Document Detail

Atherosclerosis in Octodon degus (degu) as a model for human disease.
MedLine Citation:
PMID:  20630529     Owner:  NLM     Status:  MEDLINE    
OBJECTIVE: Animal models of atherosclerosis are essential to elucidate disease mechanisms and develop new therapies. Each model features advantages and disadvantages in exemplifying the pathophysiology of human atherosclerosis. Diet-induced development of atherosclerosis in Octodon degus (degu) was examined to demonstrate the potential of the degu as a model of human atherosclerosis.
METHODS: Degus were fed for 16 weeks with either normal chow or chow containing 0.25% cholesterol and 6% palm oil to induce atherosclerosis. The lipid compositions of plasma lipoproteins and aortas were determined. Locations of aortic lesions were mapped by imaging of fluorescently stained aortic lesions. Lesion morphology in the brachiocephalic artery was detected by histological staining.
RESULTS: Total plasma cholesterol in chow-fed degus was distributed approximately 60% in HDL, 30% in LDL and less than 10% in VLDL. Cholesterol-fed degus exhibited 4- to 5-fold increases in total plasma cholesterol, principally in the VLDL and LDL fractions. Cholesteryl ester transfer protein activity of similar magnitude to that in human plasma was detected in chow-fed degu plasma. Cholesterol-fed degus developed cholesteryl ester-rich atherosclerotic lesions throughout the aorta. Histological examination of lesions in the brachiocephalic artery showed well-formed, foam cell-rich lesions populated with inflammatory cells. It is also noteworthy that all the degus in this study exhibited hyperglycemia.
CONCLUSION: These results demonstrate that degus have a human-like lipoprotein metabolism and develop extensive atherosclerosis with cholesterol feeding in the presence of hyperglycemia. These features, combined with the manageable size and handling characteristics, point to the potential of the degu as a useful model for atherosclerosis research.
Reynold Homan; Jeffrey C Hanselman; Sandra Bak-Mueller; Michelle Washburn; Patrick Lester; Heather E Jensen; Stephen L Pinkosky; Christine Castle; Bruce Taylor
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Publication Detail:
Type:  Journal Article     Date:  2010-06-11
Journal Detail:
Title:  Atherosclerosis     Volume:  212     ISSN:  1879-1484     ISO Abbreviation:  Atherosclerosis     Publication Date:  2010 Sep 
Date Detail:
Created Date:  2010-09-03     Completed Date:  2010-12-28     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0242543     Medline TA:  Atherosclerosis     Country:  Ireland    
Other Details:
Languages:  eng     Pagination:  48-54     Citation Subset:  IM    
Copyright Information:
Copyright 2010 Elsevier Ireland Ltd. All rights reserved.
AlphaCore Pharma, 333 Parkland Plaza, Suite 5, Ann Arbor, MI, USA.
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MeSH Terms
Aorta / metabolism,  pathology
Aortic Diseases* / blood,  etiology,  pathology
Atherosclerosis* / blood,  etiology,  pathology
Biological Markers / blood
Blood Glucose / metabolism
Brachiocephalic Trunk / metabolism,  pathology
Cholesterol Ester Transfer Proteins / blood
Cholesterol, Dietary / blood
Cholesterol, HDL / blood
Cholesterol, LDL / blood
Cholesterol, VLDL / blood
Disease Models, Animal*
Hyperglycemia / blood,  etiology
Plant Oils
Time Factors
Reg. No./Substance:
0/Biological Markers; 0/Blood Glucose; 0/Cholesterol Ester Transfer Proteins; 0/Cholesterol, Dietary; 0/Cholesterol, HDL; 0/Cholesterol, LDL; 0/Cholesterol, VLDL; 0/Plant Oils; 8002-75-3/palm oil
Comment In:
Atherosclerosis. 2010 Sep;212(1):32-3   [PMID:  20638066 ]

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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