Aberrant expression of agouti signaling protein (ASIP) as a cause of monogenic severe childhood obesity.


Journal

Nature metabolism
ISSN: 2522-5812
Titre abrégé: Nat Metab
Pays: Germany
ID NLM: 101736592

Informations de publication

Date de publication:
12 2022
Historique:
received: 08 09 2022
accepted: 31 10 2022
pubmed: 20 12 2022
medline: 24 12 2022
entrez: 19 12 2022
Statut: ppublish

Résumé

Here we report a heterozygous tandem duplication at the ASIP (agouti signaling protein) gene locus causing ubiquitous, ectopic ASIP expression in a female patient with extreme childhood obesity. The mutation places ASIP under control of the ubiquitously active itchy E3 ubiquitin protein ligase promoter, driving the generation of ASIP in patient-derived native and induced pluripotent stem cells for all germ layers and hypothalamic-like neurons. The patient's phenotype of early-onset obesity, overgrowth, red hair and hyperinsulinemia is concordant with that of mutant mice ubiquitously expressing the homolog nonagouti. ASIP represses melanocyte-stimulating hormone-mediated activation as a melanocortin receptor antagonist, which might affect eating behavior, energy expenditure, adipocyte differentiation and pigmentation, as observed in the index patient. As the type of mutation escapes standard genetic screening algorithms, we rescreened the Leipzig Childhood Obesity cohort of 1,745 patients and identified four additional patients with the identical mutation, ectopic ASIP expression and a similar phenotype. Taken together, our data indicate that ubiquitous ectopic ASIP expression is likely a monogenic cause of human obesity.

Identifiants

pubmed: 36536132
doi: 10.1038/s42255-022-00703-9
pii: 10.1038/s42255-022-00703-9
pmc: PMC9771800
doi:

Substances chimiques

Agouti Signaling Protein 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

1697-1712

Subventions

Organisme : NIDDK NIH HHS
ID : P30 DK036836
Pays : United States
Organisme : NIDDK NIH HHS
ID : R01 DK102898
Pays : United States
Organisme : NIDDK NIH HHS
ID : R01 DK132469
Pays : United States

Commentaires et corrections

Type : CommentIn
Type : CommentIn

Informations de copyright

© 2022. The Author(s).

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Auteurs

Elena Kempf (E)

University Hospital for Children and Adolescents, Center for Pediatric Research, Medical Faculty, University of Leipzig, Leipzig, Germany.

Kathrin Landgraf (K)

University Hospital for Children and Adolescents, Center for Pediatric Research, Medical Faculty, University of Leipzig, Leipzig, Germany.

Robert Stein (R)

University Hospital for Children and Adolescents, Center for Pediatric Research, Medical Faculty, University of Leipzig, Leipzig, Germany.
Helmholtz Institute for Metabolic Obesity and Vascular Research (HI-MAG) of the Helmholtz Zentrum München at the University of Leipzig and University Hospital Leipzig, Leipzig, Germany.

Martha Hanschkow (M)

University Hospital for Children and Adolescents, Center for Pediatric Research, Medical Faculty, University of Leipzig, Leipzig, Germany.

Anja Hilbert (A)

Department of Psychosomatic Medicine and Psychotherapy, Medical Faculty, University of Leipzig, Leipzig, Germany.

Rami Abou Jamra (R)

University Medical Center Leipzig, Institute of Human Genetics, Medical Faculty, University of Leipzig, Leipzig, Germany.

Paula Boczki (P)

University Hospital for Children and Adolescents, Center for Pediatric Research, Medical Faculty, University of Leipzig, Leipzig, Germany.

Gunda Herberth (G)

Department of Environmental Immunology, Helmholtz Centre for Environmental Research-UFZ, Leipzig, Germany.

Andreas Kühnapfel (A)

Institute for Medical Informatics, Statistics and Epidemiology, Medical Faculty, University of Leipzig, Leipzig, Germany.

Yu-Hua Tseng (YH)

Section on Integrative Physiology and Metabolism, Joslin Diabetes Center, Harvard Medical School, Boston, MA, USA.

Claudia Stäubert (C)

Division of Molecular Biochemistry, Rudolf Schönheimer Institute of Biochemistry, Medical Faculty, University of Leipzig, Leipzig, Germany.

Torsten Schöneberg (T)

Division of Molecular Biochemistry, Rudolf Schönheimer Institute of Biochemistry, Medical Faculty, University of Leipzig, Leipzig, Germany.

Peter Kühnen (P)

Institute for Experimental Pediatric Endocrinology, Charité Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, Berlin, Germany.

N William Rayner (NW)

Institute of Translational Genomics, Helmholtz Zentrum München - German Research Center for Environmental Health, Neuherberg, Germany.

Eleftheria Zeggini (E)

Institute of Translational Genomics, Helmholtz Zentrum München - German Research Center for Environmental Health, Neuherberg, Germany.
TUM School of Medicine, Translational Genomics, Technical University of Munich and Klinikum Rechts der Isar, Munich, Germany.

Wieland Kiess (W)

University Hospital for Children and Adolescents, Center for Pediatric Research, Medical Faculty, University of Leipzig, Leipzig, Germany.
LIFE-Leipzig Research Center for Civilization Diseases, Medical Faculty, University of Leipzig, Leipzig, Germany.

Matthias Blüher (M)

Helmholtz Institute for Metabolic Obesity and Vascular Research (HI-MAG) of the Helmholtz Zentrum München at the University of Leipzig and University Hospital Leipzig, Leipzig, Germany.
Medical Department III-Endocrinology, Nephrology, Rheumatology, University of Leipzig, Leipzig, Germany.

Antje Körner (A)

University Hospital for Children and Adolescents, Center for Pediatric Research, Medical Faculty, University of Leipzig, Leipzig, Germany. antje.koerner@medizin.uni-leipzig.de.
Helmholtz Institute for Metabolic Obesity and Vascular Research (HI-MAG) of the Helmholtz Zentrum München at the University of Leipzig and University Hospital Leipzig, Leipzig, Germany. antje.koerner@medizin.uni-leipzig.de.
LIFE-Leipzig Research Center for Civilization Diseases, Medical Faculty, University of Leipzig, Leipzig, Germany. antje.koerner@medizin.uni-leipzig.de.

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