Interleukin-6 and cachexia in ApcMin/+ mice

Kristen A. Baltgalvis, Franklin G. Berger, Maria Marjorette O. Pena, J. Mark Davis, Stephanie J. Muga, James Carson

Research output: Contribution to journalArticle

145 Citations (Scopus)

Abstract

The ApcMin/+ mouse has a mutation in the Apc tumor suppressor gene and develops intestinal polyps, beginning at 4 wk of age. This mouse develops cachexia by 6 mo, characterized by significant loss of muscle and fat tissue. The purpose of the present study was to determine the role of circulating interleukin-6 (IL-6) and the polyp burden for the development of cachexia in ApcMin/+ mice. At 26 wk of age, mice exhibiting severe cachectic symptoms had a 61% decrease in gastrocnemius muscle weight, complete loss of epididymal fat, a 10-fold increase in circulating IL-6 levels, and an 89% increase in intestinal polyps compared with mildly cachectic animals. ApcMin/+/IL-6-/- mice did not lose gastrocnemius muscle mass or epididymal fat pad mass while overall polyp number decreased by 32% compared with ApcMin/+ mice. Plasmid-based IL-6 overexpression in ApcMin/+/IL-6-/- mice led to a decrease in gastrocnemius muscle mass and epididymal fat pad mass and increased intestinal polyp burden. IL-6 overexpression did not induce cachexia in non-tumor-bearing mice. These data demonstrate that IL-6 is necessary for the onset of adipose and skeletal muscle wasting in the ApcMin/+ mouse and that circulating IL-6 can regulate ApcMin/+ mouse tumor burden.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Regulatory Integrative and Comparative Physiology
Volume294
Issue number2
DOIs
StatePublished - Feb 1 2008
Externally publishedYes

Fingerprint

Cachexia
Interleukin-6
Intestinal Polyps
Skeletal Muscle
Polyps
Adipose Tissue
Fats
Tumor Burden
Tumor Suppressor Genes
Weight Loss
Plasmids
Muscles
Mutation
mouse interleukin-6

All Science Journal Classification (ASJC) codes

  • Physiology
  • Physiology (medical)

Cite this

Interleukin-6 and cachexia in ApcMin/+ mice. / Baltgalvis, Kristen A.; Berger, Franklin G.; Pena, Maria Marjorette O.; Davis, J. Mark; Muga, Stephanie J.; Carson, James.

In: American Journal of Physiology - Regulatory Integrative and Comparative Physiology, Vol. 294, No. 2, 01.02.2008.

Research output: Contribution to journalArticle

Baltgalvis, Kristen A. ; Berger, Franklin G. ; Pena, Maria Marjorette O. ; Davis, J. Mark ; Muga, Stephanie J. ; Carson, James. / Interleukin-6 and cachexia in ApcMin/+ mice. In: American Journal of Physiology - Regulatory Integrative and Comparative Physiology. 2008 ; Vol. 294, No. 2.
@article{97b9392714214e85bb9b9ee2f16f2784,
title = "Interleukin-6 and cachexia in ApcMin/+ mice",
abstract = "The ApcMin/+ mouse has a mutation in the Apc tumor suppressor gene and develops intestinal polyps, beginning at 4 wk of age. This mouse develops cachexia by 6 mo, characterized by significant loss of muscle and fat tissue. The purpose of the present study was to determine the role of circulating interleukin-6 (IL-6) and the polyp burden for the development of cachexia in ApcMin/+ mice. At 26 wk of age, mice exhibiting severe cachectic symptoms had a 61{\%} decrease in gastrocnemius muscle weight, complete loss of epididymal fat, a 10-fold increase in circulating IL-6 levels, and an 89{\%} increase in intestinal polyps compared with mildly cachectic animals. ApcMin/+/IL-6-/- mice did not lose gastrocnemius muscle mass or epididymal fat pad mass while overall polyp number decreased by 32{\%} compared with ApcMin/+ mice. Plasmid-based IL-6 overexpression in ApcMin/+/IL-6-/- mice led to a decrease in gastrocnemius muscle mass and epididymal fat pad mass and increased intestinal polyp burden. IL-6 overexpression did not induce cachexia in non-tumor-bearing mice. These data demonstrate that IL-6 is necessary for the onset of adipose and skeletal muscle wasting in the ApcMin/+ mouse and that circulating IL-6 can regulate ApcMin/+ mouse tumor burden.",
author = "Baltgalvis, {Kristen A.} and Berger, {Franklin G.} and Pena, {Maria Marjorette O.} and Davis, {J. Mark} and Muga, {Stephanie J.} and James Carson",
year = "2008",
month = "2",
day = "1",
doi = "10.1152/ajpregu.00716.2007",
language = "English (US)",
volume = "294",
journal = "American Journal of Physiology",
issn = "0363-6119",
publisher = "American Physiological Society",
number = "2",

}

TY - JOUR

T1 - Interleukin-6 and cachexia in ApcMin/+ mice

AU - Baltgalvis, Kristen A.

AU - Berger, Franklin G.

AU - Pena, Maria Marjorette O.

AU - Davis, J. Mark

AU - Muga, Stephanie J.

AU - Carson, James

PY - 2008/2/1

Y1 - 2008/2/1

N2 - The ApcMin/+ mouse has a mutation in the Apc tumor suppressor gene and develops intestinal polyps, beginning at 4 wk of age. This mouse develops cachexia by 6 mo, characterized by significant loss of muscle and fat tissue. The purpose of the present study was to determine the role of circulating interleukin-6 (IL-6) and the polyp burden for the development of cachexia in ApcMin/+ mice. At 26 wk of age, mice exhibiting severe cachectic symptoms had a 61% decrease in gastrocnemius muscle weight, complete loss of epididymal fat, a 10-fold increase in circulating IL-6 levels, and an 89% increase in intestinal polyps compared with mildly cachectic animals. ApcMin/+/IL-6-/- mice did not lose gastrocnemius muscle mass or epididymal fat pad mass while overall polyp number decreased by 32% compared with ApcMin/+ mice. Plasmid-based IL-6 overexpression in ApcMin/+/IL-6-/- mice led to a decrease in gastrocnemius muscle mass and epididymal fat pad mass and increased intestinal polyp burden. IL-6 overexpression did not induce cachexia in non-tumor-bearing mice. These data demonstrate that IL-6 is necessary for the onset of adipose and skeletal muscle wasting in the ApcMin/+ mouse and that circulating IL-6 can regulate ApcMin/+ mouse tumor burden.

AB - The ApcMin/+ mouse has a mutation in the Apc tumor suppressor gene and develops intestinal polyps, beginning at 4 wk of age. This mouse develops cachexia by 6 mo, characterized by significant loss of muscle and fat tissue. The purpose of the present study was to determine the role of circulating interleukin-6 (IL-6) and the polyp burden for the development of cachexia in ApcMin/+ mice. At 26 wk of age, mice exhibiting severe cachectic symptoms had a 61% decrease in gastrocnemius muscle weight, complete loss of epididymal fat, a 10-fold increase in circulating IL-6 levels, and an 89% increase in intestinal polyps compared with mildly cachectic animals. ApcMin/+/IL-6-/- mice did not lose gastrocnemius muscle mass or epididymal fat pad mass while overall polyp number decreased by 32% compared with ApcMin/+ mice. Plasmid-based IL-6 overexpression in ApcMin/+/IL-6-/- mice led to a decrease in gastrocnemius muscle mass and epididymal fat pad mass and increased intestinal polyp burden. IL-6 overexpression did not induce cachexia in non-tumor-bearing mice. These data demonstrate that IL-6 is necessary for the onset of adipose and skeletal muscle wasting in the ApcMin/+ mouse and that circulating IL-6 can regulate ApcMin/+ mouse tumor burden.

UR - http://www.scopus.com/inward/record.url?scp=38949137388&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=38949137388&partnerID=8YFLogxK

U2 - 10.1152/ajpregu.00716.2007

DO - 10.1152/ajpregu.00716.2007

M3 - Article

VL - 294

JO - American Journal of Physiology

JF - American Journal of Physiology

SN - 0363-6119

IS - 2

ER -