Gewählte Publikation:
SHR
Neuro
Krebs
Kardio
Lipid
Stoffw
Microb
Kohlsdorf, K; Nunziata, A; Funcke, JB; Brandt, S; von Schnurbein, J; Vollbach, H; Lennerz, B; Fritsch, M; Greber-Platzer, S; Fröhlich-Reiterer, E; Luedeke, M; Borck, G; Debatin, KM; Fischer-Posovszky, P; Wabitsch, M.
Early childhood BMI trajectories in monogenic obesity due to leptin, leptin receptor, and melanocortin 4 receptor deficiency.
INT J OBESITY. 2018; 42(9): 1602-1609.
Doi: 10.1038/s41366-018-0049-6
Web of Science
PubMed
FullText
FullText_MUG
- Co-Autor*innen der Med Uni Graz
-
Fritsch Maria
-
Fröhlich-Reiterer Elke
- Altmetrics:
- Dimensions Citations:
- Plum Analytics:
- Scite (citation analytics):
- Abstract:
-
To evaluate whether early childhood body mass index (BMI) is an appropriate indicator for monogenic obesity.
A cohort of n = 21 children living in Germany or Austria with monogenic obesity due to congenital leptin deficiency (group LEP, n = 6), leptin receptor deficiency (group LEPR, n = 6) and primarily heterozygous MC4 receptor deficiency (group MC4R, n = 9) was analyzed. A control group (CTRL) was defined that consisted of n = 22 obese adolescents with no mutation in the above mentioned genes. Early childhood (0-5 years) BMI trajectories were compared between the groups at selected time points.
The LEP and LEPR group showed a tremendous increase in BMI during the first 2 years of life with all patients displaying a BMI >27 kg/m2 (27.2-38.4 kg/m2) and %BMIP95 (percentage of the 95th percentile BMI for age and sex) >140% (144.8-198.6%) at the age of 2 years and a BMI > 33 kg/m2 (33.3-45.9 kg/m2) and %BMIP95 > 184% (184.1-212.6%) at the age of 5 years. The MC4R and CTRL groups had a later onset of obesity with significantly lower BMI values at both time points (p < 0.01).
As result of the investigation of early childhood BMI trajectories in this pediatric cohort with monogenic obesity we suggest that BMI values >27.0 kg/m2 or %BMIP95 > 140% at the age of 2 years and BMI values >33.0 kg/m2 or %BMIP95 > 184% at the age of 5 years may be useful cut points to identify children who should undergo genetic screening for monogenic obesity due to functionally relevant mutations in the leptin gene or leptin receptor gene.