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

Patrick B. White, Kathryn M. Ziegler, Deborah A. Swartz-Basile, Sue S. Wang, Keith D. Lillemoe, Henry A. Pitt, Nicholas Zyromski

Research output: Contribution to journalArticle

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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 (R2 = 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 (R2 = 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.

Original languageEnglish
Pages (from-to)1680-1685
Number of pages6
JournalJournal of Gastrointestinal Surgery
Volume16
Issue number9
DOIs
StatePublished - Sep 2012

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High Fat Diet
Pancreatic Neoplasms
Obesity
Tumor Burden
Fats
Body Weight
Apoptosis
Growth
Diet
Adiponectin
Inbred C57BL Mouse
Adipocytes
Neoplasms
Analysis of Variance
Serum

Keywords

  • Adipokines
  • Diet-induced obesity
  • High-fat diet
  • Obesity
  • Pancreatic cancer

ASJC Scopus subject areas

  • Surgery
  • Gastroenterology

Cite this

White, P. B., Ziegler, K. M., Swartz-Basile, D. A., Wang, S. S., Lillemoe, K. D., Pitt, H. A., & Zyromski, N. (2012). Obesity, But Not High-Fat Diet, Promotes Murine Pancreatic Cancer Growth. Journal of Gastrointestinal Surgery, 16(9), 1680-1685. https://doi.org/10.1007/s11605-012-1931-5

Obesity, But Not High-Fat Diet, Promotes Murine Pancreatic Cancer Growth. / White, Patrick B.; Ziegler, Kathryn M.; Swartz-Basile, Deborah A.; Wang, Sue S.; Lillemoe, Keith D.; Pitt, Henry A.; Zyromski, Nicholas.

In: Journal of Gastrointestinal Surgery, Vol. 16, No. 9, 09.2012, p. 1680-1685.

Research output: Contribution to journalArticle

White, PB, Ziegler, KM, Swartz-Basile, DA, Wang, SS, Lillemoe, KD, Pitt, HA & Zyromski, N 2012, 'Obesity, But Not High-Fat Diet, Promotes Murine Pancreatic Cancer Growth', Journal of Gastrointestinal Surgery, vol. 16, no. 9, pp. 1680-1685. https://doi.org/10.1007/s11605-012-1931-5
White PB, Ziegler KM, Swartz-Basile DA, Wang SS, Lillemoe KD, Pitt HA et al. Obesity, But Not High-Fat Diet, Promotes Murine Pancreatic Cancer Growth. Journal of Gastrointestinal Surgery. 2012 Sep;16(9):1680-1685. https://doi.org/10.1007/s11605-012-1931-5
White, Patrick B. ; Ziegler, Kathryn M. ; Swartz-Basile, Deborah A. ; Wang, Sue S. ; Lillemoe, Keith D. ; Pitt, Henry A. ; Zyromski, Nicholas. / Obesity, But Not High-Fat Diet, Promotes Murine Pancreatic Cancer Growth. In: Journal of Gastrointestinal Surgery. 2012 ; Vol. 16, No. 9. pp. 1680-1685.
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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 (R2 = 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 (R2 = 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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AU - Lillemoe, Keith D.

AU - Pitt, Henry A.

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N2 - 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 (R2 = 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 (R2 = 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.

AB - 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 (R2 = 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 (R2 = 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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