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OBJECTIVE: To investigate the effects of hormone replacement therapy (HRT) and social stress on body fat distribution in an animal model of women's health, the female cynomolgus macaque (Macaca fascicularis). DESIGNaSUBJECTS: Adult female cynomolgus monkeys were ovariectomized and fed an atherogenic diet for two years while housed in social groups of 3 ± 8 monkeys each. Animals were then fed a lipid-lowering diet and randomized into four experimental groups: a baseline group which was necropsied immediately and not included in the study reported here, 26 females fed diet only (CONTROL), 22 females fed diet plus conjugated equine estrogens (CEE), and 21 females fed the diet plus CEE and medroxyprogesterone acetate (CEE MPA). Treatment lasted 30 months. MEASUREMENTS: During the last nine months of treatment, social status was determined three times at three month intervals. At the end of the study, whole body obesity and fat distribution patterns were determined using anthropometry and computerized tomography (CT). RESULTS: The addition of a progestin to the estrogen replacement regimen administered to surgically postmenopausal monkeys, increased all anthropometric and CT measures of obesity except intra-abdominal fat. HRT had no effect on patterns of fat distribution. Socially-dominant, ovariectomized females were more obese than subordinates using both anthropometric and CT measurements of whole body obesity. Dominant females were more likely to have their fat deposited centrally as measured anthropometrically. However, CT measures revealed a trend for dominants to preferentially deposit fat in the subcutaneous abdominal depot in contrast to subordinates who deposited fat in the intra-abdominal depot. CONCLUSIONS: The results of this study suggest that progestins, when administered in combination with estrogens, may increase fat deposition, particularly in subcutaneous depots. In addition, the social stress experienced by subordinate monkeys, may have mild effects on fat deposition patterns, even after removal of ovarian function as a factor. These observations may have implications for treatment recommendations in postmenopausal women. Lastly, CT may measure different characteristics of fat distribution than skinfolds and circumferences.

Inbred Carworth Farms Nelson (CFN) congenitally hyperlipidemic rats had significantly shorter coagulation and prothrombin times and higher levels of coagulation factors, II, V, VII, VIII, and X than did controls. Conversely, congenitally hypolipidemic rats of the same strain had significantly longer coagulation and prothrombin times and lower levels of factors II, V, VII, X and XII and of blood platelets than did controls. A loop-shaped polyethylene cannula was inserted into the aorta to assess the potential for thrombosis. The hyperlipidemic group obstructed this significantly faster and the hypolipidemic group slower than did the controls. Normal CFN rats made hypertensive by unilateral renal artery clip developed hypertension together with significantly elevated serum cholesterol and factor VII and X levels. Rhesus monkeys with diet-induced hyperlipidemia showed shorter prothrombin times and higher factor X levels than did controls on normal diet. By selective breeding, two groups of squirrel monkeys were obtained. Both groups had similar serum cholesterol levels on a normal diet but one group (hyperresponders) showed higher serum cholesterol levels on a cholesterol-containing diet than did the other (hyporesponder) group. Both groups showed significantly elevated levels of factors II, V, VII, IX and X on a cholesterol-containing diet. There was good correlation between the levels of many coagulation factors and serum cholesterol in both rats and monkeys. If thrombosis is important in the genesis of atherosclerosis, these findings could indicate that elevation of plasma lipids may play a role, via the coagulation pathway, in the production of human vascular disease.

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