Prevention of pancreatic cancer induction in hamsters by metformin

Matthias B. Schneider, Hosei Matsuzaki, James Haorah, Alexis Ulrich, Jens Standop, Xian Zhong Ding, Thomas E. Adrian, Parviz M. Pour

Research output: Contribution to journalArticlepeer-review

258 Scopus citations

Abstract

Background & Aims: Our previous study suggested that the known promotional effect of a high fat diet, which in hamsters induces peripheral insulin resistance, is related to a compensatory proliferation of islet cells. The present study was to examine whether the prevention of islet cell proliferation can inhibit the promotional effect of a high-fat diet in pancreatic carcinogenesis. Methods: Two groups of high fat-fed hamsters were used. One group received Metformin in drinking water for life (HF+Met group), and the other group served as a control (HF group). At the time when the normalization of the plasma insulin level was expected, all hamsters were treated with the pancreatic carcinogen, N-nitrosobis-(2-oxopropyl)amine, and the experiment was terminated 42 weeks later. Results: Although 50% of the hamsters in the high-fat group developed malignant lesions, none was found in the HF+Met group (P < 0.05). Also, significantly more hyperplastic and premalignant lesions, most of which were found within the islets, were detected in the high-fat group (8.6 lesions/hamster) than in the HF+Met group (1.8 lesions/hamster). Conclusions: The results lend further support on the significant role of islet cells in pancreatic carcinogenesis and may explain the association between pancreatic cancer and obesity, which is usually associated with peripheral insulin resistance.

Original languageEnglish (US)
Article number56493
Pages (from-to)1263-1270
Number of pages8
JournalGastroenterology
Volume120
Issue number5
DOIs
StatePublished - 2001
Externally publishedYes

All Science Journal Classification (ASJC) codes

  • Hepatology
  • Gastroenterology

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