Blocking a digestive hormone may help prevent the spread of diet-induced pancreatic tumours to other areas of the body, a study has found.
Researchers from Georgetown University in the US found that a high-fat diet may promote the growth of pancreatic cancer independent of obesity because of the interaction between dietary fat and cholecystokinin (CCK), a digestive hormone.
CCK is released by the small intestine and is associated with obesity, according to the study published in the American Journal of Physiology - Gastrointestinal and Liver Physiology.
Dietary fat triggers the secretion of CCK; those who follow a diet high in saturated fats often have high levels of CCK.
Previous research has shown that obesity and high-fat diets both together and independently increase the risk of pancreatic cancer.
CCK also regulates regeneration that takes place after partial surgical removal of the pancreas.
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Pancreatic growth and regeneration occurs through interaction of CCK with CCK receptors, proteins that bind to CCK to produce a physiological reaction.
The researchers conducted separate mouse studies involving the interactions between dietary fat, CCK and pancreatic cancer cell growth.
In all studies, half the mice were fed a high-fat diet and the other half followed a normal diet.
In the first study, half of the animals were treated with proglumide, a medication that blocks CCK.
In the second study, the mice had tumours lacking CCK.
In the third study, the mice were deficient in CCK and had pancreatic tumours.
The researchers found that mice treated with proglumide had less tumour growth than the untreated mice, even when fed a high-fat diet.
The mice lacking CCK also did not respond to a high-fat diet. These results suggest that CCK is needed to stimulate the growth of pancreatic cancer.
The high-fat diet-fed mice lacking CCK receptors did not show any tumour growth, suggesting that without receptors to bind to, increased CCK from dietary fat is unable to promote cancer.
Proglumide treatment also protected the mice from the development of excessive fibrous tissue (fibrosis) that can be associated with cancer metastases and resistance to chemotherapy.