The cause of death in non-metastasizing sarcoma-bearing mice

Pharmacological interference with tissue hypercatabolism in tumour-bearing rats

“…In spite of the sustained elevation of plasma corticosterone and catecholamines in AH-130 tumour hosts (Tessitore et al, 1993b), ADX did not substantially alter the general course of cachexia, in agreement with previous findings (Svaninger et al, 1987b). By contrast, a partial but quite evident prevention of body-weight loss and muscle wasting was afforded by ASA at day 4 after tumour transplantation, though no longer at day 7; such effects may well be accounted for by the ability of this drug to interfere with the peripheral action of PGE2 or TNF, both of which are elevated in AH-130 tumour hosts (Tessitore et al, 1993b).…”

Pharmacological interference with tissue hypercatabolism in tumour-bearing rats

“…In spite of the sustained elevation of plasma corticosterone and catecholamines in AH-130 tumour hosts (Tessitore et al, 1993b), ADX did not substantially alter the general course of cachexia, in agreement with previous findings (Svaninger et al, 1987b). By contrast, a partial but quite evident prevention of body-weight loss and muscle wasting was afforded by ASA at day 4 after tumour transplantation, though no longer at day 7; such effects may well be accounted for by the ability of this drug to interfere with the peripheral action of PGE2 or TNF, both of which are elevated in AH-130 tumour hosts (Tessitore et al, 1993b).…”

The Role of the Melanocortin‐3 Receptor in Cachexia

“…Because LPS produces a relatively short‐term illness, we tested the role of the melanocortin system in chronic disease models. We initially chose to study tumor models, as there were several well‐documented models that reliably produced cachexia and exhaustion of metabolic fuels without obvious complications of metastasis or infection 21–24. In animals implanted with cachexigenic sarcomas, we found that intracerebroventricular AGRP could both prevent and reverse the anorexia and weight loss experienced during tumor development 13.…”

Pharmacological interference with tissue hypercatabolism in tumour-bearing rats

“…In spite of the sustained elevation of plasma corticosterone and catecholamines in AH-130 tumour hosts (Tessitore et al, 1993b), ADX did not substantially alter the general course of cachexia, in agreement with previous findings (Svaninger et al, 1987b). By contrast, a partial but quite evident prevention of body-weight loss and muscle wasting was afforded by ASA at day 4 after tumour transplantation, though no longer at day 7; such effects may well be accounted for by the ability of this drug to interfere with the peripheral action of PGE2 or TNF, both of which are elevated in AH-130 tumour hosts (Tessitore et al, 1993b).…”

The Role of the Melanocortin‐3 Receptor in Cachexia

“…Because LPS produces a relatively short‐term illness, we tested the role of the melanocortin system in chronic disease models. We initially chose to study tumor models, as there were several well‐documented models that reliably produced cachexia and exhaustion of metabolic fuels without obvious complications of metastasis or infection 21–24. In animals implanted with cachexigenic sarcomas, we found that intracerebroventricular AGRP could both prevent and reverse the anorexia and weight loss experienced during tumor development 13.…”

Pharmacological interference with tissue hypercatabolism in tumour-bearing rats

“…In spite of the sustained elevation of plasma corticosterone and catecholamines in AH-130 tumour hosts (Tessitore et al, 1993b), ADX did not substantially alter the general course of cachexia, in agreement with previous findings (Svaninger et al, 1987b). By contrast, a partial but quite evident prevention of body-weight loss and muscle wasting was afforded by ASA at day 4 after tumour transplantation, though no longer at day 7; such effects may well be accounted for by the ability of this drug to interfere with the peripheral action of PGE2 or TNF, both of which are elevated in AH-130 tumour hosts (Tessitore et al, 1993b).…”

The Role of the Melanocortin‐3 Receptor in Cachexia

“…Because LPS produces a relatively short‐term illness, we tested the role of the melanocortin system in chronic disease models. We initially chose to study tumor models, as there were several well‐documented models that reliably produced cachexia and exhaustion of metabolic fuels without obvious complications of metastasis or infection 21–24. In animals implanted with cachexigenic sarcomas, we found that intracerebroventricular AGRP could both prevent and reverse the anorexia and weight loss experienced during tumor development 13.…”