Journal article | Zeitschriftenartikel
From monogenic to polygenic obesity: recent advances
The heritability of obesity and body weight in general is high. A small number of confirmed monogenic forms of obesity—the respective mutations are sufficient by themselves to cause the condition in food abundant societies—have been identified by molecular genetic studies. The elucidation of these genes, mostly based on animal and family studies, has led to the identification of important pathways to the disorder and thus to a deeper understanding of the regulation of body weight. The identification of inborn deficiency of the mostly adipocyte-derived satiety hormone leptin in extremely obese children from consanguineous families paved the way to the first pharmacological therapy for obesity based on a molecular genetic finding. The genetic predisposition to obesity for most individuals, however, has a polygenic basis. A polygenic variant by itself has a small effect on the phenotype; only in combination with other predisposing variants does a sizeable phenotypic effect arise. Common variants in the first intron of the ‘fat mass and obesity associated’ gene (FTO) result in an elevated body mass index (BMI) equivalent to approximately +0.4 kg/m² per risk allele. The FTO variants were originally detected in a genome wide association study (GWAS) pertaining to type 2 diabetes mellitus. Large meta-analyses of GWAS have subsequently identified additional polygenic variants. Up to December 2009, polygenic variants have been confirmed in a total of 17 independent genomic regions. Further study of genetic effects on human body weight regulation should detect variants that will explain a larger proportion of the heritability. The development of new strategies for diagnosis, treatment and prevention of obesity can be anticipated.
- Umfang
-
Seite(n): 297-310
- Sprache
-
Englisch
- Anmerkungen
-
Status: Postprint; begutachtet (peer reviewed)
- Erschienen in
-
European Child & Adolescent Psychiatry, 19(3)
- Thema
-
Medizin und Gesundheit
Medizin, Sozialmedizin
- Ereignis
-
Geistige Schöpfung
- (wer)
-
Hinney, Anke
Vogel, Carla I. G.
Hebebrand, Johannes
- Ereignis
-
Veröffentlichung
- (wo)
-
Deutschland
- (wann)
-
2010
- DOI
- URN
-
urn:nbn:de:0168-ssoar-214134
- Rechteinformation
-
GESIS - Leibniz-Institut für Sozialwissenschaften. Bibliothek Köln
- Letzte Aktualisierung
-
21.06.2024, 16:27 MESZ
Datenpartner
GESIS - Leibniz-Institut für Sozialwissenschaften. Bibliothek Köln. Bei Fragen zum Objekt wenden Sie sich bitte an den Datenpartner.
Objekttyp
- Zeitschriftenartikel
Beteiligte
- Hinney, Anke
- Vogel, Carla I. G.
- Hebebrand, Johannes
Entstanden
- 2010
Ähnliche Objekte (12)
From monogenic to polygenic obesity: recent advances
The Polygenic and Monogenic Basis of Paediatric Fractures
Polygenic risk alters the penetrance of monogenic kidney disease
Monogenic and polygenic concepts in chronic kidney disease (CKD)
Recent advances in polygenic scores: translation, equitability, methods and FAIR tools
The Clinical Importance of Differentiating Monogenic Familial Hypercholesterolemia from Polygenic Hypercholesterolemia
Bariatric Surgery for Monogenic Non-syndromic and Syndromic Obesity Disorders
Identifying foetal forebrain interneurons as a target for monogenic autism risk factors and the polygenic 16p11.2 microdeletion
Genetic Mechanisms Highlight Shared Pathways for the Pathogenesis of Polygenic Type 1 Diabetes and Monogenic Autoimmune Diabetes
Studying stress-related epigenetic and metabolic changes in fruit flies and mice through monogenic and polygenic models
Monogenic forms of childhood obesity due to mutations in the leptin gene
Recent advances in optimization
From monogenic to polygenic obesity: recent advances
The Polygenic and Monogenic Basis of Paediatric Fractures
Polygenic risk alters the penetrance of monogenic kidney disease
Monogenic and polygenic concepts in chronic kidney disease (CKD)
Recent advances in polygenic scores: translation, equitability, methods and FAIR tools
The Clinical Importance of Differentiating Monogenic Familial Hypercholesterolemia from Polygenic Hypercholesterolemia
Bariatric Surgery for Monogenic Non-syndromic and Syndromic Obesity Disorders
Identifying foetal forebrain interneurons as a target for monogenic autism risk factors and the polygenic 16p11.2 microdeletion
Genetic Mechanisms Highlight Shared Pathways for the Pathogenesis of Polygenic Type 1 Diabetes and Monogenic Autoimmune Diabetes
Studying stress-related epigenetic and metabolic changes in fruit flies and mice through monogenic and polygenic models
Monogenic forms of childhood obesity due to mutations in the leptin gene
Recent advances in optimization
From monogenic to polygenic obesity: recent advances
The Polygenic and Monogenic Basis of Paediatric Fractures
Polygenic risk alters the penetrance of monogenic kidney disease
Monogenic and polygenic concepts in chronic kidney disease (CKD)
Recent advances in polygenic scores: translation, equitability, methods and FAIR tools
The Clinical Importance of Differentiating Monogenic Familial Hypercholesterolemia from Polygenic Hypercholesterolemia
Bariatric Surgery for Monogenic Non-syndromic and Syndromic Obesity Disorders
Identifying foetal forebrain interneurons as a target for monogenic autism risk factors and the polygenic 16p11.2 microdeletion
Genetic Mechanisms Highlight Shared Pathways for the Pathogenesis of Polygenic Type 1 Diabetes and Monogenic Autoimmune Diabetes
Studying stress-related epigenetic and metabolic changes in fruit flies and mice through monogenic and polygenic models
Monogenic forms of childhood obesity due to mutations in the leptin gene