Evidence map›Paper›PMID 26259133›Full record

Trial reportThe Journal of clinical endocrinology and metabolism2015

Macronutrient Regulation of Ghrelin and Peptide YY in Pediatric Obesity and Prader-Willi Syndrome.

Pinar Gumus Balikcioglu, Metin Balikcioglu, Michael J Muehlbauer, Jonathan Q Purnell, David Broadhurst, Michael Freemark, Andrea M Haqq

Open access · bronzeAbstract readRandomized Controlled Trial
In one paragraph

Trial report in The Journal of clinical endocrinology and metabolism, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.7field-weighted citation impact, top 15% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

13 citing papers in PubMed, 22 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 6 institutions in 2 countries.

Pinar Gumus BalikciogluDivision 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.
Metin BalikciogluDivision 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.
Michael J MuehlbauerDivision 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.
Jonathan Q PurnellDivision 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.
David BroadhurstDivision 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.
Michael FreemarkDivision 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.
Andrea M HaqqDivision 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.
Duke Medical Center · USDuke University · USDuke University Hospital · USOregon Health & Science University · USSAS Institute (United States) · USUniversity of Alberta · CA

Funding

Developmental, nutritional and hormonal reg. of GhrelinK23RR021979 · NCRR · DUKE UNIVERSITY · PI HAQQ, ANDREA M · 2005 to 2008
$551k
NCRR NIH HHS 1K23-RR-021979NCRR NIH HHS K23 RR021979NCRR NIH HHS MO1-RR-30
6 · The paper itself

Abstract

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

objectiveWe 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).

methodsIn 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.

resultsRelative 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.

conclusionChildren 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.

Indexed as

AdolescentChildChild, PreschoolCross-Over StudiesDietary CarbohydratesDietary FatsFemaleGhrelinHuman Growth HormoneHumansMalePediatric ObesityPeptide YYPostprandial PeriodPrader-Willi SyndromeDietary CarbohydratesDietary FatsGhrelinHuman Growth HormonePeptide YY

Identifiers

PMID26259133
PMCPMC5399503
OpenAlexW1833365966

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.