The study led by Dr. Guido Eibl, a member of the Jonsson Cancer Center and a professor in the department of surgery at the David Geffen School of Medicine at UCLA, is the first to model human pancreas cancer in animals. The availability of genetically engineered model mice that have the same mutation found in human pancreas cancer patients- the KR mutation- has made the study of possible causes more feasible because changes in mouse metabolism caused by obesity are similar to those in humans.
Eibl and his colleagues set out to model diet-induced obesity and the development of pancreas cancer in a set of mice and then compare them to genetically identical mice that had not been given a high-fat, high-calorie diet.
Obesity in these mice resembles human obesity in a number of important clinical features, including weight gain and the disturbance of metabolism. The mouse model was ideal for unraveling any underlying biological mechanisms of pancreas cancer put in motion by obesity, the researchers said.
The research team also set parameters to assess the impact of the high-fat, high-calorie diet on mouse pancreas tissue, such as increased inflammation and other biological signs that indicate pancreas problems.
The study showed that the mice fed a diet high in fats and calories gained significantly more weight, had abnormalities in their metabolism and increased insulin levels, and displayed marked pancreas tissue inflammation and development of pancreas intraepithelial neoplasias.
These observations strongly suggest that such a diet leads to weight gain and metabolism disturbances, can cause pancreas inflammation, and promotes pancreas lesions that are precursors to cancer.
The study is published in the journal Cancer Prevention Research.