Analysis of glucose-dependent insulinotropic peptide receptor (GIPR) and luteinizing hormone receptor (LHCGR) expression in human adrenocortical hyperplasia

To analyze the aberrant expression of the GIPR and LHCGR in different forms of adrenocortical hyperplasia: ACTH-independent macronodular adrenal hyperplasia (AIMAH), primary pigmented nodular adrenocortical disease (PPNAD) and diffuse adrenal hyperplasia secondary to Cushing's disease (DAHCD)....

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Published in:Arquivos brasileiros de endocrinologia e metabologia 2009-04, Vol.53 (3), p.326-331
Main Authors: Costa, Marcia Helena Soares, Domenice, Sorahia, Latronico, Ana Claudia, Martin, Regina Matsunaga, Nishi, Mirian Yumie, Lucon, Antonio Marmo, Mendonca, Berenice Bilharinho, Fragoso, Maria Candida Barisson Villares
Format: Article
Language:English
Subjects:
Actins - metabolism
Adolescent
Adrenal Cortex Diseases - genetics
Adrenal Cortex Diseases - metabolism
Adrenal Glands - metabolism
Adrenal Glands - pathology
Adult
Aged
ENDOCRINOLOGY & METABOLISM
Female
Humans
Hyperplasia - metabolism
Male
Middle Aged
Pituitary ACTH Hypersecretion - genetics
Pituitary ACTH Hypersecretion - metabolism
Polymerase Chain Reaction
Receptors, Gastrointestinal Hormone - genetics
Receptors, Gastrointestinal Hormone - metabolism
Receptors, LH - genetics
Receptors, LH - metabolism
Reverse Transcriptase Polymerase Chain Reaction
RNA, Messenger - genetics
RNA, Messenger - metabolism
Young Adult
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Summary:To analyze the aberrant expression of the GIPR and LHCGR in different forms of adrenocortical hyperplasia: ACTH-independent macronodular adrenal hyperplasia (AIMAH), primary pigmented nodular adrenocortical disease (PPNAD) and diffuse adrenal hyperplasia secondary to Cushing's disease (DAHCD). We quantified GIPR and LHCGR expressions using real time PCR in 20 patients with adrenocortical hyperplasia (seven with AIMAH, five with PPNAD, and eight with DAHCD). Normal adrenals tissues were used as control and the relative expression was compared with beta-actin. GIPR and LHCGR expressions were demonstrated in all tissues studied. Median GIPR and LHCGR mRNA levels were 1.6; 0.4; 0.5 and 1.3; 0.9; 1.0 in adrenocortical tissues from AIMAH, PPNAD and DAHCD respectively. There were no differences between GIPR and LHCGR expressions in all tissues studied. GIPR and LHCGR overexpression were not identified in the studied cases, thus suggesting that this molecular mechanism is not involved in adrenocortical hyperplasia in our patients.
ISSN:0004-2730
1677-9487
1677-9487
0004-2730
DOI:10.1590/S0004-27302009000300005