In female mammals, it remains controversial whether maternal diet and particularly the source and availability of energy can influence sex of offspring born. Outbred female mice were fed ad libitum from 30 days to Ϸ45 wk of age on defined, complete diets that differed only in their relative content of fat and carbohydrate to determine whether calorie source influenced litter size and sex ratio of pups. Diet 1 (very high in saturated fat, VHF) provided 60% of calories as fat, mainly lard. Diet 2 (low in saturated fat, LF) was low in fat (10% of calories) but high in carbohydrate. Mice delivered four litters of pups, resulting in a total of 1,048 young born over 108 pregnancies. Gestation length and litter size did not differ between VHF and LF groups and did not change as mice aged. Sex ratio of pups (fraction male) born to mothers on VHF diet was unusually high (0.67) and to mothers on LF diet very low (0.39) over litters 2, 3, and 4. This skewing of sex ratio was related to diets fed and not to body mass of mothers. Age of mothers was an important variable, however. Mice that were first bred at 10 wk of age delivered similar numbers of sons and daughters, whereas virgin mice bred later than 20 wk of age produced litters that were skewed toward males or females according to diet. The data show that the source of calories provided in a nutritionally complete diet to mature female mice can influence sex of offspring born.

Since estrogens have vital functions in the uterus but might also contribute to endometrial cancer, we sought to determine the in vitro effects of methyl-piperidino-pyrazole (MPP), raloxifene, and beta-estradiol on Ishikawa and RL-95 endometrial cancer, and ovine luminal endometrial (oLE) cell lines and the in vivo effects of these compounds in the rodent uterus. MPP and raloxifene (1 nM) induced significant apoptosis in the endometrial cancer and oLE cell lines compared to beta-estradiol treated and control cells (P

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