Association of BMAL1 clock gene polymorphisms with fasting glucose in children.


Journal

Pediatric research
ISSN: 1530-0447
Titre abrégé: Pediatr Res
Pays: United States
ID NLM: 0100714

Informations de publication

Date de publication:
08 2023
Historique:
received: 11 07 2022
accepted: 18 12 2022
revised: 02 11 2022
medline: 31 7 2023
pubmed: 3 2 2023
entrez: 2 2 2023
Statut: ppublish

Résumé

The brain and muscle Arnt-like protein-1 (BMAL1) gene is an important circadian clock gene and previous studies have found that certain polymorphisms are associated with type 2 diabetes in adults. However, it remains unknown if such polymorphisms can affect fasting glucose in children and if other factors modify the associations. A school-based cross-sectional study with 947 Chinese children was conducted. A multivariable linear regression model was used to analyze the association between BMAL1 gene polymorphisms and fasting glucose level. After adjusting for age, sex, body mass index (BMI), physical activity, and unhealthy diet, GG genotype carriers of BMAL1 rs3789327 had higher fasting glucose than AA/GA genotype carriers (b = 0.101, SE = 0.050, P = 0.045). Adjusting for the same confounders, rs3816358 was shown to be significantly associated with fasting glucose (b = 0.060, SE = 0.028, P = 0.032). Furthermore, a significant interaction between rs3789327 and nutritional status on fasting glucose was identified (P BMAL1 polymorphisms were significantly associated with the fasting glucose level in children. Additionally, the observed interaction between nutritional status and BMAL1 supports promoting an optimal BMI in children genetically predisposed to higher glucose level. Polymorphisms in the essential circadian clock gene BMAL1 were associated with fasting blood glucose levels in children. Additionally, there was a significant interaction between nutritional status and BMAL1 affecting fasting glucose levels. BMAL1 rs3789327 was associated with fasting glucose only in overweight/obese children. This finding could bring novel insights into mechanisms by which nutritional status influences fasting glucose in children.

Sections du résumé

BACKGROUND
The brain and muscle Arnt-like protein-1 (BMAL1) gene is an important circadian clock gene and previous studies have found that certain polymorphisms are associated with type 2 diabetes in adults. However, it remains unknown if such polymorphisms can affect fasting glucose in children and if other factors modify the associations.
METHODS
A school-based cross-sectional study with 947 Chinese children was conducted. A multivariable linear regression model was used to analyze the association between BMAL1 gene polymorphisms and fasting glucose level.
RESULTS
After adjusting for age, sex, body mass index (BMI), physical activity, and unhealthy diet, GG genotype carriers of BMAL1 rs3789327 had higher fasting glucose than AA/GA genotype carriers (b = 0.101, SE = 0.050, P = 0.045). Adjusting for the same confounders, rs3816358 was shown to be significantly associated with fasting glucose (b = 0.060, SE = 0.028, P = 0.032). Furthermore, a significant interaction between rs3789327 and nutritional status on fasting glucose was identified (P
CONCLUSIONS
BMAL1 polymorphisms were significantly associated with the fasting glucose level in children. Additionally, the observed interaction between nutritional status and BMAL1 supports promoting an optimal BMI in children genetically predisposed to higher glucose level.
IMPACT
Polymorphisms in the essential circadian clock gene BMAL1 were associated with fasting blood glucose levels in children. Additionally, there was a significant interaction between nutritional status and BMAL1 affecting fasting glucose levels. BMAL1 rs3789327 was associated with fasting glucose only in overweight/obese children. This finding could bring novel insights into mechanisms by which nutritional status influences fasting glucose in children.

Identifiants

pubmed: 36732647
doi: 10.1038/s41390-023-02467-8
pii: 10.1038/s41390-023-02467-8
pmc: PMC10382306
doi:

Substances chimiques

ARNTL Transcription Factors 0
Glucose IY9XDZ35W2
BMAL1 protein, human 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

653-659

Informations de copyright

© 2023. The Author(s).

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Auteurs

Yi-De Yang (YD)

Department of Child and Adolescent Health, School of Medicine, Hunan Normal University, 410006, Changsha, China.
Key Laboratory of Molecular Epidemiology of Hunan Province, School of Medicine, Hunan Normal University, 410081, Changsha, China.

Yuan Zeng (Y)

Department of Child and Adolescent Health, School of Medicine, Hunan Normal University, 410006, Changsha, China.
Key Laboratory of Molecular Epidemiology of Hunan Province, School of Medicine, Hunan Normal University, 410081, Changsha, China.

Jian Li (J)

Key Laboratory of Study and Discovery of Small Targeted Molecules of Hunan Province, School of Medicine, Hunan Normal University, 410013, Changsha, China.

Jun-Hua Zhou (JH)

Key Laboratory of Molecular Epidemiology of Hunan Province, School of Medicine, Hunan Normal University, 410081, Changsha, China.

Quan-Yuan He (QY)

Key Laboratory of Molecular Epidemiology of Hunan Province, School of Medicine, Hunan Normal University, 410081, Changsha, China.

Chan-Juan Zheng (CJ)

Department of Child and Adolescent Health, School of Medicine, Hunan Normal University, 410006, Changsha, China.
Key Laboratory of Molecular Epidemiology of Hunan Province, School of Medicine, Hunan Normal University, 410081, Changsha, China.

Christoph Reichetzeder (C)

Institute of Nutritional Science, University of Potsdam, Potsdam, Germany.
HMU - Health and Medical University, Potsdam, Germany.

Bernhard K Krämer (BK)

Fifth Department of Medicine (Nephrology/Endocrinology/Rheumatology), University Medical Centre Mannheim, University of Heidelberg, Mannheim, Germany.

Berthold Hocher (B)

Key Laboratory of Study and Discovery of Small Targeted Molecules of Hunan Province, School of Medicine, Hunan Normal University, 410013, Changsha, China. berthold.hocher@medma.uni-heidelberg.de.
Fifth Department of Medicine (Nephrology/Endocrinology/Rheumatology), University Medical Centre Mannheim, University of Heidelberg, Mannheim, Germany. berthold.hocher@medma.uni-heidelberg.de.
Reproductive and Genetic Hospital of CITIC-Xiangya, Changsha, China. berthold.hocher@medma.uni-heidelberg.de.
Institute of Medical Diagnostics, IMD Berlin, Berlin, Germany. berthold.hocher@medma.uni-heidelberg.de.

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