Gastric Inhibitory Polypeptide–Dependent Cortisol Hypersecretion — A New Cause of Cushing's Syndrome
Open Access
- 1 October 1992
- journal article
- case report
- Published by Massachusetts Medical Society in New England Journal of Medicine
- Vol. 327 (14) , 974-980
- https://doi.org/10.1056/nejm199210013271402
Abstract
Corticotropin-independent nodular adrenal hyperplasia is a rare cause of Cushing's syndrome, and the factors responsible for the adrenal hyperplasia are not known. We studied a 48-year-old woman with Cushing's syndrome, nodular adrenal hyperplasia, and undetectable plasma corticotropin concentrations in whom food stimulated cortisol secretion. Cortisol secretion had an inverse diurnal rhythm in this patient, with low-to-normal fasting plasma cortisol concentrations and elevated postprandial cortisol concentrations that could not be suppressed with dexamethasone. The cortisol concentrations increased in response to oral glucose (4-fold increase) and a lipid-rich meal (4.8-fold increase) or a protein-rich meal (2.6-fold increase), but not intravenous glucose. The infusion of somatostatin blunted the plasma cortisol response to oral glucose. Intravenous infusion of gastric inhibitory polypeptide (GIP) for one hour increased the plasma cortisol concentration in the patient but not in four normal subjects. Fasting plasma GIP concentrations in the patient were similar to those in the normal subjects; feeding the patient test meals induced increases in plasma GIP concentrations that paralleled those in plasma cortisol concentrations. Cell suspensions of adrenal tissue from the patient produced more cortisol when stimulated by GIP than when stimulated by corticotropin. In contrast, adrenal cells from normal adults and fetuses or patients with cortisol-producing or aldosterone-producing adenomas responded to corticotropin but not to GIP. Nodular adrenal hyperplasia and Cushing's syndrome may be food-dependent as a result of abnormal responsiveness of adrenal cells to physiologic secretion of GIP. "Illicit" (ectopic) expression of GIP receptors on adrenal cells presumably underlies this disorder. (N Engl J Med 1992;327:974–80.)Keywords
This publication has 34 references indexed in Scilit:
- CT and MR Imaging of Massive Macronodular Adrenocortical DiseaseJournal of Computer Assisted Tomography, 1991
- Familial Cushing's Syndrome Due to Primary Pigmented Nodular Adrenocortical DiseaseNew England Journal of Medicine, 1989
- The postprandial response of gastric inhibitory polypeptide to various dietary fats in man.Journal of the American College of Nutrition, 1988
- Transition from Pituitary-Dependent to Adrenal-Dependent Cushing's SyndromeNew England Journal of Medicine, 1988
- Cushing’s Syndrome due to Bilateral Adrenal Macronodular Hyperplasia with Undetectable ACTH: Cell Culture of Adenoma Cells on Extracellular MatrixHormone Research, 1988
- Gastric inhibitory polypeptide receptor in hamster pancreatic beta cells. Direct cross-linking, solubilization and characterization as a glycoproteinEuropean Journal of Biochemistry, 1986
- Macronodular Adrenal Hyperplasia with Hypothalamic-Pituitary-Adrenal Suppression by Ultra-High-Dose DexamethasoneClinical Neuropharmacology, 1986
- Functional GIP receptors in a hamster pancreatic beta cell line, In 111: Specific binding and biological effectsBiochemical and Biophysical Research Communications, 1984
- RESPONSE OF CIRCULATING SOMATOSTATIN, INSULIN, GASTRIN AND GIP, TO INTRADUODENAL INFUSION OF NUTRIENTS IN NORMAL MANClinical Endocrinology, 1984
- Effect of a combination of gastrin, secretin, cholecystokinin, glucagon, and gastric inhibitory polypeptide on jejunal absorption in man.Gut, 1980