Adrenal incidentalomas: a manifestation of the metabolic syndrome?
Abstract
Recent evidence suggests that insulin is mitogenic on the adrenal cortex and stimulates adrenocortical tumor formation. We, investigated whether hyperinsulinemia is present in 13 patients with incidentally detected adrenal tumors. Patients with adrenal incidentalomas were obese (mean BMI 29.7 +/- 1.2 kg/m2, normal < 25; % body fat 35 +/- 1.5%, normal < 30%) with increased abdominal fat deposition (waist to hip ratio 0.92 +/- 0.02, normal < 0.85). All 13 patients were insulin resistant. Five had NIDDM, of the remaining patients 5 had fasting insulin concentrations above 15 microE/ml, and all 8 patients had elevated insulin concentrations after 75 g of glucose orally. To further investigate the potential role of insulin we examined its effects on the NCI-h295 cell line. Insulin (1-100 micrograms/ml) stimulated cell proliferation in a time and dose-dependent matter without affecting cortisol synthesis. At this concentrations insulin was equally potent to IGF I (10-80 ng/ml) or IGF II (10-100 ng/ml). We conclude that the majority of patients with adrenal incidentalomas are insulin-resistant/hyperinsulinemic. Insulin stimulates adrenal cancer cell lines in vitro. We propose that adrenal incidentalomas are a newly recognized manifestation of the metabolic syndrome comparable to insulin-mediated stimulation of the ovary in the polycystic ovary syndrome.
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Autonomous cortisol secretion in patients with adrenal incidentaloma has been associated with hypertension, insulin resistance, type 2 diabetes mellitus, obesity, metabolic syndrome, and increased mortality.
“Despite the absence of florid signs and symptoms, ACS in patients AI has been associated with hypertension (215), insulin resistance (216), type 2 diabetes mellitus (217), obesity (218), metabolic syndrome (219), and increased mortality (75).”
From Adrenal incidentaloma (2020) · cites this paper as [216]
Insulin is mitogenic, capable of stimulating adrenal cortex cell proliferation and tumor formation in a time- and dose-dependent manner without affecting cortisol synthesis.
“In fact, it has been demonstrated that insulin is mitogenic, capable of stimulating adrenal cortex cell proliferation and tumor formation in a time-and dose-dependent manner, without affecting cortisol synthesis (, ).”
From Glucose Metabolism Abnormalities in Cushing Syndrome: From Molecular Basis to Clinical Management (2017) · cites this paper as [218]
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“Despite the absence of florid signs and symptoms, ACS in patients AI has been associated with hypertension (215), insulin resistance (216), type 2 diabetes mellitus (217), obesity (218), metabolic syndrome (219), and increased mortality (75).”
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- Authors
- Reincke, M., Faßnacht, M., Väth, S., Mora, P., & Allolio, B.
- Affiliations
- University of Würzburg (DE)
- Venue
- Endocrine Research
- Publisher
- Informa UK Limited
- Published
- 1996-11
- Volume
- 22
- Issue
- 4
- Pages
- 757-761
- ISSN
- 0743-5800 (ISSN-L)
- 1532-4206
- OpenAlex
- W1904058160
- Cited by
- 133
- References
- 8
- Citations by year
- 2025: 3 · 2024: 4 · 2023: 13 · 2022: 6 · 2021: 1 · 2020: 8 · 2019: 4 · 2018: 7 · 2017: 6 · 2016: 2 · 2015: 6 · 2014: 5 · 2013: 2 · 2012: 7
- FWCI
- 2.07
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Endocrine Research (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Surgery › Adrenal and Paraganglionic Tumors
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adrenal Hormones and Disorders
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Hormonal Regulation and Hypertension
- Keywords
- adrenal incidentaloma, metabolic syndrome, hyperinsulinemia, insulin resistance, obesity, abdominal fat deposition, type 2 diabetes, insulin-like growth factor I, insulin-like growth factor II
- MeSH terms
- Adrenal Cortex Neoplasms, Body Constitution, Cell Division, Diabetes Mellitus, Type 2, Humans, Hyperinsulinism, Hypertension, Insulin, Insulin Resistance, Obesity, Body Mass Index
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