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Unlike Type 2 Diabetes, Type 1 Does Not Interact with the Codon 54 Polymorphism of the Fatty Acid Binding Protein 2 Gene

Minneapolis Veterans Affairs Medical Center (A.G.), Departments of Medicine (A.G.) and Laboratory Medicine and Pathology (O.A., M.Y.T.), University of Minnesota, Minneapolis, Minnesota 55417; and the Second Department of Medicine (M.N.), Athens University Medical School, 115 27 Athens, Greece

Address all correspondence and requests for reprints to: Angeliki Georgopoulos, M.D., Medicine Service 111M, VAMC, One Veterans Drive, Minneapolis, Minnesota 55417. E-mail: . georg003{at}tc.umn.edu

Abstract

In type 2 diabetes, the threonine (Thr) for alanine (Ala) codon 54 polymorphism of the fatty acid binding protein 2 gene is associated with elevated fasting and postprandial triglycerides and dyslipidemia when compared with the wild type (Ala-54/Ala-54). To assess whether this is the case in patients with type 1 diabetes, who usually do not manifest the metabolic syndrome, we screened 181 patients with similar glycemic control as the type 2 patients. Thirty percent were heterozygous, and 9% were homozygous for the polymorphism. Mean (±SEM) fasting plasma triglyceride levels in patients with the wild type (n = 84), those heterozygous for Ala-54/Thr-54 (n = 44), and those homozygous for the Thr-54 (n = 13) were 1.0 ± 0.07, 1.1 ± 0.17, and 1.2 ± 0.23 mmol/liter, respectively. In addition, there were no differences in total, low-density lipoprotein, high-density lipoprotein, and non-high density lipoprotein cholesterol among the three groups. After a fat load, the postprandial area under the curve of triglyceride in plasma, chylomicrons, and very low-density lipoprotein were similar between the wild type (n = 18) and the Thr-54 homozygotes (n = 12). In conclusion, in contrast to type 2, type 1 diabetes does not interact with the codon 54 polymorphism of the fatty acid binding protein 2 gene to cause hypertriglyceridemia/dyslipidemia. Insulin resistance could account possibly for this difference.