Abstract:
Background/objective:Data on metabolic impairments in Cushing's syndrome and GH deficiency all suggest that the relationship between cortisol and GH/IGF-I axis in obesity may have a role in the related diseases. However, studies focusing only on one of these hormones are often controversial in paediatrics. We aimed to explore the simultaneous relationship between cortisol and IGF-I with the metabolic alterations in paediatric obesity. Subjects/methods:Retrospective cross-sectional study in a tertiary care center. We recruited 876 (441 males and 435 females) overweight and obese children and adolescents. A complete clinical and biochemical evaluation including OGTT was performed. Cortisol and IGF-I SDS were divided in quartiles and then crossed to explore the reciprocal influence of high/high, low/low, and high/low levels of each one on the metabolic alterations of obesity. Results:Subjects in the higher quartiles of IGF-I-SDS and cortisol had an increased risk of hypertension, hypercholesterolemia, high levels of triglycerides, and reduced HDL cholesterol. Diversely, lower IGF-I-SDS quartiles were associated with higher blood glucose, insulin, insulin resistance, and reduced insulin sensitivity levels with the rise of cortisol quartiles. Conclusions:We observed that apart from glucose metabolism that is associated with low IGF-I and high cortisol levels, the other parameters known to be associated with increased cardiovascular risk were related to high levels of both IGF-I and cortisol, even if within normal range. Cortisol and IGF-I play a complex role in the comorbidities of obesity, and the evaluation of both variables could clarify some of the discordant results.
journal_name
Eur J Endocrinoljournal_title
European journal of endocrinologyauthors
Ricotti R,Solito A,Mariotti Zani E,Caputo M,Genoni G,Barone-Adesi F,Mancioppi V,Agosti E,Aimaretti G,Bellone S,Prodam Fdoi
10.1530/EJE-19-0792subject
Has Abstractpub_date
2020-03-01 00:00:00pages
255-264issue
3eissn
0804-4643issn
1479-683Xpii
EJE-19-0792journal_volume
182pub_type
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