title: Apolipoprotein E gene polymorphism alters lipids before pancreas transplantation.
abstract: BACKGROUND
  Pancreas transplantation (PTX) improves lipids in patients with type 1 diabetes mellitus. However, there are patients who have persistent abnormal lipids or develop new hyperlipidemia despite PTX. One factor that may influence the lipid profile is apolipoprotein E (Apo E) genotype. Apo E polymorphism, particularly E2 and E4 alleles, increases the risk of dyslipidemia. Apo E2 has also been found to increase risk of diabetic nephropathy and so may be more prevalent in PTX candidates.
  
  
  METHODS
  This study evaluated fasting-lipid profiles in type 1 diabetes patients who were pancreas transplant candidates to prospectively evaluate the impact of Apo E genotype on dyslipidemia before and after PTX.
  
  
  RESULTS
  Presence of one or more E4 alleles resulted in higher triglycerides ( =0.0446), lower HDL ( =0.0247), and a higher cholesterol-to-HDL (C/H) ratio ( =0.0405) before PTX when compared with those with E3/3 genotype. After PTX, lipids improved so there was no longer a difference in fasting lipids between patients with an E4 allele and E3/3 genotype. Presence of an E2 allele had no significant impact on fasting lipids before or after PTX.
  
  
  CONCLUSIONS
  Presence of an Apo E4 allele worsened HDL, triglycerides, and C/H ratio before PTX compared with those with E3/3 genotype, whereas the presence of an Apo E2 allele had no significant effect on lipids before or after PTX. Thus, Apo E4 has a larger impact than Apo E2 on fasting-lipid profile in PTX candidates, and Apo E gene polymorphism does not worsen lipid dyslipidemia after PTX, despite introduction of immunosuppressant medications known to cause dyslipidemia.
authors.affiliation: Diabetes, Endocrinology and Metabolism Section, Department of Internal Medicine, University of Nebraska Medical Center, Omaha, NE 68198-3020, USA.
authors.forename: Sajeev
authors.initials: S
authors.lastname: Balakrishnan
authors.forename: Christopher
authors.initials: C
authors.lastname: Colling
authors.forename: Tab
authors.initials: T
authors.lastname: Burkman
authors.forename: Judi
authors.initials: J
authors.lastname: Erickson
authors.forename: Elizabeth
authors.initials: E
authors.lastname: Lyden
authors.forename: Hiralal
authors.initials: H
authors.lastname: Maheshwari
authors.forename: Lynn
authors.initials: L
authors.lastname: Mack-Shipman
authors.forename: James
authors.initials: J
authors.lastname: Lane
authors.forename: Jennifer
authors.initials: J
authors.lastname: Larsen
mesh_terms: D000328:Adult; D000483:Alleles; D053329:Apolipoprotein E2; D053318:Apolipoprotein E3; D053327:Apolipoprotein E4; D001057:Apolipoproteins E / Q000235:genetics*; D002784:Cholesterol / Q000097:blood; D008076:Cholesterol, HDL / Q000097:blood; D005260:Female; D005838:Genotype; D006720:Homozygote; D006801:Humans; D006949:Hyperlipidemias / Q000097:blood / Q000235:genetics; D008055:Lipids / Q000097:blood*; D008297:Male; D016035:Pancreas Transplantation; D011110:Polymorphism, Genetic / Q000502:physiology*; D014280:Triglycerides / Q000097:blood
chemical_list: D053329:Apolipoprotein E2; D053318:Apolipoprotein E3; D053327:Apolipoprotein E4; D001057:Apolipoproteins E; D008076:Cholesterol, HDL; D008055:Lipids; D014280:Triglycerides; D002784:Cholesterol