The effect of adrenaline and Walker-256 tumour-induced cachexia upon Kupffer cell metabolism

Abstract

Kupffer cells (KC), the liver macrophages, are able to produce PGE(2), which is involved in immune suppression and in the aggravation of cancer cachexia due to interference with lipid metabolism in the liver. Since tumour-bearing (TB) rats present high plasma epinephrine levels, and this hormone is able to affect macrophage metabolism and function, we have assessed the effect of epinephrine (5 nM) upon Kupffer cell PGE(2) production. Epinephrine induced increased production of PGE(2) both by control (3.5-fold) and TB rats (27 per cent) KC, an effect blocked by propranolol. Enhancement of cAMP content in the cells by addition of isoproterenol (0.1 microM) to the incubations, however, failed to induce the same response in the cells. Nevertheless, when phenylephrine (1 microM) was added to the incubation, a similar pattern of PGE(2) production to that observed for epinephrine was found for control and TB rat KC. We propose that the effect of epinephrine upon KC PGE(2) production is mediated by alpha-adrenergic receptors and that Ca(2+) is involved in the response, since increasing concentrations of the ion added to the incubation medium (0.25, 0.5 and 1.0 mM) enhanced the eicosanoid production, while EDTA abolished the response.

Liver denervation affects hepatocyte mitochondrial fatty acid transport capacity

“…Noradrenalin release causes perisinusoidal cells to synthesize prostaglandins 11 and PGF 2 effects on ketogenesis are very similar to those of NA. 12 We have previously shown that Kupffer cells increase their PGE 2 production when incubated with adrenalin, 46 through a calcium-mediated pathway. This was also true for tumour-bearing rat liver, in which CPT II activity is reduced.…”

Exercise as a Time‐conditioning Effector in Chronic Disease: a Complementary Treatment Strategy

“…Depending on the exercise intensity and duration, the profile of secretion of these hormones and their clearance rates are substantially modified (22,56). Adrenaline, and to a lesser degree noradrenaline, seem to be responsible for the acute effects of exercise on lymphocyte dynamics and lymphocyte function (57) and NK cell activity (22). Increase in growth hormone and catecholamine levels mediates the acute effects on neutrophils whereas cortisol exerts its effects within a time lag of at least 2 h, depending on the exercise duration and intensity, and therefore may help to maintain lymphopenia and neutrocytosis only after long-term exercise (18,58).…”

Horário do dia, luminosidade ambiental e exercício físico sobre parâmetros inflamatórios e de performance em ratos nadadores

“…Durante o período claro (das 06:00h às 18:00h), empregamos lâmpadas incandescentes (Phillips®, Soft, 100W, 2700K, 565-590nm, <60lux) para evitar a retinopatia fototóxica nos animais (SUN et al, 1993;SEMPLE-ROWLAND;DAWSON, 1987). No período escuro os animais LP foram mantidos em escuridão total enquanto os animais LE foram submetidos a uma iluminação constante de espectro vermelho (Rosco®,Supergel,Fire # 19,>600nm,<15lux).…”

“…O estresse causado pelo exercício físico promove aumento transitório da contagem de células brancas do sangue NEHLSEN-CANNARELLA, 1994), geralmente associado ao aumento da liberação de catecolaminas (GABRIEL et al, 1992;SEELAENDER;KAZANTZIS;COSTA ROSA, 1999). Em estudos envolvendo o modelo Humano, a intensidade de esforço, duração e condição física do indivíduo avaliado são importantes nessas respostas (STRASNER et al, 1997;GLEESON et al, 1995;KENDALL et al, 1990), sendo o aumento das contagens de células brancas mais pronunciado em exercícios de longa duração devido a importante participação do cortisol (PEDERSEN et al, 1997;PEDERSEN, 1999).…”