Analysis of serum leptin levels and leptin gene mutations is a rapid and easy step toward the diagnosis of congenital leptin deficiency that is considered an important cause in early childhood obesity.
We aimed to investigate a possible sleep-gene interaction for childhood obesity risk, and whether the interaction in childhood longitudinally contributes to obesity risk at a 10-year follow-up and further to test if there is any mediation through the leptin pathway.
Four significant risk factors for OSA were identified: maternal obesity/diabetes during pregnancy (OR, 1.63; 95% CI, 1.21-2.21; P = .001), preterm/low birth weight (OR, 1.74; 95% CI, 1.30-2.32; P < .001), early childhood obesity (OR, 1.89; 95% CI, 1.37-2.62; P < .001), and high leptin levels in early childhood (OR, 1.94; 95% CI, 1.22-3.09; P = .005).
The present study evaluates the relationship between leptinG2548A (rs7799039) and leptin receptors (rs1137101" genes_norm="3953">Gln223Arg (rs1137101) genotyping and its leptin level and the risk of childhood obesity.
Mutations in the genes encoding leptin (LEP), the leptin receptor (LEPR), and the melanocortin 4 receptor (MC4R) are known to cause severe early-onset childhood obesity.
To the best of our knowledge, this is the first study investigating the relationship between circulating zonulin level (as a marker of intestinal permeability) and insulin resistance and leptin (as markers of metabolic disturbances associated with obesity) in childhood obesity.
The analysis was restricted to studies that examined the effect of exercise interventions on adipokines (adiponectin, leptin, resistin and visfatin) in pediatric obesity (6-18 years old).
We measured bioactive and immunoreactive leptin levels by enzyme-linked immunosorbent assays in fasting serum samples of 70 children with severe (BMI SDS >3) non-syndromic obesity with onset <3 years of life from our Leipzig childhood obesity cohort (n = 1204).
Grandparental and parental weight status and parental serum leptin levels enable us to identify childhood obesity at an early age and may help to counter the current epidemic of adult obesity.
This literature review demonstrated that (1) leptin directly interacts with the hypothalamus for energy balance regulation; (2) the measurement of free, bound and total leptin as well as soluble leptin receptor concentration are critical for our understanding of obesity in children; and (3) leptin concentration may be an important factor for determining intervention programme responsiveness in pediatric obesity.