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.