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Metabolic profiling in Prader-Willi syndrome and nonsyndromic obesity: sex differences and the role of growth hormone.
Clin Endocrinol (Oxf) 2015; 83(6):797-805CE

Abstract

OBJECTIVES

To identify metabolic factors controlling appetite and insulin sensitivity in PWS and assess effects of GH treatment.

METHODS

We compared amino acids, fatty acids and acylcarnitines in GH-treated and untreated PWS children and obese and lean controls to identify biomarkers associated with ghrelin, peptide YY and markers of insulin sensitivity (adiponectin and HOMA-IR).

RESULTS

Compared with obese controls (OC), children with PWS had fasting hyperghrelinaemia, hyperadiponectinaemia, hypoinsulinaemia and increased ghrelin/PYY. Hyperghrelinaemia, hyperadiponectinaemia and hypoinsulinaemia were more striking in PWS females than males, and decreases in BCAA were detected only in PWS females. GH-treated PWS subjects had lower leptin and higher IGF-1 and adiponectin than untreated subjects; fasting ghrelin, PYY and insulin levels were comparable. Ghrelin correlated inversely with BCAA in PWS but not OC. Adiponectin correlated negatively with BMIz and HOMA-IR in PWS; in contrast, adiponectin correlated more strongly with BCAA than BMIz or HOMA-IR in OC.

CONCLUSIONS

BCAA levels were lower in PWS females than OC females and correlated inversely with ghrelin. Low BCAA in PWS females may promote hyperghrelinaemia and hyperphagia, while hyperadiponectinaemia may maintain insulin sensitivity despite excess weight gain. GH treatment may reduce leptin and increase adiponectin, but does not affect fasting ghrelin or PYY.

Authors+Show Affiliations

Division of Pediatric Endocrinology and Diabetes, Duke University Medical Center, Durham, NC, USA.Division of Endocrinology, Metabolism, and Nutrition, Duke University Medical Center, Durham, NC, USA. Sarah W. Stedman Nutrition and Metabolism Center and the Duke Molecular Physiology Institute, Duke University, Durham, NC, USA.Departments of Pediatrics, Psychiatry and Behavioral Sciences, Kansas University Medical Center, Kansas City, KS, USA.Sarah W. Stedman Nutrition and Metabolism Center and the Duke Molecular Physiology Institute, Duke University, Durham, NC, USA.Sarah W. Stedman Nutrition and Metabolism Center and the Duke Molecular Physiology Institute, Duke University, Durham, NC, USA.Department of Pediatrics, University of Alberta, Edmonton, AB, Canada.Division of Pediatric Endocrinology and Diabetes, Duke University Medical Center, Durham, NC, USA. Sarah W. Stedman Nutrition and Metabolism Center and the Duke Molecular Physiology Institute, Duke University, Durham, NC, USA.

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

25736874

Citation

Irizarry, Krystal A., et al. "Metabolic Profiling in Prader-Willi Syndrome and Nonsyndromic Obesity: Sex Differences and the Role of Growth Hormone." Clinical Endocrinology, vol. 83, no. 6, 2015, pp. 797-805.
Irizarry KA, Bain J, Butler MG, et al. Metabolic profiling in Prader-Willi syndrome and nonsyndromic obesity: sex differences and the role of growth hormone. Clin Endocrinol (Oxf). 2015;83(6):797-805.
Irizarry, K. A., Bain, J., Butler, M. G., Ilkayeva, O., Muehlbauer, M., Haqq, A. M., & Freemark, M. (2015). Metabolic profiling in Prader-Willi syndrome and nonsyndromic obesity: sex differences and the role of growth hormone. Clinical Endocrinology, 83(6), pp. 797-805. doi:10.1111/cen.12766.
Irizarry KA, et al. Metabolic Profiling in Prader-Willi Syndrome and Nonsyndromic Obesity: Sex Differences and the Role of Growth Hormone. Clin Endocrinol (Oxf). 2015;83(6):797-805. PubMed PMID: 25736874.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Metabolic profiling in Prader-Willi syndrome and nonsyndromic obesity: sex differences and the role of growth hormone. AU - Irizarry,Krystal A, AU - Bain,James, AU - Butler,Merlin G, AU - Ilkayeva,Olga, AU - Muehlbauer,Michael, AU - Haqq,Andrea M, AU - Freemark,Michael, Y1 - 2015/04/01/ PY - 2015/01/13/received PY - 2015/01/21/revised PY - 2015/02/12/revised PY - 2015/02/26/accepted PY - 2015/3/5/entrez PY - 2015/3/5/pubmed PY - 2016/12/15/medline SP - 797 EP - 805 JF - Clinical endocrinology JO - Clin. Endocrinol. (Oxf) VL - 83 IS - 6 N2 - OBJECTIVES: To identify metabolic factors controlling appetite and insulin sensitivity in PWS and assess effects of GH treatment. METHODS: We compared amino acids, fatty acids and acylcarnitines in GH-treated and untreated PWS children and obese and lean controls to identify biomarkers associated with ghrelin, peptide YY and markers of insulin sensitivity (adiponectin and HOMA-IR). RESULTS: Compared with obese controls (OC), children with PWS had fasting hyperghrelinaemia, hyperadiponectinaemia, hypoinsulinaemia and increased ghrelin/PYY. Hyperghrelinaemia, hyperadiponectinaemia and hypoinsulinaemia were more striking in PWS females than males, and decreases in BCAA were detected only in PWS females. GH-treated PWS subjects had lower leptin and higher IGF-1 and adiponectin than untreated subjects; fasting ghrelin, PYY and insulin levels were comparable. Ghrelin correlated inversely with BCAA in PWS but not OC. Adiponectin correlated negatively with BMIz and HOMA-IR in PWS; in contrast, adiponectin correlated more strongly with BCAA than BMIz or HOMA-IR in OC. CONCLUSIONS: BCAA levels were lower in PWS females than OC females and correlated inversely with ghrelin. Low BCAA in PWS females may promote hyperghrelinaemia and hyperphagia, while hyperadiponectinaemia may maintain insulin sensitivity despite excess weight gain. GH treatment may reduce leptin and increase adiponectin, but does not affect fasting ghrelin or PYY. SN - 1365-2265 UR - https://www.unboundmedicine.com/medline/citation/25736874/Metabolic_profiling_in_Prader_Willi_syndrome_and_nonsyndromic_obesity:_sex_differences_and_the_role_of_growth_hormone_ L2 - https://doi.org/10.1111/cen.12766 DB - PRIME DP - Unbound Medicine ER -