Tumor Biology

, Volume 36, Issue 2, pp 663–667 | Cite as

RETRACTED ARTICLE: Sports-induced blood sugar utilization prevents development of pancreatic ductal adenocarcinoma

Research Article

Abstract

Pancreatic ductal adenocarcinoma (PDAC) is a malignant tumor of extremely high lethality in humans. Pancreatic intraepithelial neoplasia (PanIN) is the predominant precancerous lesion for PDAC and is frequently detected in the normal and inflamed pancreas. However, only a few of PanIN eventually progress into PDAC. Thus, understanding of the regulation of PanIN-to-PDAC conversion appears to be critical for prevention of the occurrence of PDAC. Here, we evaluated the effect of sports on the progression of PanIN into PDAC in an established mouse PDAC model (Ptf1a-Cre; K-ras fx/fx). We found that swimming (3 min twice per day) since 12 weeks of age significantly decreased the incidence of the development of PDAC in these PanIN-baring mice at 24 weeks of age. Moreover, swimming significantly decreased fasting blood sugar and improved glucose response in these mice, compared to the control. Furthermore, implantation of insulin pellets into the mice not only reduced fasting blood sugar and improved glucose response, but also significantly reduced the incidence of development of PDAC, which mimicked the effect of swimming. Taken together, our study suggests that sports-induced blood sugar utilization may prevent development of PDAC.

Keywords

Pancreatic ductal adenocarcinoma Sports Blood sugar Insulin pellet 

Notes

Conflicts of interest

None

References

  1. 1.
    Han H, Von Hoff DD. Snapshot: pancreatic cancer. Cancer Cell. 2013;23:424–4. e421.Google Scholar
  2. 2.
    Shi W, Yin J, Chen Z, Chen H, Liu L, Meng Z. Cyr61 promotes growth of pancreatic carcinoma via nuclear exclusion of p27. Tumour Biol. 2014.Google Scholar
  3. 3.
    di Magliano MP, Logsdon CD. Roles for KRAS in pancreatic tumor development and progression. Gastroenterology. 2013;144:1220–9.CrossRefPubMedPubMedCentralGoogle Scholar
  4. 4.
    Stanger BZ, Hebrok M. Control of cell identity in pancreas development and regeneration. Gastroenterology. 2013;144:1170–9.CrossRefPubMedPubMedCentralGoogle Scholar
  5. 5.
    Arda HE, Benitez CM, Kim SK. Gene regulatory networks governing pancreas development. Dev Cell. 2013;25:5–13.CrossRefPubMedPubMedCentralGoogle Scholar
  6. 6.
    Czako L, Hegyi P, Rakonczay Jr Z, Wittmann T, Otsuki M. Interactions between the endocrine and exocrine pancreas and their clinical relevance. Pancreatology. 2009;9:351–9.CrossRefPubMedGoogle Scholar
  7. 7.
    Henderson JR, Daniel PM, Fraser PA. The pancreas as a single organ: the influence of the endocrine upon the exocrine part of the gland. Gut. 1981;22:158–67.CrossRefPubMedPubMedCentralGoogle Scholar
  8. 8.
    Masoero G, Wormsley KG. Functional interrelationships of exocrine pancreas and endocrine glands in health and disease. Mount Sin J Med New York. 1980;47:261–72.Google Scholar
  9. 9.
    Malka D, Hammel P, Sauvanet A, Rufat P, O’Toole D, Bardet P, et al. Risk factors for diabetes mellitus in chronic pancreatitis. Gastroenterology. 2000;119:1324–32.CrossRefPubMedGoogle Scholar
  10. 10.
    Wang W, Guo Y, Liao Z, Zou DW, Jin ZD, Zou DJ, et al. Occurrence of and risk factors for diabetes mellitus in Chinese patients with chronic pancreatitis. Pancreas. 2011;40:206–12.CrossRefPubMedGoogle Scholar
  11. 11.
    Jackson EL, Willis N, Mercer K, Bronson RT, Crowley D, Montoya R, et al. Analysis of lung tumor initiation and progression using conditional expression of oncogenic K-ras. Genes Dev. 2001;15:3243–8.CrossRefPubMedPubMedCentralGoogle Scholar
  12. 12.
    Gidekel Friedlander SY, Chu GC, Snyder EL, Girnius N, Dibelius G, Crowley D, et al. Context-dependent transformation of adult pancreatic cells by oncogenic K-Ras. Cancer Cell. 2009;16:379–89.CrossRefPubMedPubMedCentralGoogle Scholar
  13. 13.
    Kawaguchi Y, Cooper B, Gannon M, Ray M, MacDonald RJ, Wright CV. The role of the transcriptional regulator Ptf1a in converting intestinal to pancreatic progenitors. Nat Genet. 2002;32:128–34.CrossRefPubMedGoogle Scholar
  14. 14.
    Xiao X, Wiersch J, El-Gohary Y, Guo P, Prasadan K, Paredes J, et al. TGFbeta receptor signaling is essential for inflammation-induced but not beta-cell workload-induced beta-cell proliferation. Diabetes. 2013;62:1217–26.CrossRefPubMedPubMedCentralGoogle Scholar
  15. 15.
    Can A, Dao DT, Arad M, Terrillion CE, Piantadosi SC, Gould TD. The mouse forced swim test. J Vis Exp. 2012;e3638.Google Scholar
  16. 16.
    Xiao X, Guo P, Chen Z, El-Gohary Y, Wiersch J, Gaffar I, et al. Hypoglycemia reduces vascular endothelial growth factor a production by pancreatic beta cells as a regulator of beta cell mass. J Biol Chem. 2013;288:8636–46.CrossRefPubMedPubMedCentralGoogle Scholar
  17. 17.
    Bonner-Weir S, Trent DF, Weir GC. Partial pancreatectomy in the rat and subsequent defect in glucose-induced insulin release. J Clin Invest. 1983;71:1544–53.CrossRefPubMedPubMedCentralGoogle Scholar

Copyright information

© International Society of Oncology and BioMarkers (ISOBM) 2014

Authors and Affiliations

  1. 1.Key Laboratory of Adolescent Health Assessment and Exercise Intervention, Ministry of Education, School of Physical Education and HealthEast China Normal UniversityShanghaiChina
  2. 2.School of Medical ScienceAichi Medical UniversityNagakuteJapan

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