A spontaneous
high density lipoprotein (HDL) deficiency syndrome in chickens associated with a Z-linked (sex-linked) mutation has been reported (F. Poernama et al, J
Lipid Res 1990;31:955-963). The mutant, called WHAM (Wisconsin hypo-alpha mutant), has a 70-90% reduction in plasma
HDL cholesterol and
apolipoprotein A-I (
apo A-I) concentrations. In the present study, the effect of the HDL deficiency on diet-induced or spontaneous
atherosclerosis was assessed. Control chickens maintained on a high-
cholesterol diet for 28 weeks experienced a 2.4-fold rise in the plasma
very low density lipoprotein cholesterol concentration, while the same diet induced a 3.7-fold rise in the
low density lipoprotein cholesterol concentration in WHAM chickens. The high-
cholesterol diet did not elevate the plasma
HDL cholesterol or
apo A-I concentrations in either group. Both the aortic area of involvement and the width of lesions were quantified by gross and microscopic examination, respectively.
Cholesterol feeding produced a significant increase in the area of the aorta with atherosclerotic lesions in both control and mutant chickens. The HDL deficiency in WHAM chickens did not correlate with a higher lesion area or increased lesion thickness. To assess the effect of HDL deficiency on spontaneous
atherosclerosis, a separate group of control and WHAM chickens was maintained on a low-fat,
cholesterol-free diet for 3 years. At the end of the 3-year period, the area and thickness of the spontaneous aortic lesions in control and WHAM chickens were not significantly different. Spontaneous HDL deficiency in chickens is therefore not associated with increased susceptibility to
atherosclerosis.