently emerged as novel diabetic risk factors, although their relevance to GDM and subsequent diabetes has not been characterised. Thus, we sought to determine whether adiponectin, leptin and CRP levels during pregnancy relate to the postpartum metabolic defects linking GDM with type 2 diabetes.
  
  
  METHODS
  Metabolic characterisation, including oral glucose tolerance testing, was undertaken in 487 women during pregnancy and at 3 months postpartum. Based on the antepartum OGTT, there were 137 women with GDM, 91 with gestational impaired glucose tolerance and 259 with normal glucose tolerance.
  
  
  RESULTS
  Adiponectin levels were lowest (p < 0.0001) and CRP levels highest (p = 0.0008) in women with GDM. Leptin did not differ between the glucose tolerance groups (p = 0.4483). Adiponectin (r = 0.41, p < 0.0001), leptin (r = -0.36, p < 0.0001) and CRP (r = -0.30, p < 0.0001) during pregnancy were all associated with postpartum insulin sensitivity (determined using the insulin sensitivity index of Matsuda and DeFronzo [IS(OGTT)]). Intriguingly, adiponectin levels were also related to postpartum beta cell function (insulinogenic index/HOMA of insulin resistance; r = 0.16, p = 0.0009). Indeed, on multiple linear regression analyses, adiponectin levels during pregnancy independently predicted both postpartum insulin sensitivity (t = 3.97, p < 0.0001) and beta cell function (t = 2.37, p = 0.0181), even after adjustment for GDM. Furthermore, adiponectin emerged as a significant negative independent determinant of postpartum fasting glucose (t = -3.01, p = 0.0027).
  
  
  CONCLUSIONS
  Hypoadiponectinaemia during pregnancy predicts postpartum insulin resistance, beta cell dysfunction and fasting glycaemia, and hence may be relevant to the pathophysiology relating GDM with type 2 diabetes.
authors: Leadership Sinai Centre for Diabetes, Mount Sinai Hospital, 60 Murray Street, Suite-L5-039, Mailbox-21, Toronto, ON, Canada. rretnakaran@mtsinai.on.ca
authors: R
authors: R
authors: Retnakaran
authors: Y
authors: Y
authors: Qi
authors: P W
authors: PW
authors: Connelly
authors: M
authors: M
authors: Sermer
authors: A J
authors: AJ
authors: Hanley
authors: B
authors: B
authors: Zinman
mesh_terms: D052242:Adiponectin / Q000097:blood* / Q000172:deficiency; D000328:Adult; D001786:Blood Glucose / Q000378:metabolism*; D001942:Breast Feeding; D002097:C-Reactive Protein / Q000378:metabolism; D003924:Diabetes Mellitus, Type 2 / Q000453:epidemiology; D016640:Diabetes, Gestational / Q000097:blood*; D005006:Ethnicity; D005260:Female; D005951:Glucose Tolerance Test; D006801:Humans; D007333:Insulin Resistance / Q000502:physiology*; D050417:Insulin-Secreting Cells / Q000502:physiology*; D020738:Leptin / Q000097:blood; D010298:Parity; D049590:Postpartum Period; D011247:Pregnancy / Q000097:blood*; D044469:Racial Groups; D012307:Risk Factors; D015430:Weight Gain
chemical_list: D052242:Adiponectin; D001786:Blood Glucose; D020738:Leptin; D002097:C-Reactive Protein