Obesity is associated with increased risk for postmenopausal, but not premenopausal breast cancer. Recently, we reported that intact obese Zucker rats had increased susceptibility to DMBA-induced mammary tumors compared to lean Zucker rats. In the present study, we investigated whether excessive adipose tissue would promote mammary tumor induction in the absence of ovarian estrogen. Lean and obese rats were sham-operated or ovariectomized at 40 days old and were gavaged at 50 days old with 65 mg/kg DMBA. Rats were weighed and palpated twice weekly for detection of mammary tumors and sacrificed 135 days post-DMBA treatment. Obese sham-operated (O/S) rats had a shorter latency period (102 days) compared to lean sham-operated (L/S) (134 days) and obese ovariectomized (O/O) rats (123 days). At the end of the experiment, 36% of the O/O rats developed mammary tumors while lean ovariectomized (L/O) rats developed no mammary tumors (P<0.001), and 59% of the O/S rats developed mammary tumors compared to 30% of the L/S rats (P<0.05). In summary, obesity increases the susceptibility of ovariectomized Zucker rats to DMBAinduced mammary tumors, suggesting that adipose tissuederived estrogen in obese animals may be sufficient to promote DMBA-induced tumors in this model. These results suggest that obesity in postmenopausal women may increase breast cancer risk due to increased breast tissue exposure to adipose tissue-derived estrogen. In conclusion, we have developed an animal model to further investigate the role of obesity in breast cancer development in postmenopausal women.

Blood pressure and heart rate in anaesthetized rats has been determined after i.v. injection of increasing doses of nicotine (NI) and its major metabolites, i.e. continine (CO), nornicotine (NOR), metanicotine (MN) and dihydrometanicotine (DMN). NI and MN elicited similar dose response curves, increasing blood pressure according to the dose injected. However, the dose response curve of MN was shifted to the right. Furthermore DMN caused similar pressor effects than MN and the pressor effects of NOR was even weaker. Only after injection of CO was a dose-dependent depressor effect observed and this was reversed after very high doses. CO also reduced heart rate in a dose-dependent manner, whereas NI and its other metabolites did not significantly change heart rate.

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Human and animal studies have suggested that obesity can play important role in promotion of fatty liver. Recently, we have reported that short‐term soy protein diet can reduce fatty liver. The main objective of this experiment was to investigate the long‐term effects of obesity and soy diet on liver steatosis using 7,12‐dimethylbenz(a)anthracene (DMBA)‐Induced mammary tumors in an ovariectomized obese zucker rat model. treatment. Ovariectomized lean (n=56) and Obese (n=60) Zucker rats were maintained on either casein or soy protein diet from one week before and until 155 days after DMBA treatment. All rats were orally gavaged at age 50 days with 65 mg/kg DMBA. Our results demonstrated obesity caused a significant increased on liver weight (P<0.05) and soy diet reduce liver weight in lean and obese group (P<0.05). Obesity caused a significant increase in fatty liver steatosis with rats fed casein diet had marked steatosis with small foci of mononuclear infiltration (P<0.05) but soy‐fed lean (1.00±0.0) and obese (3.20±0.26) rats significantly had lower steatosis than casein‐fed lean (1.96±.16) and obese (4.42±.10) rats. Our results suggest that long‐term dietary soy treatment can protects against liver steatosis in lean and obese ovariectomized animals. The mechanisms responsible for increasing fatty liver steatosis in obese rats are under investigation.