Assessment of dynorphin-A depletion in the anorexia of Walker-256 tumor bearing rats

• Published in: Physiology & behavior Vol. 35; no. 1; p. 117
• Main Authors: Yim, G K, Bryant, H U, Malven, P V
• Format: Journal Article
• Language: English
• Published: United States 01.01.1985
• Subjects: Animals; Anorexia - etiology; Anorexia - metabolism; Brain Chemistry; Carcinoma 256, Walker - complications; Carcinoma 256, Walker - metabolism; Dynorphins - analysis; Feeding and Eating Disorders - etiology; Male; Peptide Fragments - analysis; Pituitary Gland, Posterior - analysis; Rats; Rats, Inbred Strains
• ISSN: 0031-9384; 1873-507X
• DOI: 10.1016/0031-9384(85)90182-9

Rats bearing the Walker-256 (W-256) tumor display an anorexic profile which resembles that of normal animals forced to drink 2% NaCl [2,24], a regimen which depletes neurohypophyseal dynorphin-A (DYN) [3,9]. As expected, the naloxone reversible feeding induced by 2-deoxy-D-glucose (2-DG) was attenuated (36%) in the W-256 tumor bearing rats (TBR). Interestingly, immunoreactive (ir) levels of dynorphin-A 1-17 (DYN-17) and its postulated breakdown product, dynorphin-A 1-18 (DYN-8), were also reduced in the neurohypophysis of W-256 TBR by 42 and 50%, respectively. However, ir-DYN levels were not reduced in TBR in those brain regions which are probably involved in the regulation of appetite (e.g., hypothalamus). 2-DG itself did not consistently affect ir-DYN levels in any tissue for either controls or TBR. The ratio of DYN-8 to DYN-17 did not change in response to any treatment, including the depletion of both peptides from the NIL of TBR. In summary, the present data do not support DYN depletion as being a factor which contributes to the anorexia of the W-256 TBR.