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Diabetes. 2015 Apr;64(4):1249-61. doi: 10.2337/db14-0744. Epub 2014 Nov 12.

Evidence of early alterations in adipose tissue biology and function and its association with obesity-related inflammation and insulin resistance in children.

Author information

1
Center for Pediatric Research Leipzig, Hospital for Children and Adolescents, University of Leipzig, Leipzig, Germany Integrated Research and Treatment Center IFB Adiposity Diseases, University of Leipzig, Leipzig, Germany.
2
Center for Pediatric Research Leipzig, Hospital for Children and Adolescents, University of Leipzig, Leipzig, Germany.
3
Department of Pediatric Surgery, University of Leipzig, Leipzig, Germany.
4
Department of Orthopedic Surgery, University of Leipzig, Leipzig, Germany.
5
Integrated Research and Treatment Center IFB Adiposity Diseases, University of Leipzig, Leipzig, Germany Department of Pediatric and Adolescent Surgery, Medical University of Graz, Graz, Austria.
6
Institute of Laboratory Medicine, Clinical Chemistry and Molecular Diagnostics, University of Leipzig, Leipzig, Germany.
7
Integrated Research and Treatment Center IFB Adiposity Diseases, University of Leipzig, Leipzig, Germany Department of Medicine, Division of Endocrinology, University of Leipzig, Leipzig, Germany.
8
Center for Pediatric Research Leipzig, Hospital for Children and Adolescents, University of Leipzig, Leipzig, Germany Integrated Research and Treatment Center IFB Adiposity Diseases, University of Leipzig, Leipzig, Germany antje.koerner@medizin.uni-leipzig.de.

Abstract

Accumulation of fat mass in obesity may result from hypertrophy and/or hyperplasia and is frequently associated with adipose tissue (AT) dysfunction in adults. Here we assessed early alterations in AT biology and function by comprehensive experimental and clinical characterization of 171 AT samples from lean and obese children aged 0 to 18 years. We show an increase in adipocyte size and number in obese compared with lean children beginning in early childhood. These alterations in AT composition in obese children were accompanied by decreased basal lipolytic activity and significantly enhanced stromal vascular cell proliferation in vitro, potentially underlying the hypertrophy and hyperplasia seen in obese children, respectively. Furthermore, macrophage infiltration, including the formation of crown-like structures, was increased in AT of obese children from 6 years on and was associated with higher hs-CRP serum levels. Clinically, adipocyte hypertrophy was not only associated with leptin serum levels but was highly and independently correlated with HOMA-IR as a marker of insulin resistance in children. In summary, we show that adipocyte hypertrophy is linked to increased inflammation in AT in obese children, thereby providing evidence that obesity-associated AT dysfunction develops in early childhood and is related to insulin resistance.

PMID:
25392242
DOI:
10.2337/db14-0744
[Indexed for MEDLINE]
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