Cardiovascular disease is the leading cause of death among African Americans (AA). Reduced parasympathetic tone as measured by high frequency heart rate variability (HF
RRI
) predicts cardiovascular mortality. HF
RRI
is reduced after a high fat meal through caveolar sequestration of muscarinic M2 receptors. The fatty acid translocase CD36 is a protein abundant in the myocardium and important for heart function and lipid metabolism. CD36 plasma membrane localization and function in fatty acid uptake is modulated by its interaction with caveolin. One in four AAs are G-allele carriers for CD36 SNP rs3211938 resulting in ~50% decreased CD36 expression. CD36 deficiency also reduces fat taste perception, which might lead to higher fat intake to reach taste saturation. We tested the hypothesis that obese AAs with partial CD36 deficiency have altered parasympathetic tone during fasting and after a high-fat meal. We recruited 13 G-allele carriers and 39 non-carriers. Subjects were matched by age (P=0.820), BMI (P=0.751), and blood pressure (P=0.701). There was a trend towards reduction in heart rate in carriers (P=0.07). Baseline HF
RRI
was elevated in G carriers (557.1 [251 to 942] vs. 224 [95 to 655] ms
2
, P=0.046). Eleven subjects received a high-fat meal (700 Cal/m
2
BSA, 80% fat). HF
RRI
was measured at baseline and 30, 60, 120, 240 minutes after meal. Non-carriers (n=4) showed a time-dependent decline in the percent change in HF
RRI
(-23, -32, -70, -84, respectively). In G-allele carriers (N=6), the decline in HF
RRI
(21, -11, -61, -70 min) was attenuated.
Conclusion:
AAs with partial CD36 deficiency have enhanced fasting parasympathetic tone and a blunted response to a high fat meal.
Central and peripheral arterial stiffness responses to uninterrupted prolonged sitting combined with a high-fat meal: a randomized controlled crossover trial