Obesity, But Not High-Fat Diet, Promotes Murine Pancreatic Cancer Growth |
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Authors: | Patrick B White Kathryn M Ziegler Deborah A Swartz-Basile Sue S Wang Keith D Lillemoe Henry A Pitt Nicholas J Zyromski |
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Institution: | 1. Department of Surgery, Indiana University School of Medicine, 535 Barnhill Dr. RT 130, Indianapolis, IN, 46202, USA 2. Richard L. Roudebush VA Medical Center, Indianapolis, IN, 46202, USA
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Abstract: | 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. |
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