Obesity, But Not High-Fat Diet, Promotes Murine Pancreatic Cancer Growth

Background

Obesity accelerates pancreatic cancer growth; the mechanisms underlying this association are poorly understood. This study evaluated the hypothesis that obesity, rather than high-fat diet, is responsible for accelerated pancreatic cancer growth.

Methods

Male C57BL/6J mice were studied after 19?weeks of high-fat (60?% fat; n?=?20) or low-fat (10?% fat; n?=?10) diet and 5?weeks of Pan02 murine pancreatic cancer growth (flank).

Results

By two-way ANOVA, diet did not (p?=?0.58), but body weight, significantly influenced tumor weight (p?=?0.01). Tumor weight correlated positively with body weight (R ²?=?0.562; p?<?0.001). Tumors in overweight mice were twice as large as those growing in lean mice (1.2?±?0.2?g vs. 0.6?±?.01?g, p?<?0.01), had significantly fewer apoptotic cells than those in lean mice (0.8?±?0.4 vs 2.4?±?0.5; p?<?0.05), and greater adipocyte volume (3.7 vs. 2.2?%, p?<?0.05). Apoptosis (R ²?=?0.472; p?=?0.008) and serum adiponectin correlated negatively with tumor weight (R?=?0.45; p?<?0.05).

Conclusions

These data suggest that body weight, and not high-fat diet, is responsible for accelerated murine pancreatic cancer growth observed in this model of diet-induced obesity. Decreased tumor apoptosis appears to play an important mechanistic role in this process. The concept that decreased apoptosis is potentiated by hypoadiponectinemia (seen in obesity) deserves further investigation.