Adipose Tissue Mediates Associations of Birth Weight with Glucose Metabolism Disorders in Children.


Journal

Obesity (Silver Spring, Md.)
ISSN: 1930-739X
Titre abrégé: Obesity (Silver Spring)
Pays: United States
ID NLM: 101264860

Informations de publication

Date de publication:
05 2019
Historique:
received: 04 10 2018
accepted: 24 12 2018
pubmed: 28 2 2019
medline: 12 3 2020
entrez: 28 2 2019
Statut: ppublish

Résumé

This study aimed to examine the associations between low birth weight (LBW) versus high birth weight (HBW) and dysglycemia, including insulin resistance (IR) and impaired fasting glucose (IFG) in children, and aimed to explore the role of adipose tissue in these relationships. A total of 2,935 subjects aged 6 to 18 years were recruited to examine the relationship between birth weight and IR (defined as homeostasis model assessment of IR > 2.3) and IFG. Mediation analyses were conducted to examine the roles of various adipokines and anthropometrics in these relationships. Children with LBW had a nearly twofold increased risk of IR and IFG compared with children with normal birth weight, even after adjusting for BMI. Decreased circulating adiponectin levels contributed to 21.2% of the LBW-IR relationship, whereas none of the selected adipose markers mediated the LBW-IFG relationship. In contrast, after controlling for current BMI or waist circumference, HBW reduced the risk of IR by 34%, but it was not associated with IFG. The HBW-IR relationship was significantly mediated by reduced leptin levels (21.4%) and fat mass percentage (8.8%), after controlling for BMI. These findings suggest the potential role of adipose tissue dysfunction as an underlying mechanism for the birth weight-type 2 diabetes relationship.

Identifiants

pubmed: 30811103
doi: 10.1002/oby.22421
doi:

Substances chimiques

Blood Glucose 0

Banques de données

ClinicalTrials.gov
['NCT03421444']

Types de publication

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

Langues

eng

Sous-ensembles de citation

IM

Pagination

746-755

Informations de copyright

© 2019 The Obesity Society.

Auteurs

Yunpeng Wu (Y)

Department of Endocrinology, NHC Key Laboratory of Endocrinology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.

Xinting Yu (X)

Department of Endocrinology, NHC Key Laboratory of Endocrinology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.
Department of Nutrition, Harvard T. H. Chan School of Public Health, Harvard University, Boston, Massachusetts, USA.

Yu Li (Y)

Department of Endocrinology, NHC Key Laboratory of Endocrinology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.

Ge Li (G)

Department of Endocrinology, NHC Key Laboratory of Endocrinology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.

Hong Cheng (H)

Department of Epidemiology, Capital Institute of Pediatrics, Beijing, China.

Xinghua Xiao (X)

Department of Endocrinology, NHC Key Laboratory of Endocrinology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.

Jie Mi (J)

Department of Epidemiology, Capital Institute of Pediatrics, Beijing, China.

Shan Gao (S)

Department of Endocrinology, Beijing Chaoyang Hospital, Capital Medical University, Beijing, China.

Steven M Willi (SM)

Division of Endocrinology, The Children's Hospital of Philadelphia, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA.

Ming Li (M)

Department of Endocrinology, NHC Key Laboratory of Endocrinology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.

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