Hepatic amino acid and protein metabolism in non-anorectic, moderately cachectic tumor-bearing rats

Blaauw, Ivo de; Deutz, N.E.P.; Boers, W.; Meyenfeldt, M.F. von

doi:10.1016/s0168-8278(97)80058-x

Cited by 18 publications

(9 citation statements)

References 55 publications

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“…It is possible that urea production by Walker‐256 cells contributed to the increased uremia because the time sequence of blood urea level increase followed the profile of tumour growth (Table ). Moreover, these results could be attributed, partly at least, to the increased blood arginine and liver arginase activity in tumour‐bearing rats.…”

Section: Discussionmentioning

confidence: 96%

Changes in blood metabolic parameters during the development of Walker‐256 tumour‐induced cachexia in rats are not caused by decreased food intake

Cassolla

Moreira

Liboni

et al. 2011

Cell Biochemistry & Function

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Blood metabolic parameters of Walker-256 tumour-bearing rats, on days 5, 8, 11 and 14 after implantation of tumour, were compared with those of rats without tumour fed ad libitum (free-fed control) or with reduced feeding (pair-fed control), similar to the anorexic tumour-bearing rats. Cachexia parameters and tumour mass also were investigated. In general, especially on day 14 after implantation of tumour, there was reduction of body mass, gastrocnemius muscle mass, food intake and glycemia and increase of blood triacylglycerol, free fatty acids, lactate and urea, compared with free-fed controls rats. These changes did not occur in pair-fed control, except a slight reduction of glycemia. Pair-fed control showed no significant changes in blood cholesterol and glycerol in comparison with free-fed control, although there was reduction of cholesterol and increase of blood glycerol on day 14 after tumour implantation compared with pair-fed control. The results demonstrate that, besides the characteristic signs of the cachexia syndrome such as anorexia, weight loss and muscle catabolism, Walker-256 tumour-bearing rats show several blood metabolic alterations, some of which begin as early as day 5 after implantation of tumour, and are accentuated during the development of cachexia. Evidence that the alterations of blood metabolic parameters of tumour-bearing rats were not found in pair-fed control indicate that they were not caused by decreased food intake. These changes were probably mediated by factors produced by tumour or host tissue in response to the presence of tumour.

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Section: Discussionmentioning

confidence: 96%

Changes in blood metabolic parameters during the development of Walker‐256 tumour‐induced cachexia in rats are not caused by decreased food intake

Cassolla

Moreira

Liboni

et al. 2011

Cell Biochemistry & Function

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“…2 Although the use of amino acids for gluconeogenesis in the liver of cachectic individuals is generally mentioned, a study performed in cachectic rats similarly observed an up-regulation of APR protein synthesis at the expense of glucose production. 60 They showed that despite an increase in liver uptake of essential and glucogenic amino acids, glucose and urea production remained unchanged. They concluded that the liver was, in this context, an efficient nitrogen-sparing and active protein-synthesizing organ.…”

Section: Amino Acids Are Captured By the Liver Of Cachectic Mice Mainmentioning

confidence: 99%

Multi‐compartment metabolomics and metagenomics reveal major hepatic and intestinal disturbances in cancer cachectic mice

Pötgens

Thibaut

Joudiou

et al. 2021

J cachexia sarcopenia muscle

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Background Cancer cachexia is a multifactorial syndrome characterized by multiple metabolic dysfunctions. Besides the muscle, other organs such as the liver and the gut microbiota may also contribute to this syndrome. Indeed, the gut microbiota, an important regulator of the host metabolism, is altered in the C26 preclinical model of cancer cachexia. Interventions targeting the gut microbiota have shown benefits, but mechanisms underlying the host-microbiota crosstalk in this context are still poorly understood. Methods To explore this crosstalk, we combined proton nuclear magnetic resonance ( 1 H-NMR) metabolomics in multiple compartments with 16S rDNA sequencing. These analyses were complemented by molecular and biochemical analyses, as well as hepatic transcriptomics.Results 1 H-NMR revealed major changes between control (CT) and cachectic (C26) mice in the four analysed compartments (i.e. caecal content, portal vein, liver, and vena cava). More specifically, glucose metabolism pathways in the C26 model were altered with a reduction in glycolysis and gluconeogenesis and an activation of the hexosamine pathway, arguing against the existence of a Cori cycle in this model. In parallel, amino acid uptake by the liver, with an up to four-fold accumulation of nine amino acids (q-value <0.05), was mainly used for acute phase response proteins synthesis rather than to fuel the tricarboxylic acid cycle and gluconeogenesis. We also identified a 35% reduction in hepatic carnitine levels (q-value <0.05) and a lower activation of the phosphatidylcholine pathway as potential contributors to the hepatic steatosis present in this model. Our work also reveals a reduction of different beneficial intestinal bacterial activities in cancer cachexia. We found decreased levels of two short-chain fatty acids, acetate and butyrate (72% and 88% reduction in C26 caecal content; q-value <0.001), and a reduction in aromatic amino acid metabolites, which may contribute to the altered intestinal homeostasis in these mice. A member of the Ruminococcaceae family (ASV 2) was identified as the main bacterium responsible for the drop in butyrate. Finally, we report a two-fold intestinal transit acceleration (P-value <0.001) as a key factor shaping the gut microbiota composition and activity in cancer cachexia, which together lead to a faecal loss of proteins and amino acids. Conclusions Our work highlights new metabolic pathways potentially involved in cancer cachexia and further supports the interest of exploring the gut microbiota composition and activity, as well as intestinal transit, in cancer patients with and without cachexia.

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“…In the presence of an inflammatory stress, however, increases in liver weight, associated with increased circulating levels of APPs, have been found in cachectic tumor-bearing rats [16].…”

Section: Effects Of Nutritional Depletion On the Immune Systemmentioning

confidence: 99%

Nutritional Depletion and Dietary Manipulation: Effects on the Immune Response

et al. 1999

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The association between nutritional depletion and the increased susceptibility for infectious diseases has been recognized for a long time. The complexity of the immune system, however, makes it difficult to unravel the underlying mechanisms. It appears that depletion adversely affects virtually all components of the immune system. This review provides an overview over the specific requirements of substrates by immune cells and the effects of nutritional depletion on various components of the immune response, with special attention to gut-associated lymphoid tissue. The literature concerning effects of dietary interventions with specific nutrients on the immune response is also discussed. Finally, we offer a hypothesis with regard to the improvement of composition of "trauma" nutrition solutions.

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Hepatic amino acid and protein metabolism in non-anorectic, moderately cachectic tumor-bearing rats

Cited by 18 publications

References 55 publications

Changes in blood metabolic parameters during the development of Walker‐256 tumour‐induced cachexia in rats are not caused by decreased food intake

Changes in blood metabolic parameters during the development of Walker‐256 tumour‐induced cachexia in rats are not caused by decreased food intake

Multi‐compartment metabolomics and metagenomics reveal major hepatic and intestinal disturbances in cancer cachectic mice

Nutritional Depletion and Dietary Manipulation: Effects on the Immune Response

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