Evaluation of Autonomic Nervous System Dysfunction in Childhood Obesity and Prader–Willi Syndrome
The autonomic nervous system (ANS) may play a role in the distribution of body fat and the development of obesity and its complications. Features of individuals with Prader–Willi syndrome (PWS) impacted by PWS molecular genetic classes suggest alterations in ANS function; however, these have been ra...
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Published in | International journal of molecular sciences Vol. 24; no. 9; p. 8013 |
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Main Authors | , , , , , , , , , , , , |
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Abstract | The autonomic nervous system (ANS) may play a role in the distribution of body fat and the development of obesity and its complications. Features of individuals with Prader–Willi syndrome (PWS) impacted by PWS molecular genetic classes suggest alterations in ANS function; however, these have been rarely studied and presented with conflicting results. The aim of this study was to investigate if the ANS function is altered in PWS. In this case-control study, we assessed ANS function in 20 subjects with PWS (6 males/14 females; median age 10.5 years) and 27 body mass index (BMI) z-score-matched controls (19 males/8 females; median age 12.8 years). Standardized non-invasive measures of cardiac baroreflex function, heart rate, blood pressure, heart rate variability, quantitative sudomotor axon reflex tests, and a symptom questionnaire were completed. The increase in heart rate in response to head-up tilt testing was blunted (p < 0.01) in PWS compared to controls. Besides a lower heart rate ratio with Valsalva in PWS (p < 0.01), no significant differences were observed in other measures of cardiac function or sweat production. Findings suggest possible altered sympathetic function in PWS. |
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AbstractList | The autonomic nervous system (ANS) may play a role in the distribution of body fat and the development of obesity and its complications. Features of individuals with Prader-Willi syndrome (PWS) impacted by PWS molecular genetic classes suggest alterations in ANS function; however, these have been rarely studied and presented with conflicting results. The aim of this study was to investigate if the ANS function is altered in PWS. In this case-control study, we assessed ANS function in 20 subjects with PWS (6 males/14 females; median age 10.5 years) and 27 body mass index (BMI) z-score-matched controls (19 males/8 females; median age 12.8 years). Standardized non-invasive measures of cardiac baroreflex function, heart rate, blood pressure, heart rate variability, quantitative sudomotor axon reflex tests, and a symptom questionnaire were completed. The increase in heart rate in response to head-up tilt testing was blunted (
< 0.01) in PWS compared to controls. Besides a lower heart rate ratio with Valsalva in PWS (
< 0.01), no significant differences were observed in other measures of cardiac function or sweat production. Findings suggest possible altered sympathetic function in PWS. The autonomic nervous system (ANS) may play a role in the distribution of body fat and the development of obesity and its complications. Features of individuals with Prader–Willi syndrome (PWS) impacted by PWS molecular genetic classes suggest alterations in ANS function; however, these have been rarely studied and presented with conflicting results. The aim of this study was to investigate if the ANS function is altered in PWS. In this case-control study, we assessed ANS function in 20 subjects with PWS (6 males/14 females; median age 10.5 years) and 27 body mass index (BMI) z-score-matched controls (19 males/8 females; median age 12.8 years). Standardized non-invasive measures of cardiac baroreflex function, heart rate, blood pressure, heart rate variability, quantitative sudomotor axon reflex tests, and a symptom questionnaire were completed. The increase in heart rate in response to head-up tilt testing was blunted (p < 0.01) in PWS compared to controls. Besides a lower heart rate ratio with Valsalva in PWS (p < 0.01), no significant differences were observed in other measures of cardiac function or sweat production. Findings suggest possible altered sympathetic function in PWS. The autonomic nervous system (ANS) may play a role in the distribution of body fat and the development of obesity and its complications. Features of individuals with Prader-Willi syndrome (PWS) impacted by PWS molecular genetic classes suggest alterations in ANS function; however, these have been rarely studied and presented with conflicting results. The aim of this study was to investigate if the ANS function is altered in PWS. In this case-control study, we assessed ANS function in 20 subjects with PWS (6 males/14 females; median age 10.5 years) and 27 body mass index (BMI) z-score-matched controls (19 males/8 females; median age 12.8 years). Standardized non-invasive measures of cardiac baroreflex function, heart rate, blood pressure, heart rate variability, quantitative sudomotor axon reflex tests, and a symptom questionnaire were completed. The increase in heart rate in response to head-up tilt testing was blunted (p < 0.01) in PWS compared to controls. Besides a lower heart rate ratio with Valsalva in PWS (p < 0.01), no significant differences were observed in other measures of cardiac function or sweat production. Findings suggest possible altered sympathetic function in PWS.The autonomic nervous system (ANS) may play a role in the distribution of body fat and the development of obesity and its complications. Features of individuals with Prader-Willi syndrome (PWS) impacted by PWS molecular genetic classes suggest alterations in ANS function; however, these have been rarely studied and presented with conflicting results. The aim of this study was to investigate if the ANS function is altered in PWS. In this case-control study, we assessed ANS function in 20 subjects with PWS (6 males/14 females; median age 10.5 years) and 27 body mass index (BMI) z-score-matched controls (19 males/8 females; median age 12.8 years). Standardized non-invasive measures of cardiac baroreflex function, heart rate, blood pressure, heart rate variability, quantitative sudomotor axon reflex tests, and a symptom questionnaire were completed. The increase in heart rate in response to head-up tilt testing was blunted (p < 0.01) in PWS compared to controls. Besides a lower heart rate ratio with Valsalva in PWS (p < 0.01), no significant differences were observed in other measures of cardiac function or sweat production. Findings suggest possible altered sympathetic function in PWS. The autonomic nervous system (ANS) may play a role in the distribution of body fat and the development of obesity and its complications. Features of individuals with Prader–Willi syndrome (PWS) impacted by PWS molecular genetic classes suggest alterations in ANS function; however, these have been rarely studied and presented with conflicting results. The aim of this study was to investigate if the ANS function is altered in PWS. In this case-control study, we assessed ANS function in 20 subjects with PWS (6 males/14 females; median age 10.5 years) and 27 body mass index (BMI) z-score-matched controls (19 males/8 females; median age 12.8 years). Standardized non-invasive measures of cardiac baroreflex function, heart rate, blood pressure, heart rate variability, quantitative sudomotor axon reflex tests, and a symptom questionnaire were completed. The increase in heart rate in response to head-up tilt testing was blunted ( p < 0.01) in PWS compared to controls. Besides a lower heart rate ratio with Valsalva in PWS ( p < 0.01), no significant differences were observed in other measures of cardiac function or sweat production. Findings suggest possible altered sympathetic function in PWS. |
Audience | Academic |
Author | Richer, Lawrence P. Tun, Hein M. Peng, Ye Ainsley, Steven Triador, Lucila Haqq, Andrea M. Freemark, Michael Butler, Merlin G. DeLorey, Darren S. Sharma, Arya M. Tan, Qiming Avedzi, Hayford M. Orsso, Camila E. |
AuthorAffiliation | 4 JC School of Public Health, Faculty of Medicine, The Chinese University of Hong Kong, Hong Kong 999077, China 5 Department of Medicine, University of Alberta, Edmonton, AB T6G 2R3, Canada 1 Department of Pediatrics, University of Alberta, Edmonton, AB T6G 2R3, Canada 7 Division of Pediatric Endocrinology, Duke University Medical Center, Durham, NC 27705, USA 6 Department of Agricultural Food & Nutritional Science, University of Alberta, Edmonton, AB T6G 2R3, Canada 2 Departments of Psychiatry & Behavioral Sciences and Pediatrics, Kansas University Medical Center, Kansas City, KS 66160, USA 3 Faculty of Kinesiology, Sport, and Recreation, University of Alberta, Edmonton, AB T6G 2R3, Canada |
AuthorAffiliation_xml | – name: 5 Department of Medicine, University of Alberta, Edmonton, AB T6G 2R3, Canada – name: 7 Division of Pediatric Endocrinology, Duke University Medical Center, Durham, NC 27705, USA – name: 1 Department of Pediatrics, University of Alberta, Edmonton, AB T6G 2R3, Canada – name: 2 Departments of Psychiatry & Behavioral Sciences and Pediatrics, Kansas University Medical Center, Kansas City, KS 66160, USA – name: 3 Faculty of Kinesiology, Sport, and Recreation, University of Alberta, Edmonton, AB T6G 2R3, Canada – name: 4 JC School of Public Health, Faculty of Medicine, The Chinese University of Hong Kong, Hong Kong 999077, China – name: 6 Department of Agricultural Food & Nutritional Science, University of Alberta, Edmonton, AB T6G 2R3, Canada |
Author_xml | – sequence: 1 givenname: Lawrence P. orcidid: 0000-0002-6897-8668 surname: Richer fullname: Richer, Lawrence P. – sequence: 2 givenname: Qiming orcidid: 0000-0001-9014-6246 surname: Tan fullname: Tan, Qiming – sequence: 3 givenname: Merlin G. orcidid: 0000-0002-2911-0524 surname: Butler fullname: Butler, Merlin G. – sequence: 4 givenname: Hayford M. orcidid: 0000-0003-1854-3364 surname: Avedzi fullname: Avedzi, Hayford M. – sequence: 5 givenname: Darren S. surname: DeLorey fullname: DeLorey, Darren S. – sequence: 6 givenname: Ye orcidid: 0000-0003-3791-2305 surname: Peng fullname: Peng, Ye – sequence: 7 givenname: Hein M. surname: Tun fullname: Tun, Hein M. – sequence: 8 givenname: Arya M. surname: Sharma fullname: Sharma, Arya M. – sequence: 9 givenname: Steven surname: Ainsley fullname: Ainsley, Steven – sequence: 10 givenname: Camila E. orcidid: 0000-0001-5989-0528 surname: Orsso fullname: Orsso, Camila E. – sequence: 11 givenname: Lucila orcidid: 0000-0002-8089-2162 surname: Triador fullname: Triador, Lucila – sequence: 12 givenname: Michael surname: Freemark fullname: Freemark, Michael – sequence: 13 givenname: Andrea M. surname: Haqq fullname: Haqq, Andrea M. |
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CitedBy_id | crossref_primary_10_3390_pediatric16010013 crossref_primary_10_1111_jne_70015 crossref_primary_10_1016_j_ijpsycho_2024_112429 crossref_primary_10_1007_s10286_024_01083_8 |
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Keywords | autonomic nervous system (ANS) genetics Prader–Willi syndrome (PWS) childhood obesity |
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SubjectTerms | Appetite Autonomic Nervous System Blood pressure Body Mass Index Case-Control Studies Child Childhood Eating behavior Female Food Gene expression Heart Heart beat Heart rate Hormones Humans Hypothalamus Male Metabolism Nervous system Obesity Obesity in children Pediatric Obesity - complications Peptides Prader-Willi Syndrome - complications Sleep Weight control |
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Title | Evaluation of Autonomic Nervous System Dysfunction in Childhood Obesity and Prader–Willi Syndrome |
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