Cushing Syndrome Due to Surreptitious Glucocorticoid Administration

Quddusi, Shaista; Browne, Patrick; Toivola, Bert; Hirsch, Irl B.

doi:10.1001/archinte.158.3.294

Cited by 32 publications

(24 citation statements)

References 5 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…[4][5][6] A case study of a Pakistani man in United Kingdom and an article by a group of rheumatologists in Pakistan suggest the problem is spread across the Indian subcontinent. 7,8 In India, misuse of many drugs is a result of easy availability of drugs over the counter. This is compounded by a lack of awareness regarding the side effects, by both the patient and the prescriber.…”

Section: Introductionmentioning

confidence: 99%

Use and misuse of glucocorticoids in the community of Raxaul Block, North Bihar

Masih¹,

Stephen²,

Armstrong³

et al. 2015

Trop Doct

View full text Add to dashboard Cite

show abstract

Section: Introductionmentioning

confidence: 99%

Use and misuse of glucocorticoids in the community of Raxaul Block, North Bihar

Masih¹,

Stephen²,

Armstrong³

et al. 2015

Trop Doct

View full text Add to dashboard Cite

show abstract

“…This has been documented in patients with Cushing's syndrome [1], during glucocorticoid treatment [2], in glucocorticoid clinical trials [3], and in conjunction with mental stress [4]. It has even been suggested that high-fat diets cause insulin resistance via increased glucocorticoid production [5].…”

Section: Introductionmentioning

confidence: 99%

Glucocorticoid-induced insulin resistance in skeletal muscles: defects in insulin signalling and the effects of a selective glycogen synthase kinase-3 inhibitor

Wagman²,

2005

View full text Add to dashboard Cite

Aims/hypothesis: Treatment with glucocorticoids, especially at high doses, induces insulin resistance. The aims of the present study were to identify the potential defects in insulin signalling that contribute to dexamethasone-induced insulin resistance in skeletal muscles, and to investigate whether the glycogen synthase-3 (GSK-3) inhibitor CHIR-637 could restore insulin-stimulated glucose metabolism. Materials and methods: Skeletal muscles were made insulin-resistant by treating male Wistar rats with dexamethasone, a glucocorticoid analogue, for 12 days. Insulin-stimulated glucose uptake, glycogen synthesis and insulin signalling were studied in skeletal muscles in vitro. Results: Dexamethasone treatment decreased the ability of insulin to stimulate glucose uptake, glycogen synthesis and glycogen synthase fractional activity. In addition, the dephosphorylation of glycogen synthase by insulin was blocked. These defects were paralleled by reduced insulin-stimulated protein kinase B (PKB) and GSK-3 phosphorylation. While expression of PKB, GSK-3 and glycogen synthase was not reduced by dexamethasone treatment, expression of the p85α subunit of phosphatidylinositol 3-kinase (PI 3-kinase) was increased. Inhibition of GSK-3 by CHIR-637 increased glycogen synthase fractional activity in soleus muscle from normal and dexamethasone-treated rats, although the effect was more pronounced in control rats. CHIR-637 did not improve insulin-stimulated glucose uptake in muscles from dexamethasone-treated rats. Conclusions/interpretation: We demonstrated that chronic dexamethasone treatment impairs insulin-stimulated PKB and GSK-3 phosphorylation, which may contribute to insulin resistance in skeletal muscles. Acute pharmacological inhibition of GSK-3 activated glycogen synthase in muscles from dexamethasone-treated rats, but GSK-3 inhibition did not restore insulinstimulated glucose uptake.

show abstract

“…GLUCOCORTICOIDS INDUCE INSULIN RESISTANCE as observed in patients with Cushing's syndrome and during glucocorticoid treatment (38,39). It is also assumed that glucocorticoids mediate insulin resistance induced by mental stress (42) and high-fat diet (27).…”

mentioning

confidence: 99%