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. 2022 Dec 6;14(23):5191.
doi: 10.3390/nu14235191.

Longitudinal Association of Telomere Dynamics with Obesity and Metabolic Disorders in Young Children

Simon Toupance  1 , Sofia I Karampatsou  2 , Carlos Labat  1 , Sofia-Maria Genitsaridi  2 , Athanasia Tragomalou  2 , Penio Kassari  2 , George Soulis  3 , Allyson Hollander  1 , Evangelia Charmandari  2   4 , Athanase Benetos  1   5
Affiliations

Longitudinal Association of Telomere Dynamics with Obesity and Metabolic Disorders in Young Children

Simon Toupance et al. Nutrients. .

Abstract

In adults, short leukocyte telomere length (LTL) is associated with metabolic disorders, such as obesity and diabetes mellitus type 2. These associations could stem from early life interactions between LTL and metabolic disorders. To test this hypothesis, we explored the associations between LTL and metabolic parameters as well as their evolution over time in children with or without obesity at baseline. Seventy-three (n = 73) children attending our Outpatient Clinic for the Prevention and Management of Overweight and Obesity in Childhood and Adolescence, aged 2-10 years (mean ± SD: 7.6 ± 2.0 years), were followed for 2 to 4 years. Anthropometric, clinical, and biological (including LTL by Southern blot) measurements were performed annually. Baseline LTL correlated negatively with BMI (p = 0.02), fat percentage (p = 0.01), and blood glucose (p = 0.0007). These associations persisted after adjustments for age and sex. No associations were found between LTL attrition during the follow-up period and any of the metabolic parameters. In young children, obesity and metabolic disturbances were associated with shorter telomeres but were not associated with more pronounced LTL attrition. These results suggest that short telomeres contribute to the development of obesity and metabolic disorders very early in life, which can have a major impact on health.

Keywords: childhood; children; determinants; metabolic disorders; obesity; telomeres.

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Conflict of interest statement

The authors declare no conflict of interest. The funders had no role in the design of the study; in the collection, analyses, or interpretation of data; in the writing of the manuscript; or in the decision to publish the results.

Figures

Figure 1
Figure 1
BMI profiles according to BMI categories at the initial visit and their evolution over the follow-up period. Values are expressed as means ± SEM; BMIc = body mass index category.
Figure 2
Figure 2
Baseline LTL (a) and LTL attrition (b) in the three BMI profiles.LTL values were age- and sex-adjusted, and LTL attrition values were age-, sex-, and initial LTL-adjusted. Values are expressed as means ± SEM, and p is derived from ANOVA. Tukey–Kramer post hoc test was used for two-by-two comparisons. LTL = leukocyte telomere length; kb = kilobase; BMI = body mass index; bp = base pair.
Figure 3
Figure 3
Relationships between baseline LTL and BMI (a), waist/hip (b), and fat percentage (c) scores. R2 and p are from Pearson’s correlation. LTL = leukocyte telomere length; kb = kilobase; BMI = body mass index.
Figure 4
Figure 4
Relationships between baseline LTL and glucose (a), insulin (b), and Hb1Ac (c) scores. R2 and p are from Pearson’s correlation. LTL = leukocyte telomere length; kb = kilobase.
See this image and copyright information in PMC

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