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The Colon-26 Carcinoma Tumor-bearing Mouse as a Model for the Study of Cancer Cachexia
Published on: November 30, 2016
[Pathomechanism of cachexia in chronic obstructive pulmonary disease]
Jerzy Jarzab1, Aleksandra Chwist-Nowak, Piotr Rozentryt
1Katedry i Oddzialu Klinicznego Chorób Wewnetrznych i Dermatologii w Zabrzu.
Abstract:
Weight loss is a characteristic for advanced chronic obstructive pulmonary disease (COPD), but its mechanism remains unexplained. The decrease of lean body mass is due to a negative energy balance with a noncatabolic hypermetabolic state. Pulmonary inflammation or tissue hypoxia might contribute to it, the decrease in protein content is accompanied by an increase in reactive oxygen forms. Tumor necrosis factor (TNF) has been implicated, other candidates are cytokines IL-1B and IL-6. Activation of apoptosis may be noticed. Pulmonary inflammation and changes in serum leptin may be interrelated. Other hormonal disturbances involve serum IGF-1 level decrease, increase of insulin resistance, raised catecholamine and cortisol levels and other mechanisms which need further investigations. Up to now the attempts undertaken to counteract the observed hormonal changes failed to success.
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