title: Interactions among pro-inflammatory cytokines, IGF system and thyroid function in pre-pubertal obese subjects.
abstract: Obesity is a state of chronic inflammation. Data on IGF system are often discrepant, and their relationships with mediators of inflammation are unknown. Furthermore, changes in thyroid function have been reported. We aimed at investigating the changes in these systems, and verify any relationships among cytokines, IGF system, thyroid function and insulin-insensitivity. Fifty obese pre-pubertal children, and 55 normal-weight subjects comparable for age and sex were enrolled. Serum IGF-I, IGF-II, IGFBP-1, IGFBP-2, IGFBP-3, IL-6 and TNF-alpha were assayed. In obese children insulin, TSH and FT4 were measured also, and the HOMA-IR index was calculated. Increased IGF-II, IL-6 and TNF-alpha, and decreased IGFBP-1 and IGFBP-2 concentrations were found in obese compared to normal-weight children. The IGF-I/IGFBP-3 molar ratio was also reduced in the obese subjects. In the obese children with high HOMA-IR index, IGFBP-1 and -2 serum concentrations were significantly decreased compared with those with normal insulin sensitivity, and in the obese subjects with increased TSH, IGFBP-2 concentrations were lower, and IGFBP-3 levels were higher compared to their counterparts with normal TSH levels. Among the significant correlations, BMISDS was correlated with IGF-II, and TSH. IGF-II concentrations showed a positive relationship with IL-6. TSH was correlated with IGFBP-2 also. The data showed interactions among IL-6, IGF system, insulin sensitivity, and thyroid function with changes being related to the degree of obesity. Chronic inflammation in obese children was confirmed. Some of the changes in the IGF system could be a consequence of insulin resistance and could account also for later complications in obese subjects.
authors.forename: M E
authors.initials: ME
authors.lastname: Street
authors.forename: A
authors.initials: A
authors.lastname: Smerieri
authors.forename: L
authors.initials: L
authors.lastname: Montanini
authors.forename: B
authors.initials: B
authors.lastname: Predieri
authors.forename: L
authors.initials: L
authors.lastname: Iughetti
authors.forename: M
authors.initials: M
authors.lastname: Valenzise
authors.forename: F
authors.initials: F
authors.lastname: De Luca
authors.forename: M
authors.initials: M
authors.lastname: Vigone
authors.forename: G
authors.initials: G
authors.lastname: Weber
authors.forename: M
authors.initials: M
authors.lastname: Maghnie
authors.forename: S
authors.initials: S
authors.lastname: Bernasconi
mesh_terms: D015992:Body Mass Index; D001835:Body Weight; D002648:Child; D016207:Cytokines / Q000097:blood*; D005260:Female; D006801:Humans; D018836:Inflammation Mediators / Q000097:blood*; D007333:Insulin Resistance; D018970:Insulin-Like Growth Factor Binding Protein 1 / Q000097:blood; D018971:Insulin-Like Growth Factor Binding Protein 2 / Q000097:blood; D018972:Insulin-Like Growth Factor Binding Protein 3 / Q000097:blood; D007334:Insulin-Like Growth Factor I / Q000378:metabolism; D007335:Insulin-Like Growth Factor II / Q000378:metabolism; D015850:Interleukin-6 / Q000097:blood; D008297:Male; D009765:Obesity / Q000097:blood* / Q000503:physiopathology*; D011627:Puberty / Q000097:blood*; D013002:Somatomedins / Q000378:metabolism*; D013961:Thyroid Gland / Q000503:physiopathology*
chemical_list: D016207:Cytokines; D018836:Inflammation Mediators; D018970:Insulin-Like Growth Factor Binding Protein 1; D018971:Insulin-Like Growth Factor Binding Protein 2; D018972:Insulin-Like Growth Factor Binding Protein 3; D015850:Interleukin-6; D013002:Somatomedins; D007334:Insulin-Like Growth Factor I; D007335:Insulin-Like Growth Factor II