ICEECE2012 Poster Presentations Pituitary Clinical (183 abstracts)
Study on IGF(CA)19 gene polymorphism in adults with GH deficiency
C Giavoli 1, , E Profka 1, , L Olgiati 1, , M Filopanti 1, , S Bergamaschi 1, , E Ferrante 1, , M Arosio 1, , B Ambrosi 1, , A Spada 1, & P Beck-Peccoz 1,
1University of Milan, Milan, Italy; 2Fondazione IRCCS Ca’ Granda, Ospedale Maggiore Policlinico, Milan, Italy; 3Ospedale San Giuseppe, Multimedica, Milan, Italy; 4IRCCS Policlinico San Donato, San Donato Milanese, Italy.
A highly polymorphic microsatellite in the IGF1 gene promoter, composed of variable cytosine-adenine (CA) repeats (n=10–24) has been linked to IGF1 serum concentrations in normal, acromegalic and GHD subjects with conflicting results. Aim of this study was to investigate whether this polymorphism may influence the clinical and biochemical characteristics of adult patients with GHD (n=97). Moreover, the response to 12-month rhGH replacement in terms of IGF1 levels, body composition (BF%), lipid profile and glucose homeostasis was evaluated. According to the most frequent 192 bp allele (equivalent to 19 CA-repeats) patients were divided in three genotype-groups: homozygous for 192 bp allele (192/192, n=7, 7.2%), heterozygous for the 192 bp allele (192/X, n=68, 70.1%) and non-carriers of the 192 bp allele (X/X, n=22, 22.7%). The IGF1 genotype did not influence the clinical and biochemical phenotype of GHD adults at baseline. However, when analyzing 12-month rhGH effects separately in the 3 groups, the increase in IGF1 levels and decrease in BF% were similar, while a worsening of insulin sensitivity, documented by a significant increase in glucose levels and HOMA-IR and by a significant decrease of QUICKI, was observed only in groups carrying at least a wild type allele (192/192 and 192/X). In conclusion, longitudinal follow-up of each genotype group showed that the absence of the wild type allele of the IGF1 gene promoter might protect GHD patients from the short-term worsening of insulin sensitivity induced by rhGH.
Declaration of interest: The authors declare that there is no conflict of interest that could be perceived as prejudicing the impartiality of the research project.
Funding: This research did not receive any specific grant from any funding agency in the public, commercial or not-for-profit sector.
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Endocrine Abstracts
ISSN 1470-3947 (print) | ISSN 1479-6848 (online)
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