Please use this identifier to cite or link to this item: https://hdl.handle.net/2440/80685
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Type: Journal article
Title: Effects of low-dose prednisolone on hepatic and peripheral insulin sensitivity, insulin secretion, and abdominal adiposity in patients with inflammatory rheumatologic disease
Author: Petersons, C.
Mangesldorf, B.
Jenkins, A.
Poljak, A.
Smith, M.
Greenfield, J.
Thompson, C.
Burt, M.
Citation: Diabetes Care, 2013; 36(9):2822-2829
Publisher: Amer Diabetes Assoc
Issue Date: 2013
ISSN: 0149-5992
1935-5548
Statement of
Responsibility: 
Carolyn J. Petersons, Brenda L. Mangelsdorf, Arthur B. Jenkins, Anne Poljak, Malcolm D. Smith, Jerry R. Greenfield, Campbell H. Thompson and Morton G. Burt
Abstract: <h4>Objective</h4>The metabolic effects of low-dose prednisolone and optimal management of glucocorticoid-induced diabetes are poorly characterized. The aims were to investigate the acute effects of low-dose prednisolone on carbohydrate metabolism and whether long-term low-dose prednisolone administration increases visceral adiposity, amplifying metabolic perturbations.<h4>Research design and methods</h4>Subjects with inflammatory rheumatologic disease without diabetes mellitus were recruited. Nine subjects (age, 59 ± 11 years) not using oral glucocorticoids were studied before and after a 7- to 10-day course of oral prednisolone 6 mg daily. Baseline data were compared with 12 subjects (age, 61 ± 8 years) using continuous long-term prednisolone (6.3 ± 2.2 mg/day). Basal endogenous glucose production (EGP) was estimated by 6,6-(2)H2 glucose infusion, insulin sensitivity was estimated by two-step hyperinsulinemic-euglycemic clamp, insulin secretion was estimated by intravenous glucose tolerance test, and adipose tissue areas were estimated by computed tomography.<h4>Results</h4>Prednisolone acutely increased basal EGP (2.44 ± 0.46 to 2.65 ± 0.35 mg/min/kg; P = 0.05) and reduced insulin suppression of EGP (79 ± 7 to 67 ± 14%; P = 0.03), peripheral glucose disposal (8.2 ± 2.4 to 7.0 ± 1.6 mg/kg/min; P = 0.01), and first-phase (5.9 ± 2.0 to 3.9 ± 1.6 mU/mmol; P = 0.01) and second-phase (4.6 ± 1.7 to 3.6 ± 1.4 mU/mmol; P = 0.02) insulin secretion. Long-term prednisolone users had attenuated insulin suppression of EGP (66 ± 14 vs. 79 ± 7%; P = 0.03) and nonoxidative glucose disposal (44 ± 24 vs. 62 ± 8%; P = 0.02) compared with nonglucocorticoid users, whereas basal EGP, insulin secretion, and adipose tissue areas were not significantly different.<h4>Conclusions</h4>Low-dose prednisolone acutely perturbs all aspects of carbohydrate metabolism. Long-term low-dose prednisolone induces hepatic insulin resistance and reduces peripheral nonoxidative glucose disposal. We conclude that hepatic and peripheral insulin sensitivity should be targeted by glucose-lowering therapy for glucocorticoid-induced diabetes.
Keywords: Liver
Humans
Rheumatic Fever
Insulin Resistance
Prednisolone
Glucose
Anti-Inflammatory Agents
Glucose Clamp Technique
Aged
Middle Aged
Female
Male
Adiposity
Carbohydrate Metabolism
Rights: © 2013 American Diabetes Association
DOI: 10.2337/dc12-2617
Published version: http://dx.doi.org/10.2337/dc12-2617
Appears in Collections:Aurora harvest
Medicine publications

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