title: Adrenocortical tumors and insulin resistance: What is the first step?
abstract: The pathogenetic mechanisms underlying the onset of adrenocortical tumors (ACTs) are still largely unknown. Recently, more attention has been paid to the role of insulin and insulin-like growth factor (IGF) system on general tumor development and progression. Increased levels of insulin, IGF-1 and IGF-2 are associated with tumor cell growth and increased risk of cancer promotion and progression in patients with type 2 diabetes. Insulin resistance and compensatory hyperinsulinemia may play a role in adrenal tumor growth through the activation of insulin and IGF-1 receptors. Interestingly, apparently non-functioning ACTs are often associated with a high prevalence of insulin resistance and metabolic syndrome. However, it is unclear if ACT develops from a primary insulin resistance and compensatory hyperinsulinemia or if insulin resistance is only secondary to the slight cortisol hypersecretion by ACT. The aim of this review is to summarize the current evidence regarding the relationship between hyperinsulinemia and adrenocortical tumors.
authors.affiliation: Institute of Medical Pathology, Division of Endocrinology and Metabolic Diseases, Catholic University, Rome, Italy.
authors.forename: Barbara
authors.initials: B
authors.lastname: Altieri
authors.affiliation: Division of Endocrinology, Department of Clinical and Molecular Sciences, Umberto I Hospital, Polytechnic University of Marche, Ancona, Italy.
authors.forename: Giacomo
authors.initials: G
authors.lastname: Tirabassi
authors.affiliation: Institute of Medical Pathology, Division of Endocrinology and Metabolic Diseases, Catholic University, Rome, Italy.
authors.forename: Silvia
authors.initials: S
authors.lastname: Della Casa
authors.affiliation: Endocrine and Diabetes Unit, Department of Internal Medicine I, University Hospital, University of Wuerzburg, Wuerzburg, Germany.
authors.forename: Cristina L
authors.initials: CL
authors.lastname: Ronchi
authors.affiliation: Division of Endocrinology, Department of Clinical and Molecular Sciences, Umberto I Hospital, Polytechnic University of Marche, Ancona, Italy.
authors.forename: Giancarlo
authors.initials: G
authors.lastname: Balercia
authors.affiliation: Department of Sports Science and Wellness, Parthenope University, Naples, Italy.|Department of Endocrinology and Diabetology, Fertility Techniques Structure, University Hospital S. Giovanni Di Dio E Ruggi D'aragona, Salerno, Italy.
authors.forename: Francesco
authors.initials: F
authors.lastname: Orio
authors.affiliation: Institute of Medical Pathology, Division of Endocrinology and Metabolic Diseases, Catholic University, Rome, Italy.
authors.forename: Alfredo
authors.initials: A
authors.lastname: Pontecorvi
authors.affiliation: Department of Clinical Medicine and Surgery, Section of Endocrinology, Federico II University, Naples, Italy.
authors.forename: Annamaria
authors.initials: A
authors.lastname: Colao
authors.affiliation: Department of Clinical Medicine and Surgery, Section of Endocrinology, Federico II University, Naples, Italy.
authors.forename: Giovanna
authors.initials: G
authors.lastname: Muscogiuri
mesh_terms: D000306:Adrenal Cortex Neoplasms / Q000378:metabolism* / Q000473:pathology / Q000628:therapy; D000310:Adrenal Gland Neoplasms / Q000378:metabolism* / Q000473:pathology / Q000628:therapy; D000818:Animals; D006801:Humans; D006854:Hydrocortisone / Q000378:metabolism; D007328:Insulin / Q000502:physiology; D007333:Insulin Resistance
chemical_list: D007328:Insulin; D006854:Hydrocortisone
keywords: IGF-1R; adrenocortical tumor; cortisol; insulin receptor; insulin resistance