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Author Notes:

Correspondence: dehoff@cop.ufl.edu

The research outlined in this manuscript stems from human subjects research. As indicated, the research protocol was approved by the Institutional Review Board at all of the enrolling sites, and all patients provided written, voluntary informed consent prior to participation in any research procedures.

The authors declare that they have no conflict of interest.


Research Funding:

This study was funded by grants from the NIH (NIGMS U01 GM074492, NIDDK U24 DK097209, and NCAT under the Award Number UL1 TR000064 (University of Florida), UL1 TR000454 (Emory University) and UL1 TR000135 (Mayo Clinic)).


  • Acylcarnitine
  • Arachidonoyl-carnitine
  • C20:4
  • Atenolol
  • Hypertension
  • Pharmacometabolomics
  • Cardiometabolic syndrome

Presence of arachidonoyl-carnitine is associated with adverse cardiometabolic responses in hypertensive patients treated with atenolol

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Journal Title:



Volume 12, Number 10


, Pages 160-160

Type of Work:

Article | Post-print: After Peer Review


Introduction: Atenolol, a commonly prescribed β blocker for hypertension, is also associated with adverse cardiometabolic effects such as hyperglycemia and dyslipidemia. Knowledge of the mechanistic underpinnings of these adverse effects of atenolol is incomplete. Objective: We sought to identify biomarkers associated with risk for these untoward effects of atenolol. We measured baseline blood serum levels of acylcarnitines (ACs) that are involved in a host of different metabolic pathways, to establish associations with adverse cardiometabolic responses after atenolol treatment. Methods: Serum samples from Caucasian hypertensive patients (n = 224) who were treated with atenolol in the Pharmacogenomic Evaluation of Antihypertensive Responses (PEAR) study were interrogated using a quantitative LC/MS assay for a large number of unique ACs in serum. For the 23 ACs that were detected in serum from ≥80 % of all patients, we conducted linear regression for changes in cardiometabolic factors with baseline AC levels, baseline cardiometabolic factors, age, sex, and BMI as covariates. For the 5 ACs that were detected in serum from 20 to 79 % of the patients, we similarly modeled changes in cardiometabolic factors, but with specifying the AC as present/absent in the regression. Results: Among the 28 ACs, the presence (vs. absence) of arachidonoyl-carnitine (C20:4) was significantly associated with increased glucose (p = 0.0002), and was nominally associated with decreased plasma HDL-C (p = 0.017) and with less blood pressure (BP) lowering (p = 0.006 for systolic BP, p = 0.002 for diastolic BP), after adjustment. Conclusion: Serum level of C20:4 is a promising biomarker to predict adverse cardiometabolic responses including glucose and poor antihypertensive response to atenolol.

Copyright information:

© 2016, Springer Science+Business Media New York.

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