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Obesity, But Not High-Fat Diet, Promotes Murine Pancreatic Cancer Growth
Authors:Patrick B. White  Kathryn M. Ziegler  Deborah A. Swartz-Basile  Sue S. Wang  Keith D. Lillemoe  Henry A. Pitt  Nicholas J. Zyromski
Affiliation: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
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?p?p?p?R 2?=?0.472; p?=?0.008) and serum adiponectin correlated negatively with tumor weight (R?=?0.45; p?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.
Keywords:
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