Key result
The FABP2 A54T mutation was associated with significantly increased HDL-TG levels in the fasting state (p=0.04) and 4 hours after a test meal (p=0.0008) in viscerally obese men.
Why the study?
Does the FABP2 A54T mutation alter triglyceride metabolism and postprandial lipid response in viscerally obese men?
Observational (n=217)
Does the FABP2 A54T mutation alter triglyceride metabolism and postprandial lipid response in viscerally obese men?
The FABP2 A54T missense mutation is associated with increased postprandial HDL-triglyceride levels in viscerally obese men, potentially contributing to an altered risk of atherosclerotic vascular disease.
Answers are grounded in this paper and cite their sources.
Supports hypothesis of FABP2 effects on HDL-TG in visceral obesity; leaves open relevance for atherosclerotic risk.
OBJECTIVE: Viscerally obese individuals are frequently characterized by a proatherogenic condition. A missense mutation (A54T) in the fatty acid binding protein type 2 (FABP2) gene has been associated with insulin resistance and obesity. This study examined the effect of this mutation on lipoprotein levels in viscerally obese hyperinsulinemic condition. RESEARCH METHODS AND PROCEDURES: A total of 217 men were assigned to one of two groups based on their FABP2 A54T polymorphism. RESULTS: The two genotypic groups showed no difference in either physiological characteristics or lipoprotein/lipid profile, before or after statistical adjustment for age. From this initial sample, 50 men accepted to have their postprandial lipid response assessed and 10 T54/A54 heterozygotes were then individually matched for visceral adipose tissue accumulation and fasting plasma triglyceride (TG) levels with 10 A54/A54 homozygotes. High-density lipoprotein (HDL)-TG levels were significantly increased in the fasting state as well as 4 hours after the test meal (p = 0.04 and p = 0.0008, respectively) in men bearing the A54T mutation. In addition, the area under the curve of postprandial HDL-TG levels was also significantly higher among T54/A54 heterozygotes than among A54/A54 homozygotes (p = 0.04). Interestingly, fasting TG concentrations in large TG-rich lipoproteins (large-TRL; S(f) > 400) were correlated with HDL-TG levels at 4 (r = 0.74, p = 0.01) and 8 hours (r = 0.73, p = 0.01) after the test meal in T54/A54 heterozygotes only. DISCUSSION: The FABP2 A54T missense mutation may contribute to the TG enrichment of HDL in the postprandial state that, in turn, may alter the risk of atherosclerotic vascular disease.
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Berthier et al. (2001) conducted an observational in Visceral obesity (n=217). FABP2 A54T mutation vs. A54/A54 homozygotes was evaluated on HDL-TG levels in the fasting state and 4 hours after the test meal (p=0.04 and 0.0008). The FABP2 A54T mutation was associated with significantly increased HDL-TG levels in the fasting state (p=0.04) and 4 hours after a test meal (p=0.0008) in viscerally obese men.
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