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A rodent model of rapid-onset diabetes induced by glucocorticoids and high-fat feeding.

Publication ,  Journal Article
Shpilberg, Y; Beaudry, JL; D'Souza, A; Campbell, JE; Peckett, A; Riddell, MC
Published in: Dis Model Mech
September 2012

Glucocorticoids (GCs) are potent pharmacological agents used to treat a number of immune conditions. GCs are also naturally occurring steroid hormones (e.g. cortisol, corticosterone) produced in response to stressful conditions that are thought to increase the preference for calorie dense 'comfort' foods. If chronically elevated, GCs can contribute to the development of type 2 diabetes mellitus (T2DM), although the mechanisms for the diabetogenic effects are not entirely clear. The present study proposes a new rodent model to investigate the combined metabolic effects of elevated GCs and high-fat feeding on ectopic fat deposition and diabetes development. Male Sprague-Dawley rats (aged 7-8 weeks) received exogenous corticosterone or wax (placebo) pellets, implanted subcutaneously, and were fed either a standard chow diet (SD) or a 60% high-fat diet (HFD) for 16 days. Animals given corticosterone and a HFD (cort-HFD) had lower body weight and smaller relative glycolytic muscle mass, but increased relative epididymal mass, compared with controls (placebo-SD). Cort-HFD rats exhibited severe hepatic steatosis and increased muscle lipid deposition compared with placebo-SD animals. Moreover, cort-HFD animals were found to exhibit severe fasting hyperglycemia (60% increase), hyperinsulinemia (80% increase), insulin resistance (60% increase) and impaired β-cell response to oral glucose load (20% decrease) compared with placebo-SD animals. Thus, a metabolic syndrome or T2DM phenotype can be rapidly induced in young Sprague-Dawley rats by using exogenous GCs if a HFD is consumed. This finding might be valuable in examining the physiological and molecular mechanisms of GC-induced metabolic disease.

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Published In

Dis Model Mech

DOI

EISSN

1754-8411

Publication Date

September 2012

Volume

5

Issue

5

Start / End Page

671 / 680

Location

England

Related Subject Headings

  • Weight Gain
  • Triglycerides
  • Receptors, Glucocorticoid
  • Rats
  • Muscular Atrophy
  • Male
  • Leptin
  • Insulin Resistance
  • Insulin
  • Hyperphagia
 

Citation

APA
Chicago
ICMJE
MLA
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Shpilberg, Y., Beaudry, J. L., D’Souza, A., Campbell, J. E., Peckett, A., & Riddell, M. C. (2012). A rodent model of rapid-onset diabetes induced by glucocorticoids and high-fat feeding. Dis Model Mech, 5(5), 671–680. https://doi.org/10.1242/dmm.008912
Shpilberg, Yaniv, Jacqueline L. Beaudry, Anna D’Souza, Jonathan E. Campbell, Ashley Peckett, and Michael C. Riddell. “A rodent model of rapid-onset diabetes induced by glucocorticoids and high-fat feeding.Dis Model Mech 5, no. 5 (September 2012): 671–80. https://doi.org/10.1242/dmm.008912.
Shpilberg Y, Beaudry JL, D’Souza A, Campbell JE, Peckett A, Riddell MC. A rodent model of rapid-onset diabetes induced by glucocorticoids and high-fat feeding. Dis Model Mech. 2012 Sep;5(5):671–80.
Shpilberg, Yaniv, et al. “A rodent model of rapid-onset diabetes induced by glucocorticoids and high-fat feeding.Dis Model Mech, vol. 5, no. 5, Sept. 2012, pp. 671–80. Pubmed, doi:10.1242/dmm.008912.
Shpilberg Y, Beaudry JL, D’Souza A, Campbell JE, Peckett A, Riddell MC. A rodent model of rapid-onset diabetes induced by glucocorticoids and high-fat feeding. Dis Model Mech. 2012 Sep;5(5):671–680.
Journal cover image

Published In

Dis Model Mech

DOI

EISSN

1754-8411

Publication Date

September 2012

Volume

5

Issue

5

Start / End Page

671 / 680

Location

England

Related Subject Headings

  • Weight Gain
  • Triglycerides
  • Receptors, Glucocorticoid
  • Rats
  • Muscular Atrophy
  • Male
  • Leptin
  • Insulin Resistance
  • Insulin
  • Hyperphagia