Hyperphagia, Severe Obesity, Impaired Cognitive Function, and Hyperactivity Associated With Functional Loss of One Copy of the Brain-Derived Neurotrophic Factor (BDNF) Gene
Hyperphagia, Severe Obesity, Impaired Cognitive Function, and Hyperactivity Associated With Functional Loss of One Copy of the Brain-Derived Neurotrophic Factor ( BDNF ) Gene Juliette Gray 1 , Giles S.H. Yeo 1 , James J. Cox 2 , Jenny Morton 3 , Anna-Lynne R. Adlam 4 , Julia M. Keogh 1 , Jack A. Yan...
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Published in | Diabetes (New York, N.Y.) Vol. 55; no. 12; pp. 3366 - 3371 |
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Main Authors | , , , , , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
Alexandria, VA
American Diabetes Association
01.12.2006
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Subjects | |
Online Access | Get full text |
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Abstract | Hyperphagia, Severe Obesity, Impaired Cognitive Function, and Hyperactivity Associated With Functional Loss of One Copy of
the Brain-Derived Neurotrophic Factor ( BDNF ) Gene
Juliette Gray 1 ,
Giles S.H. Yeo 1 ,
James J. Cox 2 ,
Jenny Morton 3 ,
Anna-Lynne R. Adlam 4 ,
Julia M. Keogh 1 ,
Jack A. Yanovski 5 ,
Areeg El Gharbawy 5 ,
Joan C. Han 5 ,
Y.C. Loraine Tung 1 ,
John R. Hodges 4 ,
F. Lucy Raymond 2 ,
Stephen O’Rahilly 1 and
I. Sadaf Farooqi 1
1 University Department of Clinical Biochemistry, Cambridge Institute for Medical Research, Addenbrooke’s Hospital, Cambridge,
U.K
2 University Department of Medical Genetics, Cambridge Institute for Medical Research, Addenbrooke’s Hospital, Cambridge, U.K
3 West Midlands Regional Genetics Service, Birmingham Women’s Hospital, Birmingham, U.K
4 Medical Research Council, Cognition and Brain Sciences Unit, and the Department of Clinical Neurosciences, Addenbrooke’s Hospital,
Cambridge, U.K
5 Unit on Growth and Obesity, Developmental Endocrinology Branch, National Institute of Child Health and Human Development,
National Institutes of Health, Bethesda, Maryland
Address correspondence and reprint requests to I. Sadaf Farooqi, University Department of Clinical Biochemistry, Cambridge
Institute for Medical Research, Addenbrooke’s Hospital, Cambridge, CB2 2XY, U.K. E-mail: isf20{at}cam.ac.uk
Abstract
The neurotrophin brain-derived neurotrophic factor (BDNF) inhibits food intake, and rodent models of BDNF disruption all exhibit
increased food intake and obesity, as well as hyperactivity. We report an 8-year-old girl with hyperphagia and severe obesity,
impaired cognitive function, and hyperactivity who harbored a de novo chromosomal inversion, 46,XX,inv(11)(p13p15.3), a region
encompassing the BDNF gene. We have identified the proximal inversion breakpoint that lies 850 kb telomeric of the 5′ end of the BDNF gene. The patient’s genomic DNA was heterozygous for a common coding polymorphism in BDNF , but monoallelic expression was seen in peripheral lymphocytes. Serum concentration of BDNF protein was reduced compared
with age- and BMI-matched subjects. Haploinsufficiency for BDNF was associated with increased ad libitum food intake, severe
early-onset obesity, hyperactivity, and cognitive impairment. These findings provide direct evidence for the role of the neurotrophin
BDNF in human energy homeostasis, as well as in cognitive function, memory, and behavior.
BAC, bacterial artificial chromosome
BDNF, brain-derived neurotrophic factor
FISH, fluorescence in situ hybridization
TrkB, tropomyosin-related kinase B
Footnotes
Additional information for this article can be found in an online appendix at http://diabetes.diabetesjournals.org .
The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore
be hereby marked “advertisement” in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
Accepted August 21, 2006.
Received April 24, 2006.
DIABETES |
---|---|
AbstractList | Hyperphagia, Severe Obesity, Impaired Cognitive Function, and Hyperactivity Associated With Functional Loss of One Copy of
the Brain-Derived Neurotrophic Factor ( BDNF ) Gene
Juliette Gray 1 ,
Giles S.H. Yeo 1 ,
James J. Cox 2 ,
Jenny Morton 3 ,
Anna-Lynne R. Adlam 4 ,
Julia M. Keogh 1 ,
Jack A. Yanovski 5 ,
Areeg El Gharbawy 5 ,
Joan C. Han 5 ,
Y.C. Loraine Tung 1 ,
John R. Hodges 4 ,
F. Lucy Raymond 2 ,
Stephen O’Rahilly 1 and
I. Sadaf Farooqi 1
1 University Department of Clinical Biochemistry, Cambridge Institute for Medical Research, Addenbrooke’s Hospital, Cambridge,
U.K
2 University Department of Medical Genetics, Cambridge Institute for Medical Research, Addenbrooke’s Hospital, Cambridge, U.K
3 West Midlands Regional Genetics Service, Birmingham Women’s Hospital, Birmingham, U.K
4 Medical Research Council, Cognition and Brain Sciences Unit, and the Department of Clinical Neurosciences, Addenbrooke’s Hospital,
Cambridge, U.K
5 Unit on Growth and Obesity, Developmental Endocrinology Branch, National Institute of Child Health and Human Development,
National Institutes of Health, Bethesda, Maryland
Address correspondence and reprint requests to I. Sadaf Farooqi, University Department of Clinical Biochemistry, Cambridge
Institute for Medical Research, Addenbrooke’s Hospital, Cambridge, CB2 2XY, U.K. E-mail: isf20{at}cam.ac.uk
Abstract
The neurotrophin brain-derived neurotrophic factor (BDNF) inhibits food intake, and rodent models of BDNF disruption all exhibit
increased food intake and obesity, as well as hyperactivity. We report an 8-year-old girl with hyperphagia and severe obesity,
impaired cognitive function, and hyperactivity who harbored a de novo chromosomal inversion, 46,XX,inv(11)(p13p15.3), a region
encompassing the BDNF gene. We have identified the proximal inversion breakpoint that lies 850 kb telomeric of the 5′ end of the BDNF gene. The patient’s genomic DNA was heterozygous for a common coding polymorphism in BDNF , but monoallelic expression was seen in peripheral lymphocytes. Serum concentration of BDNF protein was reduced compared
with age- and BMI-matched subjects. Haploinsufficiency for BDNF was associated with increased ad libitum food intake, severe
early-onset obesity, hyperactivity, and cognitive impairment. These findings provide direct evidence for the role of the neurotrophin
BDNF in human energy homeostasis, as well as in cognitive function, memory, and behavior.
BAC, bacterial artificial chromosome
BDNF, brain-derived neurotrophic factor
FISH, fluorescence in situ hybridization
TrkB, tropomyosin-related kinase B
Footnotes
Additional information for this article can be found in an online appendix at http://diabetes.diabetesjournals.org .
The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore
be hereby marked “advertisement” in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
Accepted August 21, 2006.
Received April 24, 2006.
DIABETES The neurotrophin brain-derived neurotrophic factor (BDNF) inhibits food intake, and rodent models of BDNF disruption all exhibit increased food intake and obesity, as well as hyperactivity. We report an 8-year-old girl with hyperphagia and severe obesity, impaired cognitive function, and hyperactivity who harbored a de novo chromosomal inversion, 46,XX,inv(11)(p13p15.3), a region encompassing the BDNF gene. We have identified the proximal inversion breakpoint that lies 850 kb telomeric of the 5' end of the BDNF gene. The patient's genomic DNA was heterozygous for a common coding polymorphism in BDNF, but monoallelic expression was seen in peripheral lymphocytes. Serum concentration of BDNF protein was reduced compared with age- and BMI-matched subjects. Haploinsufficiency for BDNF was associated with increased ad libitum food intake, severe early-onset obesity, hyperactivity, and cognitive impairment. These findings provide direct evidence for the role of the neurotrophin BDNF in human energy homeostasis, as well as in cognitive function, memory, and behavior. The neurotrophin brain-derived neurotrophic factor (BDNF) inhibits food intake, and rodent models of BDNF disruption all exhibit increased food intake and obesity, as well as hyperactivity. We report an 8-year-old girl with hyperphagia and severe obesity, impaired cognitive function, and hyperactivity who harbored a de novo chromosomal inversion, 46,XX,inv(11)(p13p15.3), a region encompassing the BDNF gene. We have identified the proximal inversion breakpoint that lies 850 kb telomeric of the 5' end of the BDNF gene. The patient's genomic DNA was heterozygous for a common coding polymorphism in BDNF, but monoallelic expression was seen in peripheral lymphocytes. Serum concentration of BDNF protein was reduced compared with age- and BMI-matched subjects. Haploinsufficiency for BDNF was associated with increased ad libitum food intake, severe early-onset obesity, hyperactivity, and cognitive impairment. These findings provide direct evidence for the role of the neurotrophin BDNF in human energy homeostasis, as well as in cognitive function, memory, and behavior. Diabetes 55:3366-3371, 2006 The neurotrophin brain-derived neurotrophic factor (BDNF) inhibits food intake, and rodent models of BDNF disruption all exhibit increased food intake and obesity, as well as hyperactivity. We report an 8-year-old girl with hyperphagia and severe obesity, impaired cognitive function, and hyperactivity who harbored a de novo chromosomal inversion, 46,XX,inv(11)(p13p15.3), a region encompassing the BDNF gene. We have identified the proximal inversion breakpoint that lies 850 kb telomeric of the 5′ end of the BDNF gene. The patient’s genomic DNA was heterozygous for a common coding polymorphism in BDNF , but monoallelic expression was seen in peripheral lymphocytes. Serum concentration of BDNF protein was reduced compared with age- and BMI-matched subjects. Haploinsufficiency for BDNF was associated with increased ad libitum food intake, severe early-onset obesity, hyper-activity, and cognitive impairment. These findings provide direct evidence for the role of the neurotrophin BDNF in human energy homeostasis, as well as in cognitive function, memory, and behavior. |
Audience | Professional |
Author | Giles S.H. Yeo Stephen O’Rahilly Anna-Lynne R. Adlam Y.C. Loraine Tung Jenny Morton Areeg El Gharbawy Joan C. Han F. Lucy Raymond Jack A. Yanovski John R. Hodges Julia M. Keogh I. Sadaf Farooqi Juliette Gray James J. Cox |
AuthorAffiliation | 2 University Department of Medical Genetics, Cambridge Institute for Medical Research, Addenbrooke’s Hospital, Cambridge, U.K 1 University Department of Clinical Biochemistry, Cambridge Institute for Medical Research, Addenbrooke’s Hospital, Cambridge, U.K 5 Unit on Growth and Obesity, Developmental Endocrinology Branch, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland 4 Medical Research Council, Cognition and Brain Sciences Unit, and the Department of Clinical Neurosciences, Addenbrooke’s Hospital, Cambridge, U.K 3 West Midlands Regional Genetics Service, Birmingham Women’s Hospital, Birmingham, U.K |
AuthorAffiliation_xml | – name: 1 University Department of Clinical Biochemistry, Cambridge Institute for Medical Research, Addenbrooke’s Hospital, Cambridge, U.K – name: 2 University Department of Medical Genetics, Cambridge Institute for Medical Research, Addenbrooke’s Hospital, Cambridge, U.K – name: 5 Unit on Growth and Obesity, Developmental Endocrinology Branch, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland – name: 4 Medical Research Council, Cognition and Brain Sciences Unit, and the Department of Clinical Neurosciences, Addenbrooke’s Hospital, Cambridge, U.K – name: 3 West Midlands Regional Genetics Service, Birmingham Women’s Hospital, Birmingham, U.K |
Author_xml | – sequence: 1 givenname: Juliette surname: GRAY fullname: GRAY, Juliette organization: University Department of Clinical Biochemistry, Cambridge Insti tute for Medical Research, Addenbrooke's Hospital, Cambridge, United Kingdom – sequence: 2 givenname: Giles S. H surname: YEO fullname: YEO, Giles S. H organization: University Department of Clinical Biochemistry, Cambridge Insti tute for Medical Research, Addenbrooke's Hospital, Cambridge, United Kingdom – sequence: 3 givenname: John R surname: HODGES fullname: HODGES, John R organization: Medical Research Council, Cognition and Brain Sciences Unit, and the Department of Clinical Neurosciences, Addenbrooke's Hospital, Cambridge, United Kingdom – sequence: 4 givenname: F. Lucy surname: RAYMOND fullname: RAYMOND, F. Lucy organization: University Department of Medical Genetics, Cambridge Institute for Medical Research, Addenbrooke's Hospital, Cambridge, United Kingdom – sequence: 5 givenname: Stephen surname: O'RAHILLY fullname: O'RAHILLY, Stephen organization: University Department of Clinical Biochemistry, Cambridge Insti tute for Medical Research, Addenbrooke's Hospital, Cambridge, United Kingdom – sequence: 6 givenname: I surname: SADAF FAROOQI fullname: SADAF FAROOQI, I organization: University Department of Clinical Biochemistry, Cambridge Insti tute for Medical Research, Addenbrooke's Hospital, Cambridge, United Kingdom – sequence: 7 givenname: James J surname: COX fullname: COX, James J organization: University Department of Medical Genetics, Cambridge Institute for Medical Research, Addenbrooke's Hospital, Cambridge, United Kingdom – sequence: 8 givenname: Jenny surname: MORTON fullname: MORTON, Jenny organization: West Midlands Regional Genetics Service, Birmingham Women's Hospital, Birmingham, United Kingdom – sequence: 9 givenname: Anna-Lynne R surname: ADLAM fullname: ADLAM, Anna-Lynne R organization: Medical Research Council, Cognition and Brain Sciences Unit, and the Department of Clinical Neurosciences, Addenbrooke's Hospital, Cambridge, United Kingdom – sequence: 10 givenname: Julia M surname: KEOGH fullname: KEOGH, Julia M organization: University Department of Clinical Biochemistry, Cambridge Insti tute for Medical Research, Addenbrooke's Hospital, Cambridge, United Kingdom – sequence: 11 givenname: Jack A surname: YANOVSKI fullname: YANOVSKI, Jack A organization: Unit on Growth and Obesity, Developmental Endocrinology Branch, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland, United States – sequence: 12 givenname: Areeg surname: EL GHARBAWY fullname: EL GHARBAWY, Areeg organization: Unit on Growth and Obesity, Developmental Endocrinology Branch, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland, United States – sequence: 13 givenname: Joan C surname: HAN fullname: HAN, Joan C organization: Unit on Growth and Obesity, Developmental Endocrinology Branch, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland, United States – sequence: 14 givenname: Y. C surname: LORAINE TUNG fullname: LORAINE TUNG, Y. C organization: University Department of Clinical Biochemistry, Cambridge Insti tute for Medical Research, Addenbrooke's Hospital, Cambridge, United Kingdom |
BackLink | http://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=18340140$$DView record in Pascal Francis https://www.ncbi.nlm.nih.gov/pubmed/17130481$$D View this record in MEDLINE/PubMed |
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Snippet | Hyperphagia, Severe Obesity, Impaired Cognitive Function, and Hyperactivity Associated With Functional Loss of One Copy of
the Brain-Derived Neurotrophic... The neurotrophin brain-derived neurotrophic factor (BDNF) inhibits food intake, and rodent models of BDNF disruption all exhibit increased food intake and... |
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SubjectTerms | Adult Attention deficit disorders. Hyperactivity Biological and medical sciences Brain research Brain-derived neurotrophic factor Brain-Derived Neurotrophic Factor - blood Brain-Derived Neurotrophic Factor - genetics Care and treatment Child clinical studies Chromosome Aberrations Chromosome Inversion - genetics Chromosomes, Artificial, Bacterial Cognition Disorders - genetics Diabetes. Impaired glucose tolerance DNA - genetics DNA - isolation & purification Endocrine pancreas. Apud cells (diseases) Endocrinopathies Etiopathogenesis. Screening. Investigations. Target tissue resistance Female Genetic aspects Health aspects Humans Hyperkinesis - genetics Hyperphagia - genetics Medical sciences Metabolic diseases Mutation Obesity Obesity - genetics Psychology. Psychoanalysis. Psychiatry Psychopathology. Psychiatry |
Title | Hyperphagia, Severe Obesity, Impaired Cognitive Function, and Hyperactivity Associated With Functional Loss of One Copy of the Brain-Derived Neurotrophic Factor (BDNF) Gene |
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