title: [Changes in leptin, leptin receptor and fatty acids levels during chemoradiotherapy for oesophageal cancer].
abstract: BACKGROUND
  Oesophageal cancer patients with substantial weight loss have worse prognosis. Weight loss is often refractory to the nutritional support. Causes of the weight loss are multiple: oesophageal stricture, frequent alcohol abuse, cancer related cachexia. It may be a consequence of metabolic changes mediated by cytokines, hormones and tumour derived products. Leptin, a protein produced by adipocytes, is an important signalling molecule in energy regulation, metabolism of fatty acids and it can also augment tumour growth of various cancer cell lines. Enhanced intake of poly-unsaturated fatty acids may play an important role in the reversal of cancer related weight loss.
  
  
  RESULTS
  In this study we examined the nutritional status (pre-treatment weight-loss, actual weight, body mass index), serum levels of leptin, soluble leptin receptor, TNF-alpha, IGF-1 and plasma phosphatidyl-cholin fatty acids before the beginning of treatment, after the onset of treatment and shortly before its completion. In the group of 38 pts (33 men, 5 women), mean age 58 years, statistically significant mean pre-treatment weight-loss 8 kg and significant mean weight loss 2 kg after chemoradiotherapy was observed. Concomitant chemoradiation led to transient elevation of serum leptin level despite the weight loss during chemoradiotherapy. Significant changes in the distribution of fatty acids in plasmatic phosphatidyl-cholin were observed.
  
  
  CONCLUSIONS
  Our results show the possibility for direct influence of chemoradiotherapy on body weight regulation in advanced oesophageal cancer patients.
authors.affiliation: Onkologická klinika 1. LF UK a VFN, Praha. milada.zemanova@vfn.cz
authors.forename: M
authors.initials: M
authors.lastname: Zemanová
authors.forename: L
authors.initials: L
authors.lastname: Petruzelka
authors.forename: G
authors.initials: G
authors.lastname: Pazdrová
authors.forename: M
authors.initials: M
authors.lastname: Haluzík
authors.forename: F
authors.initials: F
authors.lastname: Novák
authors.forename: A
authors.initials: A
authors.lastname: Svobodník
mesh_terms: D000328:Adult; D000368:Aged; D003131:Combined Modality Therapy; D004938:Esophageal Neoplasms / Q000097:blood* / Q000628:therapy; D005227:Fatty Acids / Q000097:blood*; D005260:Female; D006801:Humans; D007334:Insulin-Like Growth Factor I / Q000032:analysis; D020738:Leptin / Q000097:blood*; D008297:Male; D008875:Middle Aged; D010713:Phosphatidylcholines / Q000737:chemistry; D011956:Receptors, Cell Surface / Q000097:blood*; D054411:Receptors, Leptin; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis; D015431:Weight Loss
chemical_list: D005227:Fatty Acids; C515448:LEPR protein, human; D020738:Leptin; D010713:Phosphatidylcholines; D011956:Receptors, Cell Surface; D054411:Receptors, Leptin; D014409:Tumor Necrosis Factor-alpha; D007334:Insulin-Like Growth Factor I