Why the study?
Does returning to a normal diet after a high-fat, low-protein diet alter the progression of coronary artery lesions in female Swiss albino mice?
Does returning to a normal diet after a high-fat, low-protein diet alter the progression of coronary artery lesions in female Swiss albino mice?
Returning to a normal diet after a high-fat, low-protein diet paradoxically exacerbates acute coronary arterial lesions before transitioning to fibrosis and hyperplasia in a mouse model.
May indicate transient vascular vulnerability during refeeding in this model; leaves open relevance to human atherosclerosis.
Female mice of a Swiss albino stock were fed a high‐fat, low‐protein, hypolipotropic diet which produces rapid cardiovascular lesions in this stock of mice. Half of the animals were killed after 45 days and the others were placed back on a diet of normal laboratory chow and killed after one, two and three weeks of refeeding. In animals killed after receiving the experimental diet for 45 days small, focal deposits of hyalin in media of large coronary arteries of the right ventricle was the major change. During the first week of recovery (fed a normal diet) the incidence and severity of arterial lesions increased and within individual hearts arteries of all sizes and in both atria and both ventricles were involved. Following hyalinization an acute arteritis developed that involved all layers of the arterial wall and extended into the perivascular space. After two and three weeks recovery the coronary arteries were characterized by a periarterial fibrosis and by a decrease or absence of the leucocytic reaction. A subendothelial hyperplasia of smooth muscle, arranged longitudinally, was accompanied by an increase in reticular and collagenous fibers. Circular smooth muscle in the media was also hyperplastic.
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Ashburn et al. (1969) studied this question.
Synapse has enriched one closely related paper. Consider it for comparative context: