title: Maternal history of type 2 diabetes is associated with diabetic nephropathy in type 1 diabetic patients.
abstract: OBJECTIVE
  Insulin resistance is a key feature of type 2 diabetes. It is also involved in the development and progression of microvascular complications. We analysed the relationship between parental history of diabetes, insulin resistance and diabetic nephropathy (DN) and assessed the specific maternal and paternal influences of history of type 2 diabetes on DN in type 1 diabetic offspring.
  
  
  METHODS
  We recorded information regarding family history of type 2 diabetes and of cardiovascular disease in 160 consecutive, unrelated type 1 diabetic patients. Insulin resistance was assessed using a validated estimation of the glucose disposal rate (eGDR).
  
  
  RESULTS
  Type 1 diabetic patients with a maternal history of type 2 diabetes were more likely to be insulin-resistant (P=0.043) and to have renal complications (P=0.0041) than those from the reference group (without parental history of diabetes), while patients with a paternal history were not different from those from the reference group, regarding eGDR and DN. Time to development of abnormal albuminuria was significantly affected by maternal history of type 2 diabetes (log-rank=12.66; P=0.0004) and by familial history of premature cardiovascular disease (log-rank=5.48; P=0.0234). In multivariate analysis, a maternal history of type 2 diabetes was independently associated with nephropathy after adjustment for sex, diabetes duration and familial history of premature cardiovascular disease.
  
  
  CONCLUSIONS
  Maternal history of type 2 diabetes is independently associated with DN in type 1 diabetic patients. This might suggest the transmission of a maternal trait related to microvascular complications, raising the hypothesis of imprinted genes predisposing to diabetic renal disease.
authors.affiliation: Inserm EO 324, CHU de Poitiers, BP 577, 2, rue de la Milétrie, 86021 Poitiers cedex, France. s.hadjadj@chu-poitiers.fr
authors.forename: S
authors.initials: S
authors.lastname: Hadjadj
authors.forename: F
authors.initials: F
authors.lastname: Duengler
authors.forename: F
authors.initials: F
authors.lastname: Torremocha
authors.forename: G
authors.initials: G
authors.lastname: Faure-Gerard
authors.forename: F
authors.initials: F
authors.lastname: Bridoux
authors.forename: M
authors.initials: M
authors.lastname: Boissonnot
authors.forename: G
authors.initials: G
authors.lastname: Mauco
authors.forename: J
authors.initials: J
authors.lastname: Guilhot
authors.forename: R
authors.initials: R
authors.lastname: Maréchaud
mesh_terms: D001794:Blood Pressure; D015992:Body Mass Index; D049628:Body Size; D002784:Cholesterol / Q000097:blood; D003922:Diabetes Mellitus, Type 1 / Q000453:epidemiology* / Q000235:genetics*; D003924:Diabetes Mellitus, Type 2 / Q000235:genetics*; D003928:Diabetic Nephropathies / Q000453:epidemiology* / Q000235:genetics*; D005260:Female; D005602:France; D006442:Glycated Hemoglobin / Q000032:analysis; D006801:Humans; D007333:Insulin Resistance / Q000235:genetics; D008055:Lipids / Q000097:blood; D008297:Male; D008487:Medical History Taking; D009035:Mothers
chemical_list: D002784:Cholesterol; D006442:Glycated Hemoglobin; D008055:Lipids