Affiliation:
1. Oxford Centre for Diabetes, Endocrinology and Metabolism, Radcliffe Department of Medicine University of Oxford Oxford UK
2. Section on Clinical Genomics and Experimental Therapeutics National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health Bethesda Maryland USA
3. Department of Internal Medicine, Section of Gerontology and Geriatrics Leiden University Medical Center Leiden the Netherlands
4. National Institute for Health Research, Oxford Biomedical Research Centre Oxford University Hospitals National Health Service Foundation Trust Oxford UK
Abstract
AbstractObjectiveObservational studies have reported bidirectional associations between metabolic syndrome (MetS) traits and short leukocyte telomere length (LTL), a TL marker in somatic tissues and a proposed risk factor for age‐related degenerative diseases. However, in Mendelian randomization studies, longer LTL has been paradoxically associated with higher MetS risk. This study investigated the hypothesis that shorter LTL might be a consequence of metabolic dysfunction.MethodsThis study undertook univariable and multivariable Mendelian randomization. As instrumental variables for MetS traits, all of the genome‐wide significant independent signals identified in genome‐wide association studies for anthropometric, glycemic, lipid, and blood pressure traits conducted in European individuals were used. Summary‐level data for LTL were obtained from a genome‐wide association study conducted in the UK Biobank.ResultsHigher BMI was associated with shorter LTL (β = −0.039, 95% CI: −0.058 to −0.020, p = 5 × 10−5) equivalent to 1.70 years of age‐related LTL change. In contrast, higher low‐density lipoprotein cholesterol was associated with longer LTL (β = 0.022, 95% CI: 0.007 to 0.037, p = 0.003) equivalent to 0.96 years of age‐related LTL change. Mechanistically, increased low‐grade systemic inflammation, as measured by circulating C‐reactive protein, and lower circulating linoleic acid levels might link higher BMI to shorter LTL.ConclusionsOverweight and obesity might promote the development of aging‐related degenerative diseases by accelerating telomere shortening.
Subject
Nutrition and Dietetics,Endocrinology,Endocrinology, Diabetes and Metabolism,Medicine (miscellaneous)
Cited by
1 articles.
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