Key result
Circulating betatrophin levels did not differ significantly between obese and lean children (1.99 vs 2.35 ng/mL; P=0.155) and were not associated with weight status or glucose tolerance.
Why the study?
Does weight status or a 1-year lifestyle intervention affect circulating betatrophin levels in children?
Observational (n=89)
Does weight status or a 1-year lifestyle intervention affect circulating betatrophin levels in children?
Absolute Event Rate: 1.99% vs 2.35%
p-value: p=.155
Betatrophin levels are not associated with weight status, glucose tolerance, or insulin resistance in children, suggesting it is not a useful biomarker for these metabolic conditions in this population.
Betatrophin is not a useful biomarker for weight status or glucose tolerance in children; leaves open its response to interventions.
OBJECTIVE: The influences of obesity, glucose metabolism, gender, and puberty on betatrophin levels and the longitudinal relationships between weight loss, metabolic changes and betatrophin have not yet been studied in childhood. METHODS: Cross-sectional and longitudinal analysis of weight status (standard deviation score-body mass index (SDS-BMI)), homeostasis model assessment insulin resistance (HOMA-IR), gender, and pubertal stage were evaluated in 69 obese children (51% female, age 11.9 ± 2.0 years) participating in lifestyle intervention over a 1-year period. An oral glucose tolerance test was performed in 53 of the 69 children. Twenty normal weight children (50% female, age 12.3 ± 3.0 years) served as controls. RESULTS: Circulating betatrophin did not differ significantly between obese and lean children (1.99 ± 0.90 vs 2.35 ± 0.28, mean ± SD, P = .155). At baseline, betatrophin did not differ in obese patients with vs without glucose intolerance (1.89 ± 0.96 vs 2.031 ± 0.91 ng/mL; P = .591) and obese with (delta SDS-BMI >0.4) vs without successful obesity intervention (1.89 ± 0.94 vs. 2.07 ± 0.87 ng/mL; P = 0.396). In multiple linear regression analyses, pubertal stage was associated with betatrophin (b: 0.48, P = .027), while gender, age, BMI, blood pressure, fasting glucose, HOMA-IR, triglycerides, LDL- and HDL-cholesterol were not related to betatrophin at baseline. At the end of the 1-year intervention, changes of betatrophin were not significantly associated with any parameter after controlling for multiple covariates including age and changes of pubertal stages. CONCLUSIONS: Our data do not support a relationship between betatrophin and weight status or glucose tolerance, insulin resistance, and lipid metabolism in children.
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Roth et al. (2016) conducted an observational in Obesity (n=89). Obesity vs. Normal weight was evaluated on Circulating betatrophin levels (p=.155). Circulating betatrophin levels did not differ significantly between obese and lean children (1.99 vs 2.35 ng/mL; P=0.155) and were not associated with weight status or glucose tolerance.
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