In:
European Journal of Endocrinology, Oxford University Press (OUP), Vol. 162, No. 4 ( 2010-04), p. 729-735
Abstract:
Glucocorticoids (GCs), such as prednisolone, are associated with adverse metabolic effects, including glucose intolerance and diabetes. In contrast to the well known GC-induced insulin resistance, the effects of GCs on β-cell function are less well established. We assessed the acute and short-term effects of prednisolone treatment on β-cell function in healthy men. Research design and methods A randomised, double-blind, placebo-controlled trial consisting of two protocols was conducted. In protocol 1 ( n =6), placebo and a single dose of 75 mg of prednisolone were administered. In protocol 2 ( n =23), participants received 30 mg of prednisolone daily or placebo for 15 days. Both empirical and model-based parameters of β-cell function were calculated from glucose, insulin and C-peptide concentrations obtained during standardised meal tests before and during prednisolone treatment (protocols 1 and 2), and 1 day after cessation of treatment (protocol 2). Results Seventy-five milligrams of prednisolone acutely increased the area under the postprandial glucose curve (AUC gluc ; P =0.005), and inhibited several parameters of β-cell function, including AUC c-pep /AUC gluc ratio ( P =0.004), insulinogenic index ( P =0.007), glucose sensitivity ( P =0.02) and potentiation factor ratio (PFR; P =0.04). A 15-day treatment with prednisolone increased AUC gluc ( P 〈 0.001), despite augmented C-peptide secretion ( P =0.05). β-cell function parameters were impaired, including the fasting insulin secretory tone ( P =0.02) and PFR ( P =0.007). Conclusions Acute and short-term exposure to prednisolone impairs different aspects of β-cell function, which contribute to its diabetogenic effects.
Type of Medium:
Online Resource
ISSN:
0804-4643
,
1479-683X
Language:
Unknown
Publisher:
Oxford University Press (OUP)
Publication Date:
2010
detail.hit.zdb_id:
1485160-X
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