Twenty‐four‐hour profiles of plasma glucose, insulin, C‐peptide and free fatty acid in subjects with varying degrees of glucose tolerance following short‐term, medium‐dose prednisone (20 mg/day) treatment: evidence for differing effects on insulin secretion and action

Abstract

Objective To determine the time course and prandial effects of short-term, medium-dose prednisone on 24-hour metabolic patterns under standardized conditions. Context Glucocorticoids (GCs) adversely affect glucose homoeostasis but 24-hour profiles of glucose, insulin, C-peptide and free fatty acids (FFAs) following short-term, medium-dose prednisone treatment in persons with varying degrees of glucose tolerance are not well defined. Design An open-label cross-sectional interventional study. Subjects Three groups were prospectively studied: persons with type 2 diabetes (T2DM) (n = 7), persons ‘at risk’ for T2DM (AR) (n = 8) and persons with normal glucose tolerance (NGT) (n = 5). Methods Before and after 3-day treatment with prednisone 20 mg each morning, subjects underwent 24-hour frequent blood sampling. Eucaloric mixed meals were provided at 0800 h, 1200 h and 1800 h. Insulin/glucose ratio provided an estimate of â-cell response to meal stimuli. Measurements Plasma glucose, insulin, C-peptide, haemoglobin A1c and FFA. Results Prednisone induced greater increases in glucose levels from midday (P = 0.001) to midnight (P = 0.02) in the T2DM than the AR and NGT groups. In contrast, insulin (P = 0.03) and C-peptide (P = 0.04) levels decreased postbreakfast in the T2DM group, whereas no changes in the morning but higher C-peptide levels (P = 0.03) from midday to midnight were observed in the AR group. In the T2DM group, insulin/glucose ratio decreased postbreakfast (P = 0.04) and increased postdinner (P = 0.03). Fasting glucose, insulin and C-peptide levels were unchanged in all groups, and FFA levels modestly increased postdinner (P = 0.03) in the NGT group. Conclusion Short-term, medium-dose prednisone treatment induces postprandial hyperglycaemia in T2DM and AR predominantly from midday to midnight because of suppression of insulin secretion followed by decreased insulin action that dissipates overnight. Effective treatment of prednisone-induced hyperglycaemia should target both rapid onset relative insulin deficiency and a less than 24-hour total duration of effect.

Does dipeptidyl peptidase-4 inhibition prevent the diabetogenic effects of glucocorticoids in men with the metabolic syndrome? A randomized controlled trial

“…Recent studies have indicated that GCs additionally impair a and b-cell function (5, 6, 7). In particular, postprandial metabolism is disturbed by GC treatment, resulting in characteristic hyperglycemia during the day and evening (8,9).…”

Glucocorticoid-Induced Hyperglycemia Is Prevalent and Unpredictable for Patients Undergoing Cancer Therapy: An Observational Cohort Study

“…Only an increased gc dose and the interval in hours since the most recent gc dose or meal correlated with hyperglycemia for the bmt and cmt groups. Those positive correlations were expected, because increased doses of gc were previously shown to increase risk of hyperglycemia 18 , a longer interval since the administration of gc reflects the longer biologic half-life of synthetic gc (ranging from 8 hours to 72 hours 24 ), and a shorter interval since the most recent meal likely reflects the postprandial rise in serum glucose 40 . Although we collected data on the duration of gc exposure for the cmt and bmt groups, the duration of gc therapy was not significantly different in our patient groups, and we therefore cannot draw conclusions about a specific duration of gc therapy that leads to a greater hyperglycemia risk.…”

Modeling function–perfusion behavior in liver lobules including tissue, blood, glucose, lactate and glycogen by use of a coupled two-scale PDE–ODE approach

“…In the beginning of the 24-h feeding cycle, rats were fed for the first 2 h, then fasted for the remaining 22 h. For the simulation, glucose profiles corresponding to 2 h of food intake and 22 h of fasting based on 24-h profiles of plasma glucose (cf. Stanhope et al 2008;Yuen et al 2012) were used as periportal input profiles for the model (Fig. 8).…”