Leupeptin Inhibits Adrenocorticotropic Hormone-induced Protein Breakdown in the Conscious Dog

McCallister, Ben D.; Lacy, William W.; Williams, Phillip E.; Abumrad, Naji N.

doi:10.1172/jci110781

Cited by 7 publications

(1 citation statement)

References 19 publications

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“…We ignore, so far, which may be the signals and mechanisms involved in such perturbations. Yet the present model seems adequate to develop further the analysis along such directions (10,14,35,39,47,51). Hopefully, this will provide some clues to devise the rationale for an adequate corrective therapy (1 1); which seems important, considering that parenteral and overfeeding per se, while partially effective in relieving host tissue waste, carry the risk ofaccelerating thegrowth ofthc tumor itself.…”

Section: Protein Turnover Regulations In Hostmentioning

confidence: 86%

Comparative Studies on Protein Turnover Regulations in Tumor Cells and Host Tissues: Development and Analysis of an Experimental Model

et al. 1986

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The protein mass of cells and tissues is determined by the relative rates of protein synthesis (PS) and degradation (PD). A convergent modulation of both PS and PD is operated by many cell types to regulate protein accumulation and thus growth. Transformed and neoplastic cells may show markedly defective PD regulations. Yet even highly-deviated cells such as those of the transplantable Yoshida ascites hepatoma AH-130 cease growth when attaining a conspicuous population size, by operating a combined reduction of PS and acceleration of PD. As in normal cells, PD acceleration is effected through an activation of the acidic-vacuolar (lysosomal) mechanism. AH-130 tumor-bearing rats develop a markedly negative nitrogen balance early after transplantation. Tumor growth involves pronounced perturbations in host body and tissue protein metabolism. Apparently, these changes occur mostly at the level of PD rather than PS, at least in liver and skeletal muscle (gastrocnemius). These observations indicate that either tumor and host cells sense different signals for PD regulations or their thresholds for the same signals are poised differently. This model seems most suitable for further studies to elucidate which signals and mechanisms are involved in these protein metabolic perturbations and possibly, to develop the rationale for adequate corrective strategies.

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