https://www.thelancet.com/pdfs/journals/lancet/PIIS0140-6736(14)61375-1.pdf

Cushing's syndrome

I. Introduction: The Adrenal Functional Unit II. Interaction Between Adrenal Medulla and Adrenal Cortex A. Relationship between medullary and cortical cells B. Paracrine control of adrenocortical function by the adrenal medulla C. Gap junctions in the adrenal cortex D. Summary III. Innervation of the Adrenal Cortex A. Evidence for a nerve supply to the adrenal cortex B. The source of adrenocortical innervation C. Regulation of adrenocortical innervation D. Role of the splanchnic nerve in regulating adrenocortical neural function E. Influence of adrenal innervation on adrenocortical function F. Effects of neurotransmitter substances on adrenocortical function G. Summary IV. The Vascular System of the Adrenal Gland A. Regulation of blood flow B. Relationship between blood flow and steroid secretion C. Effects of vascular endothelial cell products on steroid secretion D. Summary V. The Intraadrenal CRH/ACTH System A. Extrapituitary effect of CRH B. Intraadrenal ACTH C. Intraadrenal CRH and CRH receptors D. F...

Intraadrenal Interactions in the Regulation of Adrenocortical Steroidogenesis

Cushing's syndrome is usually caused by the secretion of corticotropin or cortisol by a pituitary or adrenal tumor, respectively, or by ectopic secretion of corticotropin. It is possible to determine the specific abnormality in most patients, but it can sometimes be difficult to decide whether the patient has hypercortisolism and whether it is primary or due to major depressive disorder or to the stress of other diseases. Determining the cause of the hypercortisolism involves performing multiple tests in a logical sequence; the results should all be consistent with the same diagnosis. Treatment should aim to cure the hypercortisolism and to eliminate any tumor that threatens the patient's health, while minimizing the chance of an endocrine deficiency or long-term dependence on medications.

Cushing's Syndrome

Peptide hormones within the secretin-glucagon family are expressed in endocrine cells of the pancreas and gastrointestinal epithelium and in specialized neurons in the brain, and subserve multiple biological functions, including regulation of growth, nutrient intake, and transit within the gut, and digestion, energy absorption, and energy assimilation. Glucagon, glucagon-like peptide-1, glucagon-like peptide-2, glucose-dependent insulinotropic peptide, growth hormone-releasing hormone and secretin are structurally related peptides that exert their actions through unique members of a structurally related G protein-coupled receptor class 2 family. This review discusses advances in our understanding of how these peptides exert their biological activities, with a focus on the biological actions and structural features of the cognate receptors. The receptors have been named after their parent and only physiologically relevant ligand, in line with the recommendations of the International Union of Pharmacology Committee on Receptor Nomenclature and Drug Classification (NC-IUPHAR).

https://pharmrev.aspetjournals.org/content/pharmrev/55/1/167.full.pdf

International Union of Pharmacology. XXXV. The Glucagon Receptor Family

Background. Some patients with Cushing's syndrome have nodular adrenal hyperplasia. In most the disease is corticotropin-dependent, but in others it is corticotropin-independent. The cause of the adrenal hyperplasia in the latter patients is not known. Methods. We studied a 49-year-old woman with Cushing's syndrome and nodular adrenal hyperplasia in whom food stimulated cortisol secretion. Plasma cortisol concentrations were measured in response to the ingestion of mixed meals, glucose, protein, and fat and after the administration of various gastrointestinal and other types of hormones. We also studied the ability of the long-acting somatostatin analogue octreotide to prevent the food-induced increase in plasma cortisol concentrations and to ameliorate the clinical manifestations of Cushing's syndrome in this patient. Results. The patient's fasting plasma cortisol concentrations were subnormal, ranging from 3.0 to 7.5 μg per deciliter (83 to 207 nmol per liter), and they increased to as high as ...

https://www.nejm.org/doi/pdf/10.1056/NEJM199210013271403

Food-dependent Cushing's syndrome mediated by aberrant adrenal sensitivity to gastric inhibitory polypeptide.

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Food-dependent Cushing's syndrome mediated by aberrant adrenal sensitivity to gastric inhibitory polypeptide.