Skip to main content

Gut barrier dysfunction in the Apc(Min/+) mouse model of colon cancer cachexia.

Publication ,  Journal Article
Puppa, MJ; White, JP; Sato, S; Cairns, M; Baynes, JW; Carson, JA
Published in: Biochim Biophys Acta
December 2011

BACKGROUND: The Apc(Min/+) mouse, an animal model of colorectal cancer and cachexia, has a heterologous mutation in the Apc tumor suppressor gene, predisposing the mouse to intestinal and colon tumor development. This mouse develops intestinal polyps by ~4 weeks of age, and loses body weight gradually between ~14 and ~20 weeks of age. The strengths of this cachexia model derive from several features that mimic human cancer, including a gradual increase in tumor burden, chronic inflammation, and anemia. Little is known about the role of gut barrier dysfunction and endotoxemia in the development of cancer cachexia. We sought to determine how gut permeability and resultant endotoxemia change with the progression of cachexia. METHODS: Intestinal gut barrier integrity was assessed by permeability to FITC-dextran (MW(av)=4000kDa; FD4). Plasma glucose and triglycerides were measured by enzymatic assays, IL-6 by enzyme-linked immunosorbent assay, and endotoxin by the limulus amoebocyte assay. Body temperature was measured using a rectal probe. RESULTS: Progression of cachexia was accompanied by development of gut barrier dysfunction (permeability to FD4), hypertrophy of mesenteric lymph nodes, and an increase in plasma endotoxin concentration. Changes in blood glucose and glucose tolerance, plasma IL-6, triglycerides, and body temperature were characteristic of endotoxemia. CONCLUSION: We propose a role for gut barrier dysfunction (GBD) and subsequent endotoxemia in the development of inflammation and progression of cachexia in the Apc(Min/+) mouse.

Duke Scholars

Altmetric Attention Stats
Dimensions Citation Stats

Published In

Biochim Biophys Acta

DOI

ISSN

0006-3002

Publication Date

December 2011

Volume

1812

Issue

12

Start / End Page

1601 / 1606

Location

Netherlands

Related Subject Headings

  • Tumor Burden
  • Permeability
  • Mice, Transgenic
  • Mice, Inbred C57BL
  • Mice
  • Male
  • Lymph Nodes
  • Interleukin-6
  • Insulin Resistance
  • Hypothermia
 

Citation

APA
Chicago
ICMJE
MLA
NLM
Puppa, M. J., White, J. P., Sato, S., Cairns, M., Baynes, J. W., & Carson, J. A. (2011). Gut barrier dysfunction in the Apc(Min/+) mouse model of colon cancer cachexia. Biochim Biophys Acta, 1812(12), 1601–1606. https://doi.org/10.1016/j.bbadis.2011.08.010
Puppa, Melissa J., James P. White, Shuichi Sato, Mark Cairns, John W. Baynes, and James A. Carson. “Gut barrier dysfunction in the Apc(Min/+) mouse model of colon cancer cachexia.Biochim Biophys Acta 1812, no. 12 (December 2011): 1601–6. https://doi.org/10.1016/j.bbadis.2011.08.010.
Puppa MJ, White JP, Sato S, Cairns M, Baynes JW, Carson JA. Gut barrier dysfunction in the Apc(Min/+) mouse model of colon cancer cachexia. Biochim Biophys Acta. 2011 Dec;1812(12):1601–6.
Puppa, Melissa J., et al. “Gut barrier dysfunction in the Apc(Min/+) mouse model of colon cancer cachexia.Biochim Biophys Acta, vol. 1812, no. 12, Dec. 2011, pp. 1601–06. Pubmed, doi:10.1016/j.bbadis.2011.08.010.
Puppa MJ, White JP, Sato S, Cairns M, Baynes JW, Carson JA. Gut barrier dysfunction in the Apc(Min/+) mouse model of colon cancer cachexia. Biochim Biophys Acta. 2011 Dec;1812(12):1601–1606.

Published In

Biochim Biophys Acta

DOI

ISSN

0006-3002

Publication Date

December 2011

Volume

1812

Issue

12

Start / End Page

1601 / 1606

Location

Netherlands

Related Subject Headings

  • Tumor Burden
  • Permeability
  • Mice, Transgenic
  • Mice, Inbred C57BL
  • Mice
  • Male
  • Lymph Nodes
  • Interleukin-6
  • Insulin Resistance
  • Hypothermia