Glucocorticoid excess causes insulin resistance i.e. a reduced effectiveness of insulin to suppress hepatic glucose production and to increase glucose uptake in muscle and fat tissue. Persons who cannot compensate for the resulting additional insulin need develop overt diabetes during glucocorticoid therapy. In the field of gastroenterology, glucocorticoids are mainly employed for the therapy of chronic inflammatory bowel diseases, alcoholic and autoimmune hepatitis, and after liver transplantation. The risk of developing steroid diabetes depends among other things on the genetic predisposition, the body composition, the underlying gastrointestinal disease, the age, and the steroid dose. The treatment of glucocorticoid-induced diabetes resembles essentially the treatment of type 2-diabetes. In addition to dietary measures, oral antihypoglycemic drugs and/or insulin are applied. If oral antihypoglycemic drugs are used, specific problems that might result from the gastrointestinal diseases need to be observed. In the short and medium term, the prognosis of glucocorticoid-induced diabetes is good since it is well treatable. If glucocorticoid treatment is continued for a long time, the alterations of glucose metabolism and the resulting hyperinsulinemia may lead to increased cardiovascular risk.

Download full-text PDF

Source

Publication Analysis

Top Keywords

glucocorticoid-induced diabetes
8
oral antihypoglycemic
8
antihypoglycemic drugs
8
[glucocorticoid-induced diabetes
4
diabetes mellitus
4
mellitus gastrointestinal
4
gastrointestinal diseases]
4
diseases] glucocorticoid
4
glucocorticoid excess
4
insulin
4

Similar Publications

Adrenal insufficiency (AI) is a serious disorder characterized by the adrenal glucocorticoid deficiency. Regardless of the etiology, AI patients need long-term replacement therapy for glucocorticoids and, in some cases, for mineralocorticoids. The replacement therapy cannot completely mirror the physiological secretion patterns, and therefore, glucocorticoid excess is a common sequela in AI patients.

View Article and Find Full Text PDF

Impact of Surreptitious Glucocorticoids in Over-the-Counter Arthritis Supplements.

J Endocr Soc

January 2025

Division of Endocrinology and Diabetes, Keck Medicine of USC, Los Angeles, CA 90033, USA.

Adrenal dysfunction due to over-the-counter (OTC) health supplements containing unlabeled glucocorticoids has been previously reported. Here, we present a case series of 12 patients at an urban safety net medical center evaluated by endocrinology for iatrogenic adrenal dysfunction, Cushing syndrome (CS) and/or adrenal insufficiency (AI), associated with use of OTC arthritis supplements surreptitiously containing glucocorticoids. There were 12 patients using OTC arthritis supplements (Artri King [n = 8], Ardosons [n = 3], Ajo Rey [n = 1]) included.

View Article and Find Full Text PDF

Glucose transporter type 2 (GLUT2), encoded by the Slc2a2 gene, is essential for glucose-stimulated insulin secretion (GSIS) in pancreatic islet β-cells, and low expression of GLUT2 is associated with β-cell dysfunction during the progression of type 2 diabetes in humans and animal models. Glucocorticoids are stress hormones that regulate inflammation and metabolism through the glucocorticoid receptor (GR), a member of the nuclear receptor superfamily, and synthetic glucocorticoids are widely used for the treatment of inflammatory disorders. Prolonged exposure to glucocorticoids induces β-cell dysfunction and diabetes, but the effects of Slc2a2 gene repression in β-cells, if any, and the mechanisms involved remain unclear.

View Article and Find Full Text PDF

Context: Glucocorticoids (GCs) are widely used for their anti-inflammatory and immunosuppressive properties. Their effect on bone health is predominantly negative by decreasing bone formation and increasing risk of fractures.

Objective: This work aimed to quantify the short- and long-term changes in total hip bone mineral density (THBMD) after initiating systemic GC treatment in previously GC treatment-naive adults without bone protective agents.

View Article and Find Full Text PDF

Impact of therapeutic doses of prednisolone and other glucocorticoids on insulin secretion from human islets.

Ann Endocrinol (Paris)

December 2024

University of Lille, CHU de Lille, Inserm U1190, EGID, Institut Pasteur de Lille, 59000 Lille, France. Electronic address:

Introduction: Glucocorticoid-induced diabetes (GCID) is a prevalent health issue, generally attributed to insulin resistance. High doses of dexamethasone (DEX) are known to inhibit glucose-stimulated insulin secretion (GSIS), but the effects of lower doses, commonly used in chronic therapy, and equipotent doses of other glucocorticoids (GCs) such as hydrocortisone (HC) and prednisone (PRED) remain underexplored. This study aimed to investigate these effects in vitro, and explore variations between patients.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!