Advanced cancers are associated with a chronic inflammation, especially high interleukin-6 (IL-6) and with various levels of adipokines (leptin and adiponectin), while ghrelin counteracts the anorexigenic effect of leptin in cancer-induced anorexia-cachexia syndrome.
In conclusion, IL-6, leptin, adiponectin, and ghrelin are not associated with advanced stages of cancer or cancer-induced cachexia in older subjects with cancer, but they are significantly correlated with anthropometric factors and body composition.
Our aim was to analyze the levels of ANGPTL-4 in colorectal cancer patients with a stable weight and those with cachexia in order to establish a relationship between ANGPTL-4 and the inflammatory process.
Furthermore, 17ß-estradiol prevented cachexia's disruption in skeletal muscle signaling involving AMPK and mTORC1, in addition to improving mitochondrial function in female tumor bearing mice.
Furthermore, 17ß-estradiol prevented cachexia's disruption in skeletal muscle signaling involving AMPK and mTORC1, in addition to improving mitochondrial function in female tumor bearing mice.
Furthermore, 17ß-estradiol prevented cachexia's disruption in skeletal muscle signaling involving AMPK and mTORC1, in addition to improving mitochondrial function in female tumor bearing mice.
In multivariable analysis, weight loss >5% (HR 2.8), reduction in SM >5% (HR 5.5), an increase in CRP (HR 2.2) or CA 19.9 (HR 1.9), and resection (HR 0.4) remained independently associated with survival, whereas classical cachexia and sarcopenia did not.
In this study, weight loss, body mass index, skeletal muscle index (SMI), serum carcinoembryonic antigen, serum tumor necrosis factor (TNF)-α, serum interleukin (IL)-6, serum high mobility group box (HMGB)-1, and SDS-soluble myosin light chain 1 (SDS-MYL1) of the psoas muscle were examined in 8 autopsied cases of death from colorectal cancer (CRC) as biomarkers of cachexia.
In this study, weight loss, body mass index, skeletal muscle index (SMI), serum carcinoembryonic antigen, serum tumor necrosis factor (TNF)-α, serum interleukin (IL)-6, serum high mobility group box (HMGB)-1, and SDS-soluble myosin light chain 1 (SDS-MYL1) of the psoas muscle were examined in 8 autopsied cases of death from colorectal cancer (CRC) as biomarkers of cachexia.
We demonstrate that TLR7/8 agonist R848 induces anti-tumor responses and attenuates cachexia in murine models of pancreatic ductal adenocarcinoma (PDAC).
We have identified an endogenous mediator of insulin resistance, signal regulatory protein alpha (SIRPα), which leads to cachexia in mice and is associated with cachexia in patients with CKD.
By showing that ZAG binds fatty acids in different locations, we demonstrate an augmented mechanism for fatty acid binding in ZAG that is distinct from other known fatty acid binding proteins, and may be relevant to cachexia.
We investigated FGF-21 and MCP-1 in relations to cardiac function, inflammation, and wasting in patients with heart failure with reduced ejection fraction (HFrEF) and cardiac cachexia.
Fibroblast growth factor 21 (FGF-21) levels were elevated in patients with HFrEF and cardiac cachexia, which could be mediated by increased inflammation and muscle wasting rather than impaired cardiac function.
New research, however, clarifies that cancers evoking cachexia release microvesicles rich in heat shock proteins 70 and 90, and that these extracellular heat shock proteins induce cachexia by serving as agonists for toll-like receptor 4 (TLR4) in skeletal muscle, macrophages, and adipocytes.
The normalization of elevated plasma renin activity reduced the loss of body fat and lean mass (cachexia/sarcopenia), <i>p</i> < 0.001) and prolonged survival (<i>p</i> < 0.05).