We investigated the mechanisms by which corticosteroids affect atherosclerosis. Male New Zealand White rabbits were injected with 0.125 mg dexamethasone (n = 10) or vehicle (control group, n = 10). Both groups were fed a 1% cholesterol diet for 8 weeks. Although the dexamethasone-treated animals exhibited a greater degree of hvperlipidemia, they exhibited significantly less atherosclerotic plaque of the aortic surface than control animals (7.8% versus 47.2%). Immunofluorescence study of the aortic plaque specimens showed that dexamethasone administration reduced both macrophages and T lymphocytes. In vitro, dexamethasone suppressed the proliferation and differentiation of U937 cells and inhibited uptake and degradation of 0-very low density lipoproteins by mouse peritoneal macrophages. These findings suggest that dexamethasone suppresses the development of atherosclerosis in the aorta of rabbits by inhibiting recruitment and proliferation of macrophages and the formation of foam cells in plaques. {Arteriosclerosis and Thrombosis 1993;13:892-899)

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In 29 healthy young adults and 22 ambulatory elderly subjects, a study was made of the effects of an oral glucose load on the levels of serum immunoreactive insulin (IRI), free fatty acids (FFA), growth hormone (HGH) and blood glucose. In the elderly, the pre‐load blood glucose and serum IRI levels were higher than in the younger group, reached the peak more gradually, and took longer to return to the baseline values. There was no significant difference in the serum FFA levels between the two groups until 3 hours after the glucose load, at which time the FFA values had returned to the fasting level in the young subjects but remained depressed in the elderly subjects. Serum HGH fasting levels in the elderly males were significantly higher than in the younger males and remained so at 1–2 hours after the glucose load. For the females, the numbers were too small and the intragroup variability too great to permit drawing conclusions. The total findings lend support to Dilman's hypothesis of a genetically programmed elevation of the hypothalamic threshold to feedback suppression, with age.

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