Independent and combined actions of interleukin-1β, tumor necrosis factor α, and glucagon on amino acid metabolism in the isolated perfused rat liver

Bandt, J.-P. De; Lim, Soo-Kyung; Plassart, F.; Lucas, C.; Rey, Colette; Poupon, Raoul; Giboudeau, J; Cynober, Luc

doi:10.1016/0026-0495(94)90261-5

Cited by 18 publications

(10 citation statements)

References 38 publications

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“…Furthermore, regulatory agents, which are normaly present but whose levels are frequently altered during specific pathological conditions, may equally contribute to the net action of endotoxins. A clear demonstration of this possibility is the observation that both TNFa and IL1b are able to potentiate the action of glucagon in the isolated perfused rat liver (De Bandt et al 1994).…”

Section: Discussionmentioning

confidence: 99%

“…TNFa, as well as interleukin 1b (IL1b) were injected in rats at doses up to 10 mg/kg and gluconeogenesis from alanine was measured in the isolated perfused liver. In vivo administration was used because the direct infusion of both TNFa and IL1b in the isolated perfused rat liver does not produce significant changes in glucose production and alanine uptake although it potentiates the actions of glucagon (De Bandt et al 1994). These and other observations suggest that the hepatic metabolic response to cytokines depends on the presence of circulating factors, conditions which are difficult to reproduce in the perfused liver.…”

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confidence: 99%

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Low Doses of Tumour Necrosis Factor α and Interleukin 1β Diminish Hepatic Gluconeogenesis from Alanine in vivo

Kelmer-Bracht

Broetto-Biazon

Sá‐Nakanishi

et al. 2006

Basic Clin Pharma Tox

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Previous reports have attributed a stimulating action on hepatic gluconeogenesis to tumour necrosis factor a (TNFa) administered to rats at high doses (250 mg/kg). However, in adjuvant-induced arthritic rats, which present TNFa and other interleukins in the circulation, hepatic gluconeogenesis is diminished. The same occurs in some types of experimental cancer models as, for example, rats bearing the Walker-256 tumour. The present work represents an attempt of reproducing in rats gluconeogenesis inhibition by interleukins using low instead of high doses of both TNFa and interleukin 1b (IL1b). TNFa and IL1b at doses of up to 10 mg/kg were given endovenously to rats and, after six hours, gluconeogenesis from alanine and several related parameters were evaluated in the isolated haemoglobin-free perfused rat liver. Livers from rats injected with TNFa and IL1b, either alone or in combination, presented diminished gluconeogenesis. The degrees of inhibition caused by TNFaπIL1b, TNFa and IL1b were, respectively, 48.5, 38.8 and 30.4%. TNFa also diminished oxygen uptake. No action on urea and ammonia production was found. Possibly, both TNFa and IL1b contribute to the decreased rates of hepatic gluconeogenesis that were found in rats with arthritis, sepsis and some kinds of cancer, but not to the decreased rates of ureagenesis.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Low Doses of Tumour Necrosis Factor α and Interleukin 1β Diminish Hepatic Gluconeogenesis from Alanine in vivo

Kelmer-Bracht

Broetto-Biazon

Sá‐Nakanishi

et al. 2006

Basic Clin Pharma Tox

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“…After the rinse, the livers were perfused at constant pressure (13 cm H 2 O) through the portal vein in a recirculating system in a thermostatically controlled cabinet (+37°C) for 90 minutes [22,23]. The perfusate was KrebsHenseleit buffer (150 mL, pH 7.4) saturated with 95% O 2 / 5% CO 2 containing bovine serum albumin (30 g/L), glucose (8.5 mmol/L), and calcium (2.4 mmol/L).…”

Section: Isolated Perfused Rat Livermentioning

confidence: 99%

Consequences of head injury and static cold storage on hepatic function: ex vivo experiments using a model of isolated perfused rat liver

et al. 2009

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“…In isolated perfused rat livers, TNFa reduced by about 25% the uptake of alanine but potentiated the glucagon-1995 WILEY-LISS. IN(: induced amino acid uptake (De Bandt et al, 1994). This finding suggests that TNFa can modulate glucagon action on a short-term basis.…”

mentioning

confidence: 95%

No evidence for a tumor necrosis factor α stimulated 2‐methylaminoisobutyric acid uptake in hepatocyte monolayer

Lim

Bandt

Aussel

et al. 1995

Journal Cellular Physiology

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This study investigates the short-term effects of glucagon and human recombinant tumor necrosis factor alpha (TNF alpha) singly and in association on 2-methylaminoisobutyric acid (MeAIB) transport in hepatocyte monolayers. As expected, glucagon induced a time-dependent stimulation of MeAIB transport. In our experimental conditions, TNF alpha did not induce cytolysis. A 2 hour exposure to TNF alpha (0.05-500 ng/l) with or without glucagon (10(-9) to 10(-6) M) did not modify the basal or glucagon-stimulated MeAIB transport. Varying the duration of exposure to TNF alpha 5 ng/l up to 6 h was equally ineffective. The presence of hydrocortisone potentiated the glucagon-stimulated transport, but TNF alpha remained ineffective. Finally, the association of interferon (IFN gamma) with TNF alpha and/or glucagon was unable to modify the transport activity. These data demonstrate that TNF alpha does not exert a direct effect on MeAIB transport in hepatocytes, at least on a short-term basis.

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Independent and combined actions of interleukin-1β, tumor necrosis factor α, and glucagon on amino acid metabolism in the isolated perfused rat liver

Cited by 18 publications

References 38 publications

Low Doses of Tumour Necrosis Factor α and Interleukin 1β Diminish Hepatic Gluconeogenesis from Alanine in vivo

Low Doses of Tumour Necrosis Factor α and Interleukin 1β Diminish Hepatic Gluconeogenesis from Alanine in vivo

Consequences of head injury and static cold storage on hepatic function: ex vivo experiments using a model of isolated perfused rat liver

No evidence for a tumor necrosis factor α stimulated 2‐methylaminoisobutyric acid uptake in hepatocyte monolayer

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