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Macronutrient Regulation of Ghrelin and Peptide YY in Pediatric Obesity and Prader-Willi Syndrome.
J Clin Endocrinol Metab 2015; 100(10):3822-31JC

Abstract

BACKGROUND

The roles of macronutrients and GH in the regulation of food intake in pediatric obesity and Prader-Willi Syndrome (PWS) are poorly understood.

OBJECTIVE

We compared effects of high-carbohydrate (HC) and high-fat (HF) meals and GH therapy on ghrelin, insulin, peptide YY (PYY), and insulin sensitivity in children with PWS and body mass index (BMI) -matched obese controls (OCs).

METHODS

In a randomized, crossover study, 14 PWS (median, 11.35 y; BMI z score [BMI-z], 2.15) and 14 OCs (median, 11.97 y; BMI-z, 2.35) received isocaloric breakfast meals (HC or HF) on separate days. Blood samples were drawn at baseline and every 30 minutes for 4 hours. Mixed linear models were adjusted for age, sex, and BMI-z.

RESULTS

Relative to OCs, children with PWS had lower fasting insulin and higher fasting ghrelin and ghrelin/PYY. Ghrelin levels were higher in PWS across all postprandial time points (P < .0001). Carbohydrate was more potent than fat in suppressing ghrelin levels in PWS (P = .028); HC and HF were equipotent in OCs but less potent than in PWS (P = .011). The increase in PYY following HF was attenuated in PWS (P = .037); thus, postprandial ghrelin/PYY remained higher throughout. A lesser increase in insulin and lesser decrease in ghrelin were observed in GH-treated PWS patients than in untreated patients; PYY responses were comparable.

CONCLUSION

Children with PWS have fasting and postprandial hyperghrelinemia and an attenuated PYY response to fat, yielding a high ghrelin/PYY ratio. GH therapy in PWS is associated with increased insulin sensitivity and lesser postprandial suppression of ghrelin. The ratio Ghrelin/PYY may be a novel marker of orexigenic drive.

Authors+Show Affiliations

Division of Pediatric Endocrinology and Diabetes (P.G.B., M.F.), Duke University Medical Center, Durham, North Carolina 27710; Advanced Analytics (M.B.), SAS Institute Inc., Cary, North Carolina 27513; Duke Molecular Physiology Institute (M.J.M., M.F.), Sarah W. Stedman Nutrition and Metabolism Center, Duke University Medical Center, Durham, North Carolina 27710; Knight Cardiovascular Institute (J.Q.P.), Oregon Health & Science University, Portland, Oregon 97239; and Department of Medicine (D.B.) and Division of Pediatric Endocrinology and Diabetes (A.M.H.), University of Alberta, Edmonton, AB T6G 2R3 Canada.Division of Pediatric Endocrinology and Diabetes (P.G.B., M.F.), Duke University Medical Center, Durham, North Carolina 27710; Advanced Analytics (M.B.), SAS Institute Inc., Cary, North Carolina 27513; Duke Molecular Physiology Institute (M.J.M., M.F.), Sarah W. Stedman Nutrition and Metabolism Center, Duke University Medical Center, Durham, North Carolina 27710; Knight Cardiovascular Institute (J.Q.P.), Oregon Health & Science University, Portland, Oregon 97239; and Department of Medicine (D.B.) and Division of Pediatric Endocrinology and Diabetes (A.M.H.), University of Alberta, Edmonton, AB T6G 2R3 Canada.Division of Pediatric Endocrinology and Diabetes (P.G.B., M.F.), Duke University Medical Center, Durham, North Carolina 27710; Advanced Analytics (M.B.), SAS Institute Inc., Cary, North Carolina 27513; Duke Molecular Physiology Institute (M.J.M., M.F.), Sarah W. Stedman Nutrition and Metabolism Center, Duke University Medical Center, Durham, North Carolina 27710; Knight Cardiovascular Institute (J.Q.P.), Oregon Health & Science University, Portland, Oregon 97239; and Department of Medicine (D.B.) and Division of Pediatric Endocrinology and Diabetes (A.M.H.), University of Alberta, Edmonton, AB T6G 2R3 Canada.Division of Pediatric Endocrinology and Diabetes (P.G.B., M.F.), Duke University Medical Center, Durham, North Carolina 27710; Advanced Analytics (M.B.), SAS Institute Inc., Cary, North Carolina 27513; Duke Molecular Physiology Institute (M.J.M., M.F.), Sarah W. Stedman Nutrition and Metabolism Center, Duke University Medical Center, Durham, North Carolina 27710; Knight Cardiovascular Institute (J.Q.P.), Oregon Health & Science University, Portland, Oregon 97239; and Department of Medicine (D.B.) and Division of Pediatric Endocrinology and Diabetes (A.M.H.), University of Alberta, Edmonton, AB T6G 2R3 Canada.Division of Pediatric Endocrinology and Diabetes (P.G.B., M.F.), Duke University Medical Center, Durham, North Carolina 27710; Advanced Analytics (M.B.), SAS Institute Inc., Cary, North Carolina 27513; Duke Molecular Physiology Institute (M.J.M., M.F.), Sarah W. Stedman Nutrition and Metabolism Center, Duke University Medical Center, Durham, North Carolina 27710; Knight Cardiovascular Institute (J.Q.P.), Oregon Health & Science University, Portland, Oregon 97239; and Department of Medicine (D.B.) and Division of Pediatric Endocrinology and Diabetes (A.M.H.), University of Alberta, Edmonton, AB T6G 2R3 Canada.Division of Pediatric Endocrinology and Diabetes (P.G.B., M.F.), Duke University Medical Center, Durham, North Carolina 27710; Advanced Analytics (M.B.), SAS Institute Inc., Cary, North Carolina 27513; Duke Molecular Physiology Institute (M.J.M., M.F.), Sarah W. Stedman Nutrition and Metabolism Center, Duke University Medical Center, Durham, North Carolina 27710; Knight Cardiovascular Institute (J.Q.P.), Oregon Health & Science University, Portland, Oregon 97239; and Department of Medicine (D.B.) and Division of Pediatric Endocrinology and Diabetes (A.M.H.), University of Alberta, Edmonton, AB T6G 2R3 Canada.Division of Pediatric Endocrinology and Diabetes (P.G.B., M.F.), Duke University Medical Center, Durham, North Carolina 27710; Advanced Analytics (M.B.), SAS Institute Inc., Cary, North Carolina 27513; Duke Molecular Physiology Institute (M.J.M., M.F.), Sarah W. Stedman Nutrition and Metabolism Center, Duke University Medical Center, Durham, North Carolina 27710; Knight Cardiovascular Institute (J.Q.P.), Oregon Health & Science University, Portland, Oregon 97239; and Department of Medicine (D.B.) and Division of Pediatric Endocrinology and Diabetes (A.M.H.), University of Alberta, Edmonton, AB T6G 2R3 Canada.

Pub Type(s)

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

Language

eng

PubMed ID

26259133

Citation

Gumus Balikcioglu, Pinar, et al. "Macronutrient Regulation of Ghrelin and Peptide YY in Pediatric Obesity and Prader-Willi Syndrome." The Journal of Clinical Endocrinology and Metabolism, vol. 100, no. 10, 2015, pp. 3822-31.
Gumus Balikcioglu P, Balikcioglu M, Muehlbauer MJ, et al. Macronutrient Regulation of Ghrelin and Peptide YY in Pediatric Obesity and Prader-Willi Syndrome. J Clin Endocrinol Metab. 2015;100(10):3822-31.
Gumus Balikcioglu, P., Balikcioglu, M., Muehlbauer, M. J., Purnell, J. Q., Broadhurst, D., Freemark, M., & Haqq, A. M. (2015). Macronutrient Regulation of Ghrelin and Peptide YY in Pediatric Obesity and Prader-Willi Syndrome. The Journal of Clinical Endocrinology and Metabolism, 100(10), pp. 3822-31. doi:10.1210/jc.2015-2503.
Gumus Balikcioglu P, et al. Macronutrient Regulation of Ghrelin and Peptide YY in Pediatric Obesity and Prader-Willi Syndrome. J Clin Endocrinol Metab. 2015;100(10):3822-31. PubMed PMID: 26259133.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Macronutrient Regulation of Ghrelin and Peptide YY in Pediatric Obesity and Prader-Willi Syndrome. AU - Gumus Balikcioglu,Pinar, AU - Balikcioglu,Metin, AU - Muehlbauer,Michael J, AU - Purnell,Jonathan Q, AU - Broadhurst,David, AU - Freemark,Michael, AU - Haqq,Andrea M, Y1 - 2015/08/10/ PY - 2015/8/11/entrez PY - 2015/8/11/pubmed PY - 2016/1/14/medline SP - 3822 EP - 31 JF - The Journal of clinical endocrinology and metabolism JO - J. Clin. Endocrinol. Metab. VL - 100 IS - 10 N2 - BACKGROUND: The roles of macronutrients and GH in the regulation of food intake in pediatric obesity and Prader-Willi Syndrome (PWS) are poorly understood. OBJECTIVE: We compared effects of high-carbohydrate (HC) and high-fat (HF) meals and GH therapy on ghrelin, insulin, peptide YY (PYY), and insulin sensitivity in children with PWS and body mass index (BMI) -matched obese controls (OCs). METHODS: In a randomized, crossover study, 14 PWS (median, 11.35 y; BMI z score [BMI-z], 2.15) and 14 OCs (median, 11.97 y; BMI-z, 2.35) received isocaloric breakfast meals (HC or HF) on separate days. Blood samples were drawn at baseline and every 30 minutes for 4 hours. Mixed linear models were adjusted for age, sex, and BMI-z. RESULTS: Relative to OCs, children with PWS had lower fasting insulin and higher fasting ghrelin and ghrelin/PYY. Ghrelin levels were higher in PWS across all postprandial time points (P < .0001). Carbohydrate was more potent than fat in suppressing ghrelin levels in PWS (P = .028); HC and HF were equipotent in OCs but less potent than in PWS (P = .011). The increase in PYY following HF was attenuated in PWS (P = .037); thus, postprandial ghrelin/PYY remained higher throughout. A lesser increase in insulin and lesser decrease in ghrelin were observed in GH-treated PWS patients than in untreated patients; PYY responses were comparable. CONCLUSION: Children with PWS have fasting and postprandial hyperghrelinemia and an attenuated PYY response to fat, yielding a high ghrelin/PYY ratio. GH therapy in PWS is associated with increased insulin sensitivity and lesser postprandial suppression of ghrelin. The ratio Ghrelin/PYY may be a novel marker of orexigenic drive. SN - 1945-7197 UR - https://www.unboundmedicine.com/medline/citation/26259133/Macronutrient_Regulation_of_Ghrelin_and_Peptide_YY_in_Pediatric_Obesity_and_Prader_Willi_Syndrome_ L2 - https://academic.oup.com/jcem/article-lookup/doi/10.1210/jc.2015-2503 DB - PRIME DP - Unbound Medicine ER -