Key result
Carriers of the CAV-1 rs3807992 A allele had significantly higher odds of metabolic syndrome (OR 2.31), a risk that was exacerbated by high saturated fat intake and attenuated by high polyunsaturated fat intake.
Why the study?
CAV-1 genetic variations may correlate with dietary fatty acid intake, prompting investigation into whether CAV-1 rs3807992 interacts with types of dietary fatty acids to influence metabolic syndrome risk.
Does the CAV-1 rs3807992 genetic polymorphism interact with dietary fatty acid intake to modulate metabolic syndrome risk in overweight and obese females?
Cross-Sectional (n=404)
Does the CAV-1 rs3807992 genetic polymorphism interact with dietary fatty acid intake to modulate metabolic syndrome risk in overweight and obese females?
Higher PUFA consumption may attenuate the increased risk of metabolic syndrome associated with the CAV-1 rs3807992 A allele in overweight and obese females.
Several studies have reported a significant association between the metabolic syndrome (MetS) and mortality around the world. Caveolin-1 (CAV-1) has been widely studied in dyslipidaemia, and several studies have indicated that CAV-1 genetic variations may correlate with dietary intake of fatty acids. This study aimed to investigate the interaction of CAV-1 rs3807992 with types of dietary fatty acid in the MetS risk. This cross-sectional study was carried out on 404 overweight and obese females. Dietary intake was obtained from a 147-item FFQ. The CAV-1 genotype was measured using the PCR-restriction fragment length polymorphism method. Anthropometric values and serum levels (TC, LDL, HDL, TAG and FBS) were measured by standard methods. It was observed that the (AA + AG) group had significantly higher BMI, waist circumference and DBP ( P = 0·02, P = 0·02, and P = 0·01, respectively) and lower serum LDL, HDL and TC ( P < 0·05) than the GG group. It was found that A allele carriers were at higher odds of the MetS ( P = 0·01), abdominal obesity ( P = 0·06), increased TAG concentration ( P = 0·01), elevated blood pressure (BP) ( P = 0·01), increased glucose concentration ( P = 0·45) and decreased HDL-cholesterol concentration ( P = 0·03). Moreover, the interaction of CAV-1 and SFA intake was significant in terms of the MetS ( P = 0·03), LDL ( P = 0·03) and BP ( P = 0·01). Additionally, the (AA + AG) group was significantly related to PUFA intake in terms of the MetS ( P = 0·04), TAG ( P = 0·02), glucose ( P = 0·02) and homoeostasis model assessment insulin resistance ( P = 0·01). Higher PUFA consumption might attenuate the CAV-1 rs3807992 associations with the MetS, and individuals with greater genetic predisposition appeared to have a higher risk of the MetS, associated with higher SFA consumption.
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Abaj et al. (2021) conducted a cross-sectional in Metabolic syndrome (n=404). CAV-1 rs3807992 A allele vs. CAV-1 rs3807992 GG genotype was evaluated on Metabolic syndrome (MetS) (OR 2.31, 95% CI 1.16-4.61, p=0.01). Carriers of the CAV-1 rs3807992 A allele had significantly higher odds of metabolic syndrome (OR 2.31), a risk that was exacerbated by high saturated fat intake and attenuated by high polyunsaturated fat intake.
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