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Nutrigenomics and molecular nutrition

Reduced sCD36 following weight loss corresponds to improved insulin sensitivity, dyslipidemia and liver fat in obese children

European Journal of Clinical Nutrition volume 70, pages 1073–1077 (2016)Cite this article

Subjects

Abstract

Background/Objectives:

Childhood obesity is a major health problem with serious long-term metabolic consequences. CD36 is important for the development of obesity-related complications among adults. We aimed to investigate circulating sCD36 during weight loss in childhood obesity and its associations with insulin resistance, dyslipidemia, hepatic fat accumulation and low-grade inflammation.

Subjects/Methods:

The impact of a 10-week weight loss camp for obese children (N=113) on plasma sCD36 and further after a 12-month follow-up (N=68) was investigated. Clinical and biochemical data were collected, and sCD36 was measured by an in-house assay. Liver fat was estimated by ultrasonography and insulin resistance by the homeostasis model assessment (HOMA-IR).

Results:

Along with marked weight loss, sCD36 was reduced by 21% (P=0.0013) following lifestyle intervention, and individual sCD36 reductions were significantly associated with the corresponding decreases in HOMA-IR, triglycerides and total cholesterol. The largest sCD36 decrease occurred among children who reduced HOMA-IR and liver fat. After 12 months of follow-up, sCD36 was increased (P=0.014) and the metabolic improvements were largely lost.

Conclusions:

Weight-loss-induced sCD36 reduction, coincident with improved insulin resistance, circulating lipids and hepatic fat accumulation, proposes that sCD36 may be an early marker of long-term health risk associated with obesity-related complications.

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Acknowledgements

We thank Jane Hansen, Aarhus University Hospital, Skejby, Denmark, for the collection and processing of blood samples; Lone Larsen, Clinical Institute, Aarhus University Hospital, Denmark, for skillful laboratory assistance; Morten H Nielsen, Department of Clinical Biochemistry, Aalborg University Hospital, for assistance in preparation of figures, as well as the staff of Julemærkehjemmet, Hobro, Denmark, for their collaboration during the study. The NOVO Nordisk Foundation supported the study.

Author information

Authors and Affiliations

  1. Department of Clinical Biochemistry, Aalborg University Hospital, Aalborg, Denmark

    L Knøsgaard & A Handberg

  2. Department of Hepatology and Gastroenterology, Aarhus University Hospital, Aarhus, Denmark

    K Kazankov, H Vilstrup & H Grønbæk

  3. Department of Pediatrics, Aarhus University Hospital, Aarhus, Denmark

    N H Birkebæk, P Holland-Fischer, A Lange, K Kristensen & S Rittig

  4. Department of Radiology, Aarhus University Hospital, Aarhus, Denmark

    J Solvig & A Hørlyck

  5. Department of Clinical Medicine, Faculty of Medicine, Aalborg University, Aalborg, Denmark

    A Handberg

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  1. L Knøsgaard
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Correspondence to A Handberg.

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Competing interests

A Handberg is the inventor of two patent applications on sCD36 as a biomarker of the metabolic syndrome. The Ideas Clinic of Aalborg University Hospital owns the patent IP rights.

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Knøsgaard, L., Kazankov, K., Birkebæk, N. et al. Reduced sCD36 following weight loss corresponds to improved insulin sensitivity, dyslipidemia and liver fat in obese children. Eur J Clin Nutr 70, 1073–1077 (2016). https://doi.org/10.1038/ejcn.2016.88

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