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Research Paper|Volume 6, Issue 3|pp 176—186

Metabolic profiles of biological aging in American Indians: The strong heart family study

Jinying Zhao1, Yun Zhu1, Karan Uppal2, ViLinh T. Tran2, Tianwei Yu3, Jue Lin4, Tet Matsuguchi4, Elizabeth Blackburn4, Dean Jones2, Elisa T. Lee5, Barbara V. Howard6
  • 1Department of Epidemiology, Tulane University School of Public Health, New Orleans, LA 70112; USA
  • 2Division of Pulmonary, Emory University School of Medicine, Atlanta, GA 30322; USA
  • 3Department of Biostatistics and Bioinformatics, Emory University School of Public Health, Atlanta, GA 30322; USA
  • 4Department of Biochemistry and Biophysics, University of California, San Francisco, CA 94143, USA
  • 5Center for American Indian Health Research, University of Oklahoma Health Sciences Center, Oklahoma City, OK 73104; USA
  • 6Medstar Research Institute and Georgetown and Howard Universities Centers for Translational Sciences, Washington, DC 20007
Received: January 3, 2014Accepted: March 18, 2014Published: March 20, 2014
https://doi.org/10.18632/aging.100644

Copyright: © 2014 Zhao et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

Short telomere length, a marker of biological aging, has been associated with age-related metabolic disorders. Telomere attrition induces profound metabolic dysfunction in animal models, but no study has examined the metabolome of telomeric aging in human. Here we studied 423 apparently healthy American Indians participating in the Strong Family Heart Study. Leukocyte telomere length (LTL) was measured by qPCR. Metabolites in fasting plasma were detected by untargeted LC/MS. Associations of LTL with each metabolite and their combined effects were examined using generalized estimating equation adjusting for chronological age and other aging-related factors. Multiple testing was corrected using the q-value method (q<0.05). Of the 1,364 distinct m/z features detected, nineteen metabolites in the classes of glycerophosphoethanolamines, glycerophosphocholines, glycerolipids, bile acids, isoprenoids, fatty amides, or L-carnitine ester were significantly associated with LTL, independent of chronological age and other aging-related factors. Participants with longer (top tertile) and shorter (bottom tertile) LTL were clearly separated into distinct groups using a multi-marker score comprising of all these metabolites, suggesting that these newly detected metabolites could be novel metabolic markers of biological aging. This is the first study to interrogate the human metabolome of telomeric aging. Our results provide initial evidence for a metabolic control of LTL and may reveal previously undescribed new roles of various lipids in the aging process.