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The Journal of Clinical Endocrinology & Metabolism Vol. 85, No. 8 2801-2804
Copyright © 2000 by The Endocrine Society

Original Studies

The T 54 Allele of the Intestinal Fatty Acid-Binding Protein 2 Is Associated with a Parental History of Stroke1

Martin Carlsson, Marju Orho-Melander, Jan Hedenbro, Peter Almgren and Leif C. Groop

Department of Endocrinology, Malmo University Hospital (M.C., M.O.-M., P.A., L.C.G.), S-205 02 Malmo, Sweden; and Department of Surgery, Lund University Hospital, University of Lund (J.H.), S-221 85 Lund, Sweden

Address all correspondence and requests for reprints to: Martin Carlsson, M.D., Department of Medicine, Kalmar Hospital, S-391 85 Kalmar, Sweden. E-mail: martinC{at}ltkalmar.se


   Abstract
Top
 Abstract
Introduction
 Subjects and Methods
 Results
 Discussion
 References
 
To test the hypothesis that the A/T polymorphism of the fatty acid-binding protein 2 gene (FABP2) is associated with impaired lipid metabolism and cardiovascular disease, we compared clinical characteristics and a parental history of cardiovascular disease between 213 sibling pairs discordant for the polymorphism. Siblings with an excess of the T54 allele had higher triglyceride (P = 0.002) and cholesterol (P = 0.019) concentrations than siblings with the A54 allele. Parents of offspring with the T54T and T54A genotypes reported an increased prevalence of stroke compared to parents of offspring with the A54A genotype (P = 0.007). In summary, we have confirmed the association of the FABP2 T54 allele with increased concentrations of cholesterol and triglycerides in genotype-discordant sibling pairs. We also present novel evidence that genetic variation in the FABP2 gene may increase susceptibility to stroke.


   Introduction
Top
 Abstract
 Introduction
Subjects and Methods
 Results
 Discussion
 References
 
FATTY ACID-BINDING proteins (FABP) represent a family of proteins that is thought to be involved in intestinal fatty acid (FFA) absorption and intracellular metabolism of long-chain FFA (1, 2). Several different isoforms of FABP have been described; each encoded by different genes. A FABP2 gene on chromosome 4q encodes an intestinal isoform (IFABP) that is expressed in enterocytes (3) and has a high affinity for long-chain fatty acids (4). A common polymorphism at codon 54 of this gene results in replacement of alanine with threonine. A complete tertiary structure has been reported for the alanine 54 variant (2). In vitro, the threonine-containing protein has a greater affinity for long-chain fatty acids than the alanine-containing protein (4, 5). In addition, subjects with the threonine-encoding allele (T54) have been shown to be more insulin resistant (4, 6) and more obese (7, 8) than carriers of the alanine-encoding allele (A54). The T54 allele has also been associated with elevated triglyceride concentrations after a fat meal (9) and reduced secretion of fecal bile acids in response to different dietary fiber (10).

However, all studies have not confirmed a role for the T54 allele in lipid and glucose metabolism (11, 12, 13). In a study from Finland, the polymorphism did not modify the fatty acid composition of serum lipids (11), nor did the polymorphism affect basal metabolic rate, insulin, glucose, or lipid concentrations (12, 13). Population-based association studies are often biased by the selection of the control group. To circumvent this problem, we tested the hypothesis that the FABP2 T54 allele is associated with obesity, dyslipidemia, insulin resistance, hypertension, and diabetes in siblings discordant for the A54T polymorphism. This approach using genotype-discordant sibling pairs has earlier been shown to be a valid test of association in the presence of linkage (14, 15, 16, 17). We further investigated the possibility that the T54 allele could contribute to the risk of cardiovascular disease (CVD) by relating the parental history of CVD with the genotype status in the offspring.


   Subjects and Methods
Top
 Abstract
 Introduction
 Subjects and Methods
Results
 Discussion
 References
 
Subjects

Three groups of subjects from southern Sweden were included in the study. Group 1 consisted of 687 siblings from 210 families, 399 of which had type 2 diabetes [200 males and 199 females; age, 60.1 ± 12.3 yr; body mass index (BMI), 27.8 ± 4.7 kg/m2], 93 of whom had impaired glucose tolerance (43 males and 50 females; age, 54.8 ± 16.4 yr; BMI, 26.8 ± 4.7 kg/m2) and 195 of whom had normal glucose tolerance (84 males and 111 females; age, 48.9 ± 16.2 yr; BMI, 25.5 ± 3.9 kg/m2). All subjects in the first group had first degree relatives with type 2 diabetes (siblings or parents), whereas 73% of the subjects had 1 parent with type 2 diabetes. Group 2 consisted of 59 unrelated, morbidly obese, nondiabetic subjects without a family history of diabetes undergoing bariatric surgery (15 males and 44 females; age, 40.5 ± 12.0 yr; BMI, 41.7 ± 5. kg/m2).

For comparison of allele frequencies, we also included a third group of 59 unrelated lean nondiabetic subjects without a family history of diabetes (28 males and 31 females; age, 58.5 ± 12.2 yr; BMI, 23.6 ± 2.6 kg/m2). To compare allele frequencies between diabetic and control subjects, one diabetic patient from each family was randomly selected. To compare differences in personal and parental history of CVD, one subject from each family from group 1 was randomly selected. Data on a parental history of CVD was available from 210 unrelated subjects, all of whom had first degree relatives with diabetes. We wanted to test the hypothesis that the phenotypic difference between sibling pairs discordant for the FABP2 A54T polymorphism would differ significantly from zero. We advanced the hypothesis that there will be a dose-dependent effect of the number of T alleles on the phenotype by comparing the T54T and T54A genotypes with the A54A genotype, or the T54T with the T54A genotype. A total of 213 sibling pairs discordant for the polymorphism from 97 families were included. Of them, 158 sibling pairs had the same gender. Before participating in the study, the purpose, nature, and potential risks were explained, and informed written voluntary consent was obtained from each subject. The study protocol was approved by the ethics committee of Lund University.

Phenotypic characterization of the subjects

The studies were performed at 0800 h after a 12-h overnight fast. Height and weight were measured with subjects in light clothing. BMI was calculated as kilograms per m2. Waist was measured with a flexible tape midway between the lowest rib and the iliac crest and the hip circumference at the widest part of the gluteal region. The waist to hip ratio was calculated. Blood pressure was measured twice in the right arm with the subject in a supine position after a 15-min rest, and the mean was calculated. If the fasting blood glucose concentration was below 10 mmol/L, an oral glucose tolerance test (OGTT) was performed. During the OGTT, the subjects ingested 75 g glucose in a volume of 300 mL, and venous samples for measurement of blood glucose and serum insulin were drawn. For fasting glucose and insulin concentrations, the mean of the -5 and 0 min values was used. Venous fasting blood samples were drawn for the measurements of serum concentrations of FFA, total cholesterol, and triglycerides.

Questionnaire

Information on personal and family history of diabetes, stroke, and myocardial infarction was based upon a standardized, nurse-administered questionnaire. Myocardial infarction (MI) was defined as either fatal or nonfatal myocardial infarction. Stroke was defined as cerebral thrombosis or hemorrhage diagnosed in hospital or primary health care. The majority of cases (>85%) represented ischemic stroke. Hypertension was defined as systolic blood pressure of 160 mm Hg or more and/or a diastolic blood pressure of 95 mm Hg or more or use of antihypertensive drugs.

Assays

Blood glucose during the OGTT was measured with a HemoCue Blood Glucose Analyzer (HemoCue AB, Angelholm Sweden). Serum was separated and kept at -20 C until analyzed. FFA were measured by an enzymatic colorimetric method using a commercial kit (Wako Chemicals GmbH, Neuss, Germany). Insulin concentrations were measured by specific RIAs (DAKO Corp., Cambridgeshire, UK). Cholesterol and triglyceride concentrations were analyzed with commercially available kits using Technicon DAX 48 (Bayer Sverige AB, Gothenborg, Sweden).

Genotyping

The G to A nucleotide substitution in exon 2 of the FABP2 gene, which changes an alanine at codon 54 to a threonine (A54T), was genotyped using an earlier described PCR-restriction fragment length polymorphism method (4) with the following changes: exon 2 was PCR amplified from 25 ng genomic DNA in a 20-µL volume consisting of 1 x PCR buffer (Perkin-Elmer Corp., Foster City, CA), 0.25 mmol/L of each deoxy-NTP, 10 pmol of each primer, 2.5 mmol/L MgCl2, and 0.5 U Taq polymerase (Amersham Pharmacia Biotech, Sweden). PCR reactions were initiated by an initial denaturation (30 s at 94 C), followed by amplification for 30 cycles of denaturation (30 s at 94 C), annealing (30 s at 55 C), and extension (30 s at 72 C) and by a final extension step (10 min at 72 C). The amplified 180-bp product was digested with HhaI according to the manufacturer’s instructions (Amersham Pharmacia Biotech) and separated on a 3% agarose gel. The T54 allele lacking the HhaI site migrated as a 180-bp fragment, whereas the A54 allele was cleaved and appeared as 99- and 81-bp fragments. Twelve percentage of all samples was genotyped twice to exclude genotyping errors.

Statistical analysis

Frequency differences between the groups were tested by Pearson {chi}2 test using a BMDP statistical package (Biomedical Data processing version 7.0, 1992, Los Angeles, CA). Differences between the genotype discordant sibling pairs were estimated using a permutation test for paired replicates based upon a modified program (17, 18). The differences between continuous variables were computed as the value in sibling 1 with and excess of T54 alleles minus the value in sibling 2. In a permutation test for 213 sibling pairs, there are 2213 equally likely outcomes for each variable under the assumption of no difference between the pairs. Because of computational limitations, the two-tailed P values were estimated using a large (107) random sample from all possible permutations. If the observed sum of differences entered into the 5% region of rejection, the difference between the pairs was considered significant. Finally, for testing differences in diabetes prevalence, the McNemar test of symmetry for paired replicates was performed for a randomly chosen one genotype-discordant sibling pair per family. All statistical tests were two-sided, and P < 0.05 was considered statistically significant.


   Results
Top
 Abstract
 Introduction
 Subjects and Methods
 Results
Discussion
 References
 
Allele and genotype frequencies in different groups

Allele and genotype frequencies did not differ among unrelated type 2 diabetes patients (TT, 6%; TA, 40%; AA, 55%), obese subjects (TT, 8%; TA, 39%; AA, 53%), and lean controls (TT, 12%; TA, 36%; AA, 52%; P = NS), nor did the prevalence of diabetes differ between siblings discordant for the FABP2 polymorphism. None of the observed genotype frequency distributions deviated from Hardy-Weinberg equilibrium.

Sibling pair analysis

Of sibling pairs discordant for the T54A polymorphism, the sibling with more T54 alleles had higher triglyceride (P = 0.002) and higher cholesterol (P = 0.019) concentrations than the sibling with two A54 alleles (Table 1Go). When only siblings of the same gender were considered, the differences remained statistically significant (cholesterol, P = 0.053; triglyceride, P = 0.013).


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  		Table 1. Observed sum of differences between 213 sibling pairs discordant for the FABP2 codon 54 polymorphism analyzed by a permutation test

 
Personal and parental history of diabetes, MI, and stroke

There were only a few subjects with a personal history of MI and/or stroke (MI: TT, 0%; TA, 2.9%; AA, 2.9%; stroke: TT, 0%; TA, 1.4%; AA, 2.4%), and there was no difference in the prevalence of hypertension among the different genotype carriers (TT, 2.4%; TA, 13.8%; AA, 17%; P = NS). Given the low prevalence of CVD in the subjects, we related the genotype in the offspring to a parental history of MI, stroke, or diabetes (Table 2Go). There was a statistically significant association between parental history of stroke and the T54T and T54A genotypes in the offspring. Of subjects with a parental history of stroke, 67% were either heterozygous or homozygous for the T54 allele (P = 0.0071). Among the parents with stroke, 35% had diabetes. If only nondiabetic parents were included, 69% of the offspring had either the T54T or the T54A genotype (P = 0.011 vs. expected). If we include all subjects from the families (n = 683), stroke was more common among parents of homozygous T54T than among homozygous A54A carriers (P = 0.041) and was more common among heterozygous A54T carriers than among homozygous A54A carriers (P = 0.0011), suggesting that the T allele must have been transmitted from the parent with stroke.


View this table:
[in this window]
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  		Table 2. Prevalence of FABP2 genotypes by parental history of diabetes, myocardial infarction, and stroke in 210 subjects

 

   Discussion
Top
 Abstract
 Introduction
 Subjects and Methods
 Results
 Discussion
References
 
To test the hypothesis put forward in association and in vitro studies that the T54 allele of the FABP2 gene influences phenotypic expression, we used a genotype-discordant sibling pair approach. The study provided conclusive evidence for a dose-dependent effect of the number of T54 alleles on triglyceride and cholesterol concentrations. In contrast to population-based association studies, this approach can control for the genetic background of the control population. The common T54 allele appears to affect the intracellular transport and intestinal affinity for long-chain fatty acids (4, 5). Increased levels of FFA have been associated with insulin resistance (19, 20, 21, 22) and diabetes (23, 24, 25), and increased delivery of FFA to the liver stimulates very low density lipoprotein production. Although the T54 allele was associated with high triglyceride concentrations, we could not detect any significant association with FFA concentrations. This may be due to the fact that the subjects were tested in the fasting state. We also found an association between the T54 allele and high cholesterol concentrations. Cholesterol is either absorbed from the diet or synthesized by cells in the body. It is eliminated by the body through excretion as free cholesterol in the bile or is converted to bile acids and secreted into the intestine (26). The finding of elevated cholesterol concentrations in carriers of the T54 allele is in accordance with earlier reports showing that subjects with the T54 allele have reduced excretion of fecal bile acids (10). In a Finnish study, variants of the FABP2 gene were not associated with coronary heart disease (27), and we did not find an association with FABP2 T54 allele and MI; instead, we found a strong correlation to stroke in the parents. Although there are abundant data on the familial clustering of stroke (28, 29), we are not aware of any earlier study that has evaluated the risk of stroke in relation to any polymorphism in the FABP2 gene. However, a similar approach has been used to search for an association between the angiotensin converting enzyme gene and parental history of CVD (30). It is likely that the parental prevalence of stroke and MI in our study population was higher than that in the general population, because all subjects had first degree relatives with type 2 diabetes. However, the association between the FABP2 T54 allele and stroke was not restricted to the parents with diabetes. In fact, the association was seen even though parents with diabetes and stroke were excluded.

Stroke was more common among parents of homozygous T54T carriers than among parents of heterozygous A54T carriers and was more common among parents of heterozygous A54T carriers than among parents of homozygous A54A carriers, suggesting that the T allele must have been transmitted from the parent with stroke.

In conclusion, using a genotype-discordant sibling pair approach, we demonstrate an association between the number of T54 alleles of the FABP2 gene and elevated triglyceride and cholesterol concentrations. We also show that the T54 allele may influence the susceptibility to cardiovascular disease, as parents of offspring with the T54 allele reported an increased prevalence of stroke.


   Acknowledgments
 
We are indebted to the study subjects for their participation and to Ms. Ylva Wessman and Ms. M. Åberg for excellent technical assistance.


   Footnotes
 
1 This work was supported by grants from the Swedish Medical Research Council, the Sigrid Juselius Foundation, the Swedish Diabetes Research Foundation, the Juvenile Diabetes Foundation (Juvenile Diabetes Foundation-Wallenberg Grant K 98-990-12812-01A), the Albert Påhlssons Foundation, Malmo University Hospital, the Ernhold Lundström Foundation, the Diabetes Association in Malmo, the Anna-Lisa and Sven-Eric Lundgren Foundation, the Swedish Foundation for the Study of Diabetes, and an European Economic Community Paradigm BMH-4-CT95-0662 grant. Back

Received September 29, 1999.

Revised May 15, 2000.

Accepted May 15, 2000.


   References
Top
 Abstract
 Introduction
 Subjects and Methods
 Results
 Discussion
 References
 

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