A maternal high fat diet increases the incidence of prostate cancer in male offspring using a transgenic mouse model. — ASN Events

A maternal high fat diet increases the incidence of prostate cancer in male offspring using a transgenic mouse model. (#292)

Tina Bianco-Miotto 1 2 , Himawan Harryanto 1 , Natalie K Ryan 3 , Shalini Jindal 3 , Karen L Kind 1 , Wayne D Tilley 3 , Lisa M Butler 3 , Julie A Owens 1
  1. Robinson Research Institute, School of Paediatrics and Reproductive Health, The University of Adelaide, Adelaide, SA, Australia
  2. School of Agriculture, Food and Wine, The University of Adelaide, Adelaide, SA, Australia
  3. Dame Roma Mitchell Cancer Research Laboratories & Adelaide Prostate Cancer Research Centre, The University of Adelaide and Hanson Institute, Adelaide, SA, Australia

Prostate cancer is the most commonly diagnosed cancer in Australian men. Like many other cancers, obesity increases the risk of developing prostate cancer. Increasing evidence suggests that maternal obesity, often a result of a high fat diet (HFD), is a cause of high birth weight offspring. High birth weight offspring are more likely to be obese as adults and birth weight and adult obesity are both positively associated with cancer risk. The aim of this study was to use a transgenic mouse model of prostate cancer (TRAMP) to provide direct evidence that a HFD early in life increased the incidence of prostate cancer in adulthood. Female TRAMP mice (5 weeks of age) were fed a control (7% total fat) or HFD (23% total fat) for 3 weeks before mating and throughout pregnancy and lactation. Offspring were weaned onto standard chow at 3 weeks of age. Offspring were culled at 14 weeks when the incidence of prostate cancer in the TRAMP is 20%. There were no differences in body weights, prostate or other organ weights. However, omental and perigonadal fat was significantly higher in the male offspring exposed to a maternal HFD compared to the CON offspring (P<0.05). Preliminary histological analysis of the prostates from 12 offspring, 6 exposed to CON diet (n=3 dams) and 6 exposed to a HFD (n=3 dams) has identified 1 case of cancer in the CON group and 3 in the HFD group, each offspring from a different mum. Histological assessment from additional mice is currently underway. We have shown for the first time, using a mouse model of prostate cancer, that a maternal HFD is associated with an increased incidence of cancer in offspring. Our next step is identifying the molecular mechanisms involved and to test dietary interventions.

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