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Serum Asprosin Concentrations in Children with Prader-Willi Syndrome: Correlations with Metabolic Parameters
Maha Alsaif1, Catherine J Field1, Eloisa Colin-Ramirez2,3
1Department of Agricultural, Food and Nutritional Science, University of Alberta, Edmonton, AB T6G 2R7, Canada.
Insights
Asprosin levels did not differ in children with Prader-Willi syndrome (PWS) compared to controls. However, fasting asprosin correlated with glucose in obese children, suggesting a potential predictor for metabolic changes.
Area of Science:
- Endocrinology
- Pediatric Obesity
- Metabolic Syndrome
Background:
- Prader-Willi syndrome (PWS) is associated with severe obesity.
- Asprosin, a protein hormone from white adipose tissue, is linked to insulin resistance.
Purpose of the Study:
- To compare serum asprosin concentrations in children with PWS, overweight/obesity, and normal weight.
- To investigate postprandial asprosin changes in PWS and matched controls.
Main Methods:
- Enrolled 52 children: 23 with PWS, 8 overweight/obese, 21 normal weight.
- Measured fasting asprosin, glucose, insulin, HOMA-IR, acyl ghrelin, and leptin.
- Assessed postprandial asprosin in a subsample.
Main Results:
- No significant differences in fasting asprosin, glucose, insulin, or HOMA-IR across groups.
- No differences in fasting or postprandial asprosin in PWS or control groups.
- Fasting asprosin correlated positively with glucose in obese children (p=0.007).
Conclusions:
- Asprosin may predict early glucose metabolism alterations in obese children.
- Further research is needed on asprosin's role in PWS metabolism and obesity.
Abstract:
Children with Prader-Willi syndrome (PWS) are characterized by severe obesity. Asprosin is a newly discovered protein hormone produced by the white adipose tissue and is correlated with insulin resistance. The aim of our study was to describe the concentrations of serum asprosin in children with PWS compared to those with overweight/obesity and normal weight, and to explore the postprandial change in asprosin concentrations in participants with PWS and BMI-z matched controls. We enrolled 52 children, 23 with PWS, 8 with overweight/obesity, and 21 with normal weight. Fasting levels of asprosin, glucose, and insulin were collected in all children, and postprandial asprosin and fasting levels of acyl ghrelin (AG) and leptin were also determined in a subsample of participants. There were no significant differences among groups in fasting levels of asprosin, glucose, insulin, and HOMA-IR. Fasting serum asprosin and 1-h post-meal serum asprosin did not differ in children with PWS nor in BMI-z matched controls. Fasting asprosin showed an adjusted positive correlation with glucose in children with obesity (r = 0.93, p = 0.007) but not in children with PWS nor children with normal weight. Circulating asprosin might be a predictor of early alterations in glucose metabolism in children with obesity. More research is needed to further explain the association between asprosin, food intake, metabolism, and obesity in PWS.
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