Metabolically healthy obesity in a paediatric obesity clinic
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Diana Teixeira
Abstract
Objectives
Metabolically healthy obese (MHO) children is a described subgroup of obese children who do not exhibit traditional cardiometabolic risk factors. The aim of this study was to determine the prevalence and characterize patients with this phenotype.
Methods
Cross-sectional study, performed in a paediatric obesity clinic (tertiary university hospital) in 2019. Children were classified with “MHO” or “metabolically unhealthy obesity” according to the criteria proposed by Damanhoury based on HDL, triglycerides, systolic and diastolic blood pressure (DBP) and fasting glucose values.
Results
241 participants were included, with ages between two and 17 years. The prevalence of the MHO phenotype was 61.8%. The body mass index (Z-score) in children aged five years or older was significantly lower in those with MHO (p=0.040). In the MHO group, mean total cholesterol levels were higher (p<0.001), due to the high value of HDL (p<0.001); triglyceride levels (p<0.001), systolic blood pressure (SBP) (p=0.036), DBP (p=0.029) and the homeostasis model assessment – insulin resistance (HOMA-IR) index (p=0.001) were significantly lower. HDL (OR=1.421; 95% CI 1.279–1.579; p<0.001) and SBP (OR=0.943; 95% CI 0.903–0.985; p=0.008) were the only independent predictors for the development of MHO.
Conclusions
Almost two-thirds of the participants had an MHO phenotype. The high and low values of HDL and SBP, respectively, were the only variables that proved to be predictors of MHO.
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Research funding: This research received no specific grant from any funding agency in the public, commercial or not-for-profit sectors.
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Author contributions: All authors have accepted responsibility for the entire content of this manuscript and approved its submission. All authors conceived the study and made substantial contributions to the design of the work. Diana Teixeira and Cátia Martins contributed towards acquisition of data. Diana Teixeira and Raquel Soares performed the analysis and interpretation of the data. Diana Teixeira e Cátia Martins drafted the manuscript. Raquel Soares and Guiomar Oliveira revised it critically for important intellectual content.
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Competing interests: Authors state no conflict of interest.
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Informed consent: Written informed consent was not required according to the decision of Ethics Committee of Centro Hospitalar e Universitário de Coimbra.
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Ethical approval: The research was conducted ethically in accordance with the World Medical Association Declaration of Helsinki. This study protocol was reviewed and approved by Ethics Committee of Centro Hospitalar e Universitário de Coimbra, approval number [094/CES of 25/02/2021].
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© 2022 Walter de Gruyter GmbH, Berlin/Boston
Articles in the same Issue
- Frontmatter
- Review Article
- Effects and dose-response relationships of exercise intervention on weight loss in overweight and obese children: a meta-regression and system review
- Original Articles
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- Metabolically healthy obesity in a paediatric obesity clinic
- Universal salt iodization potentially contributes to health equity: socio-economic status of children does not affect iodine status
- Association between clinical variations and copy number variations in cases with Turner syndrome
- The mediating function of obesity on endocrine-disrupting chemicals and insulin resistance in children
- Relationship between prolactin level and puberty in girls with early breast development
- Pattern of presentation of paediatric endocrine disorders in a Nigerian tertiary institution: an 11-year survey
- Case Reports
- Novel non-stop variant of the NR0B1 gene in two siblings with adrenal hypoplasia congenita
- Identification of two novel ACAT1 variant associated with beta-ketothiolase deficiency in a 9-month-old boy
- Craniosynostosis in a patient with Fanconi–Bickel syndrome: a case report
- Severe loss of adipose tissue in a Vietnamese lipodystrophy patient caused by LMNA p.G465D mutation: a first clinical characterization and two-year follow-up
- The response to growth hormone treatment in a child with short stature, growth hormone deficiency and autosomal dominant cutis laxa type 3 – case report
- Novel homozygous inactivating mutation in the luteinizing hormone receptor gene (LHCGR) associated with 46, XY DSD in a Moroccan family
Articles in the same Issue
- Frontmatter
- Review Article
- Effects and dose-response relationships of exercise intervention on weight loss in overweight and obese children: a meta-regression and system review
- Original Articles
- Diabetic ketoacidosis in children with new-onset type 1 diabetes mellitus: demographics, risk factors and outcome: an 11 year review in Hong Kong
- Incidence tendency, etiological classification and outcome of congenital hypothyroidism in Guangzhou, China: an 11-year retrospective population-based study
- Metabolically healthy obesity in a paediatric obesity clinic
- Universal salt iodization potentially contributes to health equity: socio-economic status of children does not affect iodine status
- Association between clinical variations and copy number variations in cases with Turner syndrome
- The mediating function of obesity on endocrine-disrupting chemicals and insulin resistance in children
- Relationship between prolactin level and puberty in girls with early breast development
- Pattern of presentation of paediatric endocrine disorders in a Nigerian tertiary institution: an 11-year survey
- Case Reports
- Novel non-stop variant of the NR0B1 gene in two siblings with adrenal hypoplasia congenita
- Identification of two novel ACAT1 variant associated with beta-ketothiolase deficiency in a 9-month-old boy
- Craniosynostosis in a patient with Fanconi–Bickel syndrome: a case report
- Severe loss of adipose tissue in a Vietnamese lipodystrophy patient caused by LMNA p.G465D mutation: a first clinical characterization and two-year follow-up
- The response to growth hormone treatment in a child with short stature, growth hormone deficiency and autosomal dominant cutis laxa type 3 – case report
- Novel homozygous inactivating mutation in the luteinizing hormone receptor gene (LHCGR) associated with 46, XY DSD in a Moroccan family
