title: The APOB -516C/T polymorphism is associated with differences in insulin sensitivity in healthy males during the consumption of diets with different fat content.
abstract: Several apo B polymorphic sites have been studied for their potential use as markers for CHD in the population and for potential gene-diet interactions. Our aim was to determine whether the presence of the -516C/T polymorphism in the APOB gene promoter modifies insulin sensitivity to dietary fat. We studied fifty-nine healthy volunteers (thirty men and twenty-nine women, thirty-six homozygotes for the -516C allele (C/C) (nineteen males and seventeen females) and twenty-three heterozygotes for the -516T allele (C/T) (eleven males and twelve females)). Subjects consumed three diets during the feeding study, 4 weeks each: an SFA-rich diet (38 % fat, 20 % SFA), followed by a carbohydrate (CHO)-rich diet (30 % fat, 55 % CHO) or a MUFA-rich diet (38 % fat, 22 % MUFA) following a randomised cross-over design. For each diet, we investigated peripheral insulin sensitivity with the insulin suppression test. Male carriers of the -516T allele showed a significantly greater decrease in steady-state plasma glucose concentrations when changing from the SFA-rich diet (9.18 (sd 1.35) mmol/l) to the MUFA (6.55 (sd 0.74) mmol/l) or the CHO (6.31 (sd 0.93) mmol/l) diets than did those who were homozygous for the C allele (P = 0.040). Furthermore, C/T subjects presented higher plasma NEFA values after consumption of the SFA diet compared with the MUFA and CHO diets (P = 0.001). This effect was not observed in females (P = 0.908). Our findings show that male carriers of the -516T allele, C/T, have a significant increase in insulin resistance after consumption of all diets, but the difference is more exaggerated after the SFA diet compared with the MUFA- and CHO-rich diets.
authors.affiliation: Unit of Lipids and Atherosclerosis, Hospital Universitario Reina Sofía, Avda. Menéndez Pidal, s/n. 14004, Córdoba, Spain. pablopermar@yahoo.es
authors.forename: Pablo
authors.initials: P
authors.lastname: Pérez-Martínez
authors.forename: Francisco
authors.initials: F
authors.lastname: Pérez-Jiménez
authors.forename: José María
authors.initials: JM
authors.lastname: Ordovás
authors.forename: Juan Antonio
authors.initials: JA
authors.lastname: Moreno
authors.forename: Rafael
authors.initials: R
authors.lastname: Moreno
authors.forename: Francisco
authors.initials: F
authors.lastname: Fuentes
authors.forename: Juan
authors.initials: J
authors.lastname: Ruano
authors.forename: Purificación
authors.initials: P
authors.lastname: Gómez
authors.forename: Carmen
authors.initials: C
authors.lastname: Marín
authors.forename: José
authors.initials: J
authors.lastname: López-Miranda
mesh_terms: D000328:Adult; D001053:Apolipoproteins / Q000097:blood; D001055:Apolipoproteins B / Q000235:genetics*; D001786:Blood Glucose / Q000378:metabolism; D018592:Cross-Over Studies; D004032:Diet; D004041:Dietary Fats / Q000008:administration & dosage*; D005260:Female; D006801:Humans; D007333:Insulin Resistance / Q000235:genetics*; D008055:Lipids / Q000097:blood; D008297:Male; D011110:Polymorphism, Genetic; D011401:Promoter Regions, Genetic / Q000235:genetics
chemical_list: D001053:Apolipoproteins; D001055:Apolipoproteins B; D001786:Blood Glucose; D004041:Dietary Fats; D008055:Lipids