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Correlations between endocrine-metabolic characteristics and body fat distribution, appetite, growth, and memory in
Ying Zhang1, Xiang Li1, Jian Wen1
1Department of Paediatrics, Pu'er People's Hospital, Pu'er City, Yunnan Province, China.
Insights
Children with Prader-Willi Syndrome (PWS) exhibit significant endocrine-metabolic issues impacting body fat, growth, and memory. These findings highlight multisystem damage in hereditary obesity and guide targeted interventions.
Area of Science:
- Pediatric Endocrinology
- Metabolic Disorders
- Neurodevelopmental Genetics
Background:
- Prader-Willi Syndrome (PWS) is a rare genetic disorder characterized by hyperphagia, obesity, and developmental issues.
- Endocrine and metabolic dysfunctions are common in PWS, but their specific correlations with clinical manifestations require further elucidation.
Purpose of the Study:
- To investigate the relationship between endocrine-metabolic profiles and body fat distribution, appetite, growth, and memory in children with PWS.
- To compare these characteristics between children with PWS, simple obesity, and healthy controls.
Main Methods:
- A cross-sectional study involving 46 children with PWS, 46 with simple obesity, and a healthy control group.
- Measurements included physical development, hyperphagia severity, memory function, hormone levels (e.g., ghrelin, IGF-1, thyroid hormones), and lipid profiles.
- Statistical analyses compared endocrine-metabolic differences and explored correlations within the PWS cohort.
Main Results:
- Children with PWS showed increased overweight, growth retardation, higher body fat, elevated hyperphagia, and reduced memory compared to controls.
- Distinct endocrine-metabolic profiles in PWS included higher ghrelin, triglycerides, total cholesterol, LDL-C, HOMA-IR, and C-peptide, with lower IGF-1, T3, T4, TSH, and HDL-C.
- Significant correlations were found between metabolic markers (e.g., ghrelin, HOMA-IR) and body fat, hyperphagia, BMI, and memory deficits.
Conclusions:
- PWS is associated with significant endocrine-metabolic abnormalities contributing to abnormal body composition, hyperphagia, growth impairment, and cognitive deficits.
- These findings clarify the multisystemic impact of PWS and support the need for tailored clinical management strategies.
- Understanding these correlations is crucial for developing targeted interventions for children with PWS.
Objective:
To explore the correlations between endocrine-metabolic characteristics and body fat distribution, appetite, growth, and memory in children with Prader-Willi Syndrome (PWS).
Methods:
Forty-six children with PWS and forty-six with simple obesity were studied, alongside a healthy control group. Researchers measured physical development, hyperphagia, memory, hormone levels, and lipid profiles. They compared endocrine-metabolic differences across groups and examined correlations between these indicators and body fat, appetite, growth, and memory in children with PWS.
Results:
The PWS group presented overweight, growth retardation, increased body fat, elevated hyperphagia scores and reduced memory scores relative to simple obesity and healthy control groups, with distinct plasma metabolic and endocrine profiles (higher ghrelin, Triglycerides [TG], Total Cholesterol [TC], Low-Density Lipoprotein Cholesterol [LDL-C], Homeostatic Model Assessment of Insulin Resistance [HOMA-IR] and C-peptide; lower Insulin-like Growth Factor-1 [IGF-1], Triiodothyronine [T3], Thyroxine [T4], Thyroid-Stimulating Hormone [TSH] and High-Density Lipoprotein Cholesterol [HDL-C]). Correlation analyses confirmed positive associations of ghrelin, cortisol, and HOMA-IR with Fat Mass Index (FMI); of cortisol and HOMA-IR with hyperphagia score; of TSH, TG, HOMA-IR, and C-peptide with Body Mass Index (BMI); and of IGF-1 and T3 with memory score, as well as negative associations of IGF-1 with FMI and hyperphagia score; of HDL-C with BMI; and of ghrelin with memory score (all p < 0.05).
Conclusion:
Children with PWS present major endocrine-metabolic abnormalities associated with abnormal body fat, hyperphagia, growth retardation, and memory impairment, which help clarify multisystem damage in hereditary obesity and guide targeted clinical interventions.
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