European Journal of Cardiovascular Medicine

Pediatric obesity has emerged as a major global health challenge, affecting millions of children worldwide and contributing to numerous adverse health outcomes. The increasing prevalence of obesity among children has profound implications on growth trajectories, pubertal development, and metabolic health, which in turn influences long-term well-being and risks for chronic diseases. Children with obesity often demonstrate altered growth patterns compared to their normal-weight peers, characterized by greater height during early childhood but with an earlier cessation of growth and advanced pubertal timing. Early puberty in obese children has been associated with complex hormonal and metabolic changes, including increased leptin and sex hormone levels, which mediate growth and the onset of secondary sexual characteristics. These alterations in pubertal timing can have significant physiological and psychological effects, potentially increasing the risk of metabolic syndrome, insulin resistance, cardiovascular diseases, and psychosocial challenges in adolescence and adulthood.^[1][2]

Moreover, pediatric obesity is strongly linked to metabolic dysregulation, including abnormalities in lipid profiles, glucose metabolism, and inflammatory markers. Obese children exhibit higher insulin levels, impaired glucose tolerance, elevated triglycerides, and altered cholesterol fractions when compared to their normal-weight peers. These metabolic disturbances not only predispose children to type 2 diabetes and cardiovascular disease early in life but also reflect the complex interplay between excess adiposity, endocrine function, and genetic and environmental factors.^[3]

Despite extensive research characterizing obesity-related complications, comparative studies evaluating growth patterns, pubertal timing, and metabolic profiles concurrently in pediatric obesity relative to normal-weight children remain limited. Understanding these interrelations is crucial for the development of targeted interventions aimed at optimizing growth and preventing metabolic derangements during critical developmental windows.^[4]

Aim

To compare growth patterns, pubertal timing, and metabolic profile in pediatric obese children versus normal-weight peers.

Objectives

1. To assess and compare physical growth measurements between obese and normal-weight children.
2. To evaluate differences in pubertal timing and progression between the two groups.
3. To analyze metabolic parameters including glucose, insulin, and lipid profiles in obese and normal-weight children.

Source of Data

Data were collected from pediatric patients attending the outpatient pediatric outpatient department of a tertiary care hospital.

Study Design

This was a cross-sectional comparative study examining growth, pubertal development, and metabolic parameters between obese and normal-weight pediatric populations.

Study Location

The study was conducted at the Department of Pediatrics, SRTR Medical College Ambajogai.

Study Duration

The study was carried out from January 2024 to June 2025.

Sample Size

A total of 200 children were enrolled in the study, with 100 children classified as obese and 100 as normal-weight controls, matched by age and sex.

Inclusion Criteria

• Children aged between 6 and 13 years.
• For the obese group: BMI ≥95th percentile for age and sex based on standardized growth charts.
• For the normal-weight group: BMI between 5th and 85th percentile for age and sex.
• Informed consent obtained from parents or guardians.

Exclusion Criteria

• Children with chronic illnesses affecting growth or metabolism (e.g., hypothyroidism, diabetes mellitus, genetic syndromes).
• Use of medications known to affect weight, growth, or pubertal development.
• Children with endocrine disorders or significant acute illness at the time of study.

Procedure and Methodology

Participants underwent detailed clinical evaluation including anthropometric measurements (height, weight, BMI calculation). Pubertal staging was assessed using Tanner’s criteria by a trained pediatrician. Blood samples were collected after overnight fasting to measure metabolic parameters including fasting glucose, insulin, lipid profile (total cholesterol, LDL, HDL, triglycerides). Insulin resistance was estimated using the Homeostasis Model Assessment of Insulin Resistance (HOMA-IR).

Sample Processing

Blood samples were processed in the central laboratory of the hospital using standardized assays. Plasma glucose was measured using the glucose oxidase method, insulin by enzyme-linked immunosorbent assay (ELISA), and lipid profile by enzymatic colorimetric techniques. Quality controls and calibration of instruments were conducted regularly to ensure accuracy.

Statistical Methods

Data were analyzed using SPSS version 25. Continuous variables were tested for normality using the Shapiro-Wilk test. Means were compared using independent t-tests or Mann-Whitney U tests as appropriate. Categorical data were analyzed using chi-square tests. Correlations between metabolic parameters and pubertal stages were assessed with Pearson’s or Spearman’s correlation coefficients. A p-value <0.05 was considered statistically significant.

Data Collection

Relevant demographic, clinical and laboratory data were collected using standardized data collection forms. Pubertal staging and anthropometric measurements were recorded during clinic visits, while laboratory data were retrieved from the hospital laboratory reports. Data confidentiality was maintained throughout.

Table 1: Comparison of Growth, Pubertal Timing, and Metabolic Profile

The data summarized in Table 1 indicate that children with obesity had significantly greater height compared to their normal-weight peers, with mean heights of 138.96 cm versus 135.25 cm, respectively (mean difference 3.72 cm; 95% CI 0.98 to 6.45; p=0.008). However, the age at puberty onset was notably earlier in obese children (mean 9.32 years) than in normal-weight children (mean 10.91 years), with a mean difference of -1.60 years (95% CI -2.12 to -1.08) indicating accelerated pubertal timing in obesity. Metabolically, obese children showed higher fasting glucose levels (94.33 vs. 86.85 mg/dL), fasting insulin (22.17 vs. 12.97 µIU/mL), and triglycerides (156.86 vs. 110.78 mg/dL) compared to normal-weight peers, all with statistically significant differences and clear confidence intervals not crossing zero.

Table 2: Physical Growth Measurements Comparison

Table 2 further details the physical growth comparisons, showing obese children to have significantly higher weight (54.40 kg vs. 37.29 kg), body mass index (BMI) (27.18 vs. 18.41 kg/m²), and waist circumference (88.17 cm vs. 61.01 cm) than the normal-weight group. Height differences echo those from Table 1. All differences were statistically significant with p-values less than 0.01 and clinically meaningful confidence intervals.

Table 3: Pubertal Timing and Progression

Table 3 demonstrates differences in pubertal progression using Tanner staging. Notably, a smaller proportion of obese children were in Tanner stage 1 (6%) compared to normal-weight children (22%), whereas obese children had higher proportions in advanced stages such as stage 4 (28% vs. 15%) and stage 5 (8% vs. 4%). The chi-square test showed a significant overall distribution difference between groups (χ²=14.83, p=0.005), corroborating the earlier puberty onset observed in obese children.

Table 4: Metabolic Parameters Comparison

Metabolic parameters in Table 4 show that obese children had significantly elevated fasting glucose, insulin, and triglycerides compared to normal-weight peers, consistent with increased metabolic risk. Furthermore, obese children exhibited lower HDL cholesterol (39.39 vs. 50.21 mg/dL) and higher LDL cholesterol (114.51 vs. 94.36 mg/dL), underscoring a more atherogenic lipid profile. All these differences were statistically robust, highlighting the metabolic dysregulation associated with pediatric obesity.

Table 1 demonstrated that obese children had significantly greater height than their normal-weight peers, consistent with studies indicating that obese children tend to be taller in early childhood but may have an earlier cessation of growth later in puberty due to advanced skeletal maturation. The observation of significantly earlier pubertal onset among obese children aligns with numerous cross-sectional and longitudinal investigations. Calcaterra V et al. (2025)^[6] in a large multiethnic cohort confirmed childhood obesity is associated with earlier puberty in both girls and boys, with more pronounced effects among girls. Likewise, Li Z et al. (2025)^[7] reported clear trends for earlier thelarche and menarche in obese girls, while pubertal timing in boys showed more variability but a tendency toward earlier gonadarche with obesity. These findings further underscore the role of excess adiposity and its hormonal milieu, such as increased leptin and insulin resistance, in modulating hypothalamic-pituitary-gonadal axis activation. Handakas E et al. (2022)^[8]

Table 2’s physical growth measurements reiterated that obese children presented substantially higher weight, BMI, and waist circumference compared to normal-weight children, paralleling global trends reported by WHO and other epidemiological studies. Central obesity specifically has been implicated as a critical determinant of metabolic risk and pubertal alterations. Shalitin S et al. (2022)^[9]

The pubertal staging differences in Table 3, with obese children distributed more into advanced Tanner stages than their normal-weight counterparts, aligns with the earlier onset and accelerated tempo of puberty observed in obesity. This significant chi-square result highlights the altered pubertal progression pattern in obese children. Jaksic M et al. (2021)^[10]

The metabolic disruptions documented in Table 4, including elevated fasting glucose, insulin, triglycerides, and LDL cholesterol along with reduced HDL cholesterol in obese children, are concordant with established links between pediatric obesity and metabolic syndrome risk factors noted by multiple authors. These lipid and glucose abnormalities contribute to early atherosclerosis and cardiovascular risk. Such metabolic shifts often precede and potentially contribute to altered pubertal timing and accelerated biological aging. Marcus C et al. (2022)^[11]

This comparative study highlights significant differences in growth patterns, pubertal timing and metabolic profiles between pediatric obese children and their normal-weight peers. Obese children showed greater height and physical growth measures while entering puberty significantly earlier than normal-weight peers, indicating accelerated biological maturation. The metabolic profile of obese children was markedly altered, with elevated fasting glucose, insulin, triglycerides, and LDL cholesterol levels accompanied by decreased HDL cholesterol, all reflecting early metabolic risk. These findings emphasize the complex interplay of excess adiposity with endocrine and metabolic pathways in childhood, underscoring the critical importance of early identification and comprehensive management of obesity in children to prevent long-term adverse health outcomes.

LIMITATIONS

The study has several limitations to consider. The cross-sectional design precludes causal inferences about the temporal relationship between obesity and pubertal timing or metabolic changes. The sample size, while moderate, was limited to a single center, which may affect generalizability across different populations and ethnicities. Pubertal staging was assessed clinically without hormonal quantification, which may impact precision. Potential confounders such as socioeconomic status, dietary habits, physical activity, and genetic factors were not controlled and might influence growth and metabolic outcomes. Finally, the study did not include long-term follow-up to evaluate the impact of altered pubertal timing and metabolic profiles on adult health.

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