ArticleClinics (Sao Paulo, Brazil)2026
Correlations between endocrine-metabolic characteristics and body fat distribution, appetite, growth, and memory in children with Prader-Willi syndrome.
Article in Clinics (Sao Paulo, Brazil), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
objectiveTo explore the correlations between endocrine-metabolic characteristics and body fat distribution, appetite, growth, and memory in children with Prader-Willi Syndrome (PWS).
methodsForty-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.
resultsThe 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).
conclusionChildren 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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