Comparison of aortic and adrenal glandular lipids between non-arteriosclerotic and arteriosclerotic rats

Abstract

Repeatedly bred male and female rats develop arteriosclerosis spontaneously. Despite hyperlipidaemia, fatty liver and obesity the arterial lesions contain minuscule quantities of lipid. Because histopathological lipid techniques may not detect bound or “masked” lipid, we used thin layer chromatography, which affords extra sensitivity in detecting small quantities of lipids. A survey was made of the lipids in female breeder aortae on the basis of the severity of their grossly-visible arteriosclerosis. The aortae were divided into arch, thoracic and abdominal aortic segments to further delineate any lipid changes, according to the anatomical pathogenesis of the arterial disease. Adrenal lipid changes were also analysed by the TLC procedure, comparing adrenal glands of non-arteriosclerotic animals with those having severe, grossly visible arteriosclerosis.

The TLC method demonstrated that small quantities of lipid accumulate in the aortae of repeatedly bred rats, first in the abdominal aortic segment, increasing in concentration with progressive severity of arteriosclerosis and spreading from abdominal aorta to arch and thoracic aorta. Specifically, phospholipids, free fatty acids, cholesterol, di- and triglycerides are increased whereas cholesterol ester is decreased as arteriosclerosis becomes more advanced. Adrenocortical di- and triglycerides were found to be greatly increased in those animals having severe, grossly visible arteriosclerosis. However, total cholesterol was reduced. These adrenal lipid changes are construed to be a reflection of the eventual impairment of the steroidogenic capacity of arteriosclerotic breeder rats. Our conclusions are that the stimulation of the hypothalamic-pituitary-adrenal-gonadal axis occasioned by repeated breeding invokes first a condition of hyperadrenocorticism, followed by adrenal “exhaustion”. The excess adrenal (and gonadal) steroids condition these animals towards hyperlipidaemia, fatty metamorphosis of the liver and obesity. However, these endogenous lipid changes do not contribute directly to the pathogenesis of the arterial lesions.