We investigated the role of fasting hormones and pro-inflammatory cytokines in cancer patients. Hormones (ghrelin, adiponectin, and leptin) and cytokines (TNF-alpha, IFN-gamma, and IL-6) were measured by ELISA or RIA in lung cancer and colorectal cancer patients before the administration of cancer therapy, and measurements were repeated every 2 months for 6 months. From June 2006 to August 2008, 42 patients (19 with colorectal cancer and 23 with lung cancer) were enrolled. In total, 21 patients were included in the cachexia group and the others served as a comparison group. No significant difference in the initial adiponectin, ghrelin, TNF-alpha, IFN-gamma, or IL-6 level was observed between groups, although leptin was significantly lower in cachectic patients than in the comparison group (15.3 +/- 19.5 vs 80.9 +/- 99.0 pg/mL, P = 0.007). During the follow-up, the patients who showed a > 5% weight gain had higher ghrelin levels after 6 months. Patients exhibiting elevated IL-6 levels typically showed a weight loss > 5% after 6 months. A blunted adiponectin or ghrelin response to weight loss may contribute to cancer cachexia and IL-6 may be responsible for inducing and maintaining cancer cachexia.
Adiponectin/analysis ; Aged ; Antineoplastic Agents/therapeutic use ; Cachexia/*physiopathology ; Colorectal Neoplasms/drug therapy/*metabolism/mortality ; Cytokines/*analysis ; Female ; Follow-Up Studies ; Ghrelin/analysis ; Humans ; Interferon-gamma/analysis/physiology ; Interleukin-6/analysis ; Leptin/analysis ; Lung Neoplasms/drug therapy/*metabolism/mortality ; Male ; Middle Aged ; Peptide Hormones/*analysis ; Prognosis ; Prospective Studies ; Survival Rate ; Tumor Necrosis Factor-alpha/analysis ; Weight Gain ; Weight Loss

Recently, gastric Helicobacter pylori (H. pylori) colonization has been shown to affect the expression of leptin and ghrelin, hormones that control appetite and satiety. Gastric leptin, produced by chief and parietal cells and released in response to meals, may play a role in weight gain after eradication of H. pylori infection, whereas ghrelin, produced by X/A-like enteroendocrine cells in oxyntic gland, is released during fasting, and suppressed by feeding and leptin. Whether either that H. pylori genes represent microbial contributions to the complement of thrifty genes of humans, or that H. pylori disappearance plays a role in adiposity remains to be determined. Simply, ghrelin-leptin might tango in body weight regulation, gastric inflammation, and gastric motility. In the current review about the possible role of ghrelin in gastric inflammation, we found that high serum albumin condition decreased ghrelin expression, whereas serum albumin deprivation significantly increased ghrelin expression, however, of which regulation was abolished after H. pylori infection. Ghrelin significantly attenuated the inflammatory stimuli imposed after H. pylori, shown with inactivation of phospho-extracellular signal-regulated kinase (p-ERK) and nuclear factor-KappaB (NF-KappaB)-DNA binding activities. Conclusively, besides orexigenic and weight gaining actions of gastric hormone, ghrelin, it likely endows the stomach the protective effect from exogenous damages.
Amino Acid Sequence ; Appetite Stimulants ; Gastritis/*metabolism/microbiology ; Ghrelin/*blood/chemistry ; Helicobacter Infections/*metabolism ; *Helicobacter pylori ; Humans ; Insulin-Like Growth Factor I/analysis ; Leptin/*blood ; Mitogen-Activated Protein Kinases/metabolism ; Molecular Sequence Data ; NF-kappa B/metabolism ; Neurosecretory Systems/*metabolism ; Peptide Hormones/*blood ; Signal Transduction ; Weight Gain