Omega-3 Red Blood Cell Content Is Associated with Fat Mass Index and Leptin in Subjects with Obesity and Heart Failure with Preserved Ejection Fraction (P21-001-19).
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ABSTRACT: AbstractObjectivesOverweight and obesity affect 80% of patients with heart failure and preserved ejection fraction (HFpEF). Exercise intolerance is a cardinal manifestation of HFpEF and is associated with excess fat mass (FM). Dietary polyunsaturated fatty acids (PUFA) have been associated with lower FM. However, the relationship between Omega-3 (N-3) PUFA and FM in HFpEF remains unclear. Red blood cell membrane (RBC) N-3 and omega-6 (N-6) PUFA content may serve as better objective measures of intake than subject-reported data. We hypothesized that increased RBC omega-3 (N-3) content is associated with lower FM and leptin in subjects with obesity and HFpEF.MethodsTwenty-four consecutive subjects with HFpEF underwent body composition measurement with bioelectrical impedance analysis to obtain FM Index (FMI; kg/m) and venipuncture to obtain RBC total percentage of N-3 PUFA content (RBC N-3%) as well as the ratio of N-6 to N-3 PUFA (N-6/N-3 ratio).ResultsFourteen subjects were female (58%) with a median age of 53 (interquartile range [IQR] 48–63). Median BMI was 42.4 kg/m (38.1–47.4) and FMI was 18.7 kg/m (14.2–22.7). Median leptin was 82.5 ng/mL (63.5–116.5), RBC N-3% was 7.4% (6.6–8.9), and N-6/N-3 ratio was 5.00 (4.03–5.70). RBC N-3% was inversely associated with FMI ( = ?0.406, = 0.049), while N-6/N-3 ratio was positively associated with FMI ( = +0.472, = 0.020) (). N-6/N-3 ratio was also associated with leptin ( = +0.462, = 0.023), while RBC N-3% presented an inverse trend with leptin ( = ?0.388, = 0.061) ().ConclusionsHigher percentage of N-3 PUFA in RBC membranes is associated with lower FMI and leptin in subjects with obesity and HFpEF. These findings suggest that increasing dietary N-3 intake and reducing N-6/N-3 ratio may protect against adiposity in HFpEF.Funding SourcesThis cross-sectional analysis was performed from baseline data of the DHART2 clinical trial (NCT02173548) and was funded by the NIH (1R34HL11348-01A1).Supporting Tables, Images and/or Graphs
SUBMITTER: Billingsley H
PROVIDER: S-EPMC6578465 | biostudies-literature | 2019 Jun
REPOSITORIES: biostudies-literature
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