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



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).



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.



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.
Department of Clinical Biochemistry, Aalborg University Hospital, Aalborg, Denmark.
L
L
Knøsgaard
Department of Hepatology and Gastroenterology, Aarhus University Hospital, Aarhus, Denmark.
K
K
Kazankov
Department of Pediatrics, Aarhus University Hospital, Aarhus, Denmark.
N H
NH
Birkebæk
Department of Pediatrics, Aarhus University Hospital, Aarhus, Denmark.
P
P
Holland-Fischer
Department of Pediatrics, Aarhus University Hospital, Aarhus, Denmark.
A
A
Lange
Department of Radiology, Aarhus University Hospital, Aarhus, Denmark.
J
J
Solvig
Department of Radiology, Aarhus University Hospital, Aarhus, Denmark.
A
A
Hørlyck
Department of Pediatrics, Aarhus University Hospital, Aarhus, Denmark.
K
K
Kristensen
Department of Pediatrics, Aarhus University Hospital, Aarhus, Denmark.
S
S
Rittig
Department of Hepatology and Gastroenterology, Aarhus University Hospital, Aarhus, Denmark.
H
H
Vilstrup
Department of Hepatology and Gastroenterology, Aarhus University Hospital, Aarhus, Denmark.
H
H
Grønbæk
Department of Clinical Biochemistry, Aalborg University Hospital, Aalborg, Denmark.|Department of Clinical Medicine, Faculty of Medicine, Aalborg University, Aalborg, Denmark.
A
0000-0001-5719-203X
A
Handberg
D000273:Adipose Tissue / Q000378:metabolism; D000293:Adolescent; D015415:Biomarkers / Q000097:blood / Q000378:metabolism; D001786:Blood Glucose / Q000378:metabolism; D015992:Body Mass Index; D018955:CD36 Antigens / Q000097:blood*; D002648:Child; D002784:Cholesterol / Q000097:blood; D050171:Dyslipidemias / Q000097:blood*; D005234:Fatty Liver / Q000097:blood*; D005260:Female; D006801:Humans; D007249:Inflammation / Q000097:blood; D007328:Insulin / Q000097:blood; D007333:Insulin Resistance; D008055:Lipids / Q000097:blood*; D008099:Liver / Q000378:metabolism; D008297:Male; D024821:Metabolic Syndrome / Q000097:blood; D063766:Pediatric Obesity / Q000097:blood / Q000150:complications / Q000628:therapy*; D014280:Triglycerides / Q000097:blood; D015431:Weight Loss / Q000502:physiology*
D015415:Biomarkers; D001786:Blood Glucose; D018955:CD36 Antigens; D007328:Insulin; D008055:Lipids; D014280:Triglycerides; D002784:Cholesterol