Inhibition of atherosclerosis and myocardial lesions in the JCR:LA-cp rat by beta, beta'-tetramethylhexadecanedioic acid (MEDICA 16).
Atherosclerosis-prone, insulin-resistant JCR:LA-cp male rats were treated from 6 weeks to 39 weeks of age with beta,beta'-tetramethylhexadecanedioic acid (MEDICA 16). Body weights were reduced (13%, P < .001) at 36 weeks without any accompanying decrease in food consumption. The treatment did not cause any significant change in plasma glucose or fasting insulin concentrations. There was a significant decrease in the extreme hyperplasia of the islets of Langerhans (38%, P < .05). The marked VLDL hypertriglyceridemia was decreased by 70% (P < .001), with an accompanying significant reduction in cholesterol concentrations. The severity of raised atherosclerotic lesions on the aortic arch was very markedly reduced (P < .01) in treated rats. This was accompanied by a reduction (P < .01) in the incidence of ischemic myocardial lesions. We conclude that long-term (33 weeks) MEDICA 16 treatment of an animal model for the obesity/insulin-resistant/hyperlipidemic syndrome not only markedly improved lipid metabolism, but also inhibited the development of advanced cardiovascular disease.
Russell
J C
JC
Department of Surgery, University of Alberta, Edmonton, Canada.
Amy
R M
RM
Graham
S E
SE
Dolphin
P J
PJ
Wood
G O
GO
Bar-Tana
J
J
D000818:Animals; D001011:Aorta / Q000473:pathology; D001161:Arteriosclerosis / Q000473:pathology / Q000517:prevention & control*; D001835:Body Weight; D009202:Cardiomyopathies / Q000473:pathology / Q000517:prevention & control*; D004730:Endothelium, Vascular / Q000473:pathology; D008055:Lipids / Q000097:blood; D008264:Macrophages / Q000473:pathology; D008297:Male; D008855:Microscopy, Electron, Scanning; D010169:Palmitic Acids / Q000627:therapeutic use*; D010179:Pancreas / Q000473:pathology; D051381:Rats; D011922:Rats, Mutant Strains
D008055:Lipids; D010169:Palmitic Acids; C056166:MEDICA 16