ArticleBMC endocrine disorders2026
Metabolic risk profiling in childhood obesity through hormonal dysfunction and genetic variants: findings from a retrospective study.
Article in BMC endocrine disorders, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundChildhood obesity is frequently accompanied by endocrine dysfunction and genetic susceptibility, but their combined contribution to metabolic risk remains insufficiently defined. This retrospective study evaluated hormonal, metabolic, and genetic determinants of metabolic syndrome (MetS) in children and adolescents with obesity.
methodsElectronic medical records from January 2021 to May 2025 were reviewed. A total of 429 children and adolescents with obesity were included. Clinical, biochemical, endocrine, and targeted SNP genotyping data for FTO rs9939609, MC4R rs17782313, and LEPR rs1137101 were analyzed. MetS was defined according to pediatric criteria. Multivariable logistic regression and receiver operating characteristic analysis were performed.
resultsMetS was present in 187 participants (43.6%). Fasting glucose averaged 5.3 ± 0.5 mmol/L, HbA1c averaged 5.24 ± 0.22%, and median HOMA-IR was 4.4 (2.7-5.7). Insulin resistance was observed in 68.0% of Tanner stage I participants and 73.3% of Tanner stage II-V participants. Elevated HOMA-IR was strongly associated with MetS (OR = 2.89, 95% CI: 1.71-4.99, P < 0.001). Leptin was positively associated with MetS risk (OR = 1.32, 95% CI: 1.02-1.70, P = 0.033), whereas adiponectin was inversely associated (OR = 0.63, 95% CI: 0.49-0.80, P < 0.001). FTO and MC4R risk allele carriage independently predicted MetS, with ORs of 1.88 and 1.71, respectively. The combined endocrine-genetic model showed acceptable discrimination (AUC = 0.751).
conclusionInsulin resistance, adipokine imbalance, and FTO/MC4R variants were independently associated with MetS in pediatric obesity. Integrated endocrine-genetic profiling may improve early metabolic risk stratification. CLINICAL TRIAL NUMBER: Not applicable.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.