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Pediatr Obes. 2019 May;14(5):e12493. doi: 10.1111/ijpo.12493. Epub 2018 Dec 27.

Obestatin and adropin in Prader-Willi syndrome and nonsyndromic obesity: Associations with weight, BMI-z, and HOMA-IR.

Author information

1
Department of Agricultural, Food and Nutritional Science, University of Alberta, Edmonton, Canada.
2
Department of Pharmacology and Physiology, Saint Louis University School of Medicine, Saint Louis University, St. Louis, Missouri, United States.
3
Sarah W. Stedman Nutrition and Metabolism Center, Duke University Medical Center, Durham, North Carolina, United States.
4
Department of Kinesiology, California State University, Fullerton, California, United States.
5
Departments of Psychiatry, Behavioral Sciences, and Pediatrics, Kansas University Medical Center, Kansas City, Kansas, United States.
6
Division of Pediatric Endocrinology, Duke University Medical Center, Durham, North Carolina, United States.
7
Department of Pediatrics, University of Alberta, Edmonton, Canada.

Abstract

The roles of obestatin and adropin in paediatric obesity are poorly understood. We compared obestatin and adropin concentrations in younger (n = 21) and older children (n = 14) with Prader-Willi syndrome (PWS) and age and BMI-z-matched controls (n = 31). Fasting plasma obestatin and adropin were higher in younger children with PWS than controls; adropin was also higher in older children with PWS. Growth hormone treatment had no effects on obestatin or adropin in PWS. The ratio of ghrelin to obestatin declined from early to late childhood but was higher in older PWS than older controls. Adropin correlated with fasting glucose in the PWS group only. Changes in the ratio of ghrelin to obestatin may suggest changes in the processing of preproghrelin to ghrelin and obestatin during development and differential processing of preproghrelin in PWS.

KEYWORDS:

Prader-Willi syndrome; adropin; obesity; obestatin

PMID:
30589518
DOI:
10.1111/ijpo.12493
[Indexed for MEDLINE]

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