Cancer cachexia

Michael J. Tisdale

Research output: Contribution to journalReview article

Abstract

Purpose of review: Although cachexia has a major effect on both the morbidity and mortality of cancer patients, information on the mechanisms responsible for this condition is limited. This review summarizes recent data in this area. Recent findings: Cachexia is defined as loss of muscle, with or without fat, frequently associated with anorexia, inflammation and insulin resistance. Loss of adipose mass is due to an increased lipolysis through an increased expression of hormone-sensitive lipase. Adipose tissue does not contribute to the inflammatory response. There is an increased phosphorylation of both protein kinase R (PKR) and eukaryotic initiation factor 2 on the α-subunit in skeletal muscle of cachectic cancer patients, which would lead to muscle atrophy through a depression in protein synthesis and an increase in degradation. Mice lacking the ubiquitin ligase MuRF1 are less susceptible to muscle wasting under amino acid deprivation. Expression of MuRF1 and atrogin-1 is increased by oxidative stress, whereas nitric oxide may protect against muscle atrophy. Levels of interleukin (IL)-6 correlate with cachexia and death due to an increase in tumour burden. Ghrelin analogues and melanocortin receptor antagonists increase food intake and may have a role in the treatment of cachexia. Summary: These findings provide impetus for the development of new therapeutic agents.

LanguageEnglish
Pages146-151
Number of pages6
JournalCurrent Opinion in Gastroenterology
Volume26
Issue number2
DOIs
Publication statusPublished - Mar 2010

Fingerprint

Cachexia
Muscular Atrophy
Neoplasms
Muscle Neoplasms
Eukaryotic Initiation Factor-2
Melanocortin Receptors
Ghrelin Receptor
Sterol Esterase
Muscles
Lipolysis
Anorexia
Ligases
Ubiquitin
Tumor Burden
Protein Kinases
Insulin Resistance
Adipose Tissue
Interleukin-6
Nitric Oxide
Skeletal Muscle

Keywords

  • lipolysis
  • muscle atrophy
  • neuropetides
  • pro-inflammatory cytokines

Cite this

Tisdale, Michael J. / Cancer cachexia. In: Current Opinion in Gastroenterology. 2010 ; Vol. 26, No. 2. pp. 146-151.
@article{c24116cbc6654731bf22efe092bc4248,
title = "Cancer cachexia",
abstract = "Purpose of review: Although cachexia has a major effect on both the morbidity and mortality of cancer patients, information on the mechanisms responsible for this condition is limited. This review summarizes recent data in this area. Recent findings: Cachexia is defined as loss of muscle, with or without fat, frequently associated with anorexia, inflammation and insulin resistance. Loss of adipose mass is due to an increased lipolysis through an increased expression of hormone-sensitive lipase. Adipose tissue does not contribute to the inflammatory response. There is an increased phosphorylation of both protein kinase R (PKR) and eukaryotic initiation factor 2 on the α-subunit in skeletal muscle of cachectic cancer patients, which would lead to muscle atrophy through a depression in protein synthesis and an increase in degradation. Mice lacking the ubiquitin ligase MuRF1 are less susceptible to muscle wasting under amino acid deprivation. Expression of MuRF1 and atrogin-1 is increased by oxidative stress, whereas nitric oxide may protect against muscle atrophy. Levels of interleukin (IL)-6 correlate with cachexia and death due to an increase in tumour burden. Ghrelin analogues and melanocortin receptor antagonists increase food intake and may have a role in the treatment of cachexia. Summary: These findings provide impetus for the development of new therapeutic agents.",
keywords = "lipolysis, muscle atrophy, neuropetides, pro-inflammatory cytokines",
author = "Tisdale, {Michael J.}",
year = "2010",
month = "3",
doi = "10.1097/MOG.0b013e3283347e77",
language = "English",
volume = "26",
pages = "146--151",
journal = "Current Opinion in Gastroenterology",
issn = "0267-1379",
publisher = "Lippincott Williams and Wilkins",
number = "2",

}

Cancer cachexia. / Tisdale, Michael J.

In: Current Opinion in Gastroenterology, Vol. 26, No. 2, 03.2010, p. 146-151.

Research output: Contribution to journalReview article

TY - JOUR

T1 - Cancer cachexia

AU - Tisdale, Michael J.

PY - 2010/3

Y1 - 2010/3

N2 - Purpose of review: Although cachexia has a major effect on both the morbidity and mortality of cancer patients, information on the mechanisms responsible for this condition is limited. This review summarizes recent data in this area. Recent findings: Cachexia is defined as loss of muscle, with or without fat, frequently associated with anorexia, inflammation and insulin resistance. Loss of adipose mass is due to an increased lipolysis through an increased expression of hormone-sensitive lipase. Adipose tissue does not contribute to the inflammatory response. There is an increased phosphorylation of both protein kinase R (PKR) and eukaryotic initiation factor 2 on the α-subunit in skeletal muscle of cachectic cancer patients, which would lead to muscle atrophy through a depression in protein synthesis and an increase in degradation. Mice lacking the ubiquitin ligase MuRF1 are less susceptible to muscle wasting under amino acid deprivation. Expression of MuRF1 and atrogin-1 is increased by oxidative stress, whereas nitric oxide may protect against muscle atrophy. Levels of interleukin (IL)-6 correlate with cachexia and death due to an increase in tumour burden. Ghrelin analogues and melanocortin receptor antagonists increase food intake and may have a role in the treatment of cachexia. Summary: These findings provide impetus for the development of new therapeutic agents.

AB - Purpose of review: Although cachexia has a major effect on both the morbidity and mortality of cancer patients, information on the mechanisms responsible for this condition is limited. This review summarizes recent data in this area. Recent findings: Cachexia is defined as loss of muscle, with or without fat, frequently associated with anorexia, inflammation and insulin resistance. Loss of adipose mass is due to an increased lipolysis through an increased expression of hormone-sensitive lipase. Adipose tissue does not contribute to the inflammatory response. There is an increased phosphorylation of both protein kinase R (PKR) and eukaryotic initiation factor 2 on the α-subunit in skeletal muscle of cachectic cancer patients, which would lead to muscle atrophy through a depression in protein synthesis and an increase in degradation. Mice lacking the ubiquitin ligase MuRF1 are less susceptible to muscle wasting under amino acid deprivation. Expression of MuRF1 and atrogin-1 is increased by oxidative stress, whereas nitric oxide may protect against muscle atrophy. Levels of interleukin (IL)-6 correlate with cachexia and death due to an increase in tumour burden. Ghrelin analogues and melanocortin receptor antagonists increase food intake and may have a role in the treatment of cachexia. Summary: These findings provide impetus for the development of new therapeutic agents.

KW - lipolysis

KW - muscle atrophy

KW - neuropetides

KW - pro-inflammatory cytokines

UR - http://www.scopus.com/inward/record.url?scp=77149130208&partnerID=8YFLogxK

U2 - 10.1097/MOG.0b013e3283347e77

DO - 10.1097/MOG.0b013e3283347e77

M3 - Review article

VL - 26

SP - 146

EP - 151

JO - Current Opinion in Gastroenterology

T2 - Current Opinion in Gastroenterology

JF - Current Opinion in Gastroenterology

SN - 0267-1379

IS - 2

ER -