title: Association of insulin sensitivity to lipids across the lifespan in people with Type 1 diabetes.
abstract: OBJECTIVE
  Insulin resistance and dyslipidaemia both increase cardiovascular risk in Type 1 diabetes. However, little data exist on the associations of insulin resistance to lipids in Type 1 diabetes. Our objective was to explore the associations between insulin resistance (assessed by glucose infusion rate) and lipids in people with Type 1 diabetes and determine whether adiposity and/or average glycaemia influence these associations.
  
  
  METHODS
  Hyperinsulinaemic-euglycaemic clamp studies were performed in 60 subjects with Type 1 diabetes aged 12-19 years (age 15±2 years, 57% female, duration of diabetes 6.3±3.8 years, HbA(1c) 8.6±1.5%, IFCC=70 mmol/mol) and 40 subjects with Type 1 diabetes aged 27-61 years (age 45±9 years, 53% female, duration of diabetes 23±8 years, HbA(1c) 7.5±0.9%, IFCC=58 mmol/mol). Multiple linear regression models were fit to examine the association between glucose infusion rate and fasting lipid levels with adjustment for possible confounders.
  
  
  RESULTS
  Lower glucose infusion rate was significantly associated with lower levels of HDL cholesterol in youths with Type 1 diabetes and with higher levels of triglycerides and higher triglyceride/HDL ratio in both youths and adults. The magnitude of the associations between glucose infusion rate and lipid levels translate into interquartile differences of 0.098 mmol/l for HDL cholesterol, 0.17 mmol/l for triglycerides and 1.06 for triglycerides/HDL in the adolescents and 0.20 mmol/l for triglycerides and 1.01 for triglycerides/HDL in the adults. The associations were attenuated and no longer statistically significant by adjustment for adiposity among adults, while adjustment for HbA(1c) had a small effect in youths and adults.
  
  
  CONCLUSIONS
  Lower insulin sensitivity is associated with a more atherogenic lipid profile in both youths and adults with Type 1 diabetes.
authors.affiliation: Barbara Davis Center for Childhood Diabetes, University of Colorado, Denver, CO, USA.
authors.forename: D M
authors.initials: DM
authors.lastname: Maahs
authors.forename: K
authors.initials: K
authors.lastname: Nadeau
authors.forename: J K
authors.initials: JK
authors.lastname: Snell-Bergeon
authors.forename: I
authors.initials: I
authors.lastname: Schauer
authors.forename: B
authors.initials: B
authors.lastname: Bergman
authors.forename: N A
authors.initials: NA
authors.lastname: West
authors.forename: M
authors.initials: M
authors.lastname: Rewers
authors.forename: S R
authors.initials: SR
authors.lastname: Daniels
authors.forename: L G
authors.initials: LG
authors.lastname: Ogden
authors.forename: R F
authors.initials: RF
authors.lastname: Hamman
authors.forename: D
authors.initials: D
authors.lastname: Dabelea
mesh_terms: D000293:Adolescent; D000328:Adult; D002114:Calcinosis / Q000503:physiopathology*; D002648:Child; D008076:Cholesterol, HDL / Q000097:blood; D003324:Coronary Artery Disease / Q000378:metabolism / Q000401:mortality / Q000503:physiopathology*; D003922:Diabetes Mellitus, Type 1 / Q000378:metabolism / Q000401:mortality / Q000503:physiopathology*; D003925:Diabetic Angiopathies / Q000378:metabolism / Q000401:mortality / Q000503:physiopathology*; D005260:Female; D006442:Glycated Hemoglobin / Q000378:metabolism; D006801:Humans; D007333:Insulin Resistance / Q000502:physiology*; D008055:Lipids / Q000097:blood*; D008297:Male; D008875:Middle Aged; D012307:Risk Factors; D014280:Triglycerides / Q000097:blood; D055815:Young Adult
chemical_list: D008076:Cholesterol, HDL; D006442:Glycated Hemoglobin; D008055:Lipids; D014280:Triglycerides