| A rodent model of rapid-onset diabetes (ROD) induced by glucocorticoids and high-fat feeding. | |
| | |
MedLine Citation:
|
PMID: 22184636 Owner: NLM Status: Publisher |
Abstract/OtherAbstract:
|
Glucocorticoids (GC) 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 may contribute to the development of type 2 diabetes mellitus (T2DM), although mechanisms 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 various indexes of insulin resistance that induces rapid-onset diabetes (ROD). Male Sprague-Dawley rats (aged 4 weeks) received exogenous corticosterone or wax (placebo) (4 x 100 mg each) pellets, implanted subcutaneously, and fed either a standard chow diet (SD) or a 60% high-fat diet (HFD) for 16 days (n= 8-10). Animals given corticosterone and a HFD (cort-HFD) had lower body weight (226.1±9.05 versus 358.9±5.57 g, mean ± SEM, p<0.05) and smaller relative glycolytic muscle mass (0.14±0.01 versus 0.09±0.02 g/kg body mass for the epitroclearis muscle, p<0.05), but increased relative epididymal mass (9.81±1.65 versus 4.56±0.54 g/kg, p<0.05), compared to controls (placebo-SD). Cort-HFD rats exhibited severe hepatic steatosis and increased muscle lipid deposition compared to 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 beta cell response (20% decrease) to oral glucose load compared to placebo-SD animals. Thus, a metabolic syndrome/T2DM phenotype can be rapidly induced in young Sprague-Dawley rats by using exogenous GCs if a HFD is consumed. This finding may be valuable in examining the physiological and molecular mechanisms of GC-induced metabolic disease. |
| | |
Authors:
|
Yaniv Shpilberg; Jacqueline L Beaudry; Anna D'Souza; Jonathan E Campbell; Ashley Peckett; Michael C Riddell |
Related Documents
:
|
15817266 - Dietary supplementation with blueberries, spinach, or spirulina reduces ischemic brain ... 18216516 - A biomechanical and morphologic analysis of capsule formation around implanted piezoele... 2912146 - Saturated fatty acid diet prevents radiation-associated decline in intestinal uptake. 12916896 - Heat and mass transfer scale-up issues during freeze-drying, i: atypical radiation and ... 11606036 - Acquisition of texture-cued fasting-anticipatory meal-size change in rats with adequate... 2820026 - High-carbohydrate and fibre diets in the treatment of diabetes. |
Publication Detail:
|
Type: JOURNAL ARTICLE Date: 2011-12-19 |
Journal Detail:
|
Title: Disease models & mechanisms Volume: - ISSN: 1754-8411 ISO Abbreviation: - Publication Date: 2011 Dec |
Date Detail:
|
Created Date: 2011-12-20 Completed Date: - Revised Date: - |
Medline Journal Info:
|
Nlm Unique ID: 101483332 Medline TA: Dis Model Mech Country: - |
Other Details:
|
Languages: ENG Pagination: - Citation Subset: - |
Affiliation:
|
York University, Toronto, Ontario, Canada. |
Export Citation:
|
APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
|
|
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
Previous Document: High-mobility group nucleosome-binding protein 1 acts as an alarmin and is critical for lipopolysacc...
Next Document: Identification of Cis-Acting Promoter Elements in Cold- and Dehydration-Induced Transcriptional Path...