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West Ashley Library
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Phone: (843) 766-6635
Folly Beach Library
9 a.m. - 5:30 p.m.
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Edgar Allan Poe/Sullivan's Island Library
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Wando Mount Pleasant Library
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Phone: (843) 805-6888
Village Library
9 a.m. - 6 p.m.
Phone: (843) 884-9741
St. Paul's/Hollywood Library
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Glucose metabolism during tumorigenesis in the genetic mouse model of pancreatic cancer.
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- Author(s): Pasquale, Valentina; Dugnani, Erica; Liberati, Daniela; Marra, Paolo; Citro, Antonio; Canu, Tamara; Policardi, Martina; Valla, Libera; Esposito, Antonio; Piemonti, Lorenzo
- Source:
Acta Diabetologica; Sep2019, Vol. 56 Issue 9, p1013-1022, 10p- Subject Terms:
- Source:
- Additional Information
- Abstract: Aim: More than 40% of pancreatic ductal adenocarcinoma (PDAC) patients have glucose intolerance or diabetes. The association has led to two hypotheses: PDAC causes diabetes or diabetes shares risk factors for the development of PDAC. In order to elucidate the relationship between diabetes and PDAC, we investigated the glucose metabolism during tumorigenesis in the LSL-KrasG12D/+; LSL-Trp53R172H/+; and Pdx-1-Cre (KPC) mouse, a genetically engineered model of PDAC. Methods: Male and female KPCs have been fed with standard diet (SD) or high-fat diet (HFD). The imaging-based 4-class tumor staging was used to follow pancreatic cancer development. Not fasting glycemia, 4-h fasting glycemia, insulin, C-peptide, glucose tolerance after OGTT and abdominal fat volume were measured during tumorigenesis. Results: PDAC development did not lead to an overt diabetic phenotype or to any alterations in glucose tolerance in KPC fed with SD. Consumption of HFD induced higher body weight/abdominal fat volume and worsened glucose homeostasis both in control CRE mice and only in early tumorigenesis stages of the KPC mice, excluding that the cancer development itself acts as a trigger for the onset of dysmetabolic features. Conclusion: Our data demonstrate that carcinogenesis in KPC mice is not associated with paraneoplastic diabetes. [ABSTRACT FROM AUTHOR]
- Abstract: Copyright of Acta Diabetologica is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
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