Efficiency of oxidative phosphorylation in liver mitochondria is decreased in a rat model of peritoneal carcinosis

Dumas, Jean‐François; Goupille, Caroline; Julienne, Cloé Mimsy; Pinault, Michelle; Chevalier, Stéphan; Bougnoux, Philippe; Servais, Stéphane; Couet, Charles

doi:10.1016/j.jhep.2010.08.012

Cited by 45 publications

(45 citation statements)

References 43 publications

(50 reference statements)

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“…Activated macrophages in the liver parenchyma may provide a local source of IL-6 production, which stimulates the synthesis of hepatic acute-phase protein (Castell et al 1989). Preclinical investigations have shown that hepatic oxidative phosphorylation is reduced in a rat model of peritoneal carcinosis, concomitant with increased energy wasting and production of reactive oxygen species (Dumas et al 2010). Furthermore, clinical investigations have shown that hepatic gluconeogenesis is increased in cancer patients (Yoshikawa et al 1999).…”

Section: The Role Of the Liver In Cancer Cachexiamentioning

confidence: 99%

Mechanisms of metabolic dysfunction in cancer-associated cachexia

2016

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Metabolic dysfunction contributes to the clinical deterioration observed in advanced cancer patients and is characterized by weight loss, skeletal muscle wasting, and atrophy of the adipose tissue. This systemic syndrome, termed cancer-associated cachexia (CAC), is a major cause of morbidity and mortality. While once attributed solely to decreased food intake, the present description of cancer cachexia is a disorder of multiorgan energy imbalance. Here we review the molecules and pathways responsible for metabolic dysfunction in CAC and the ideas that led to the current understanding.

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Section: The Role Of the Liver In Cancer Cachexiamentioning

confidence: 99%

Mechanisms of metabolic dysfunction in cancer-associated cachexia

2016

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“…Furthermore, the large amount of lactate produced by tumor cells that show intense glycolytic metabolism is converted to glucose by hepatic gluconeogenesis, which is available in the plasma, constituting the Cori cycle (1). Recent studies conducted on animal models of cancer cachexia indicate that mitochondrial dysfunction and reduced ATP synthesis could participate in energy wastage (9,10). All these factors contribute to intense basal energy expenditure, body mass loss, and debility in a cachectic patient.…”

Section: Introductionmentioning

confidence: 99%

Chronic Supplementation With Shark Liver Oil for Reducing Tumor Growth and Cachexia in Walker 256 Tumor-Bearing Rats

Iagher

Belo

Naliwaiko

et al. 2011

Nutrition and Cancer

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We investigated the effect of chronic supplementation with shark liver oil (SLO), an antitumor supplement source of n-3 fatty acids and 1-O-alkylglycerols, alone and combined with coconut fat (CF), a source of saturated fatty acids, on Walker 256 tumor growth and cachexia. Male rats were supplemented daily and orally with SLO and/or CF (1 g per kg body weight) for 7 wk. After 7 wk, 50% of animals were subcutaneously inoculated with 3 × 10(7) Walker 256 tumor cells. After 14 days, the rats were killed, the tumors were removed for lipid peroxidation measurement, and blood was collected for glycemia, triacylglycerolemia, and lacticidemia evaluation. Liver samples were obtained for glycogen measurement. Unlike CF, supplementation with SLO promoted gain in body weight, reduction of tumor weight, and maintained glycemia, triacylglycerolemia, lacticidemia, and liver glycogen content to values similar to non-tumor-bearing rats. Combined supplementation of SLO with CF also showed a reversion of cachexia with gain in body mass, reduction of lacticidemia, maintaining the liver glycogen store, and reduction in tumor weight. SLO, alone or combined with CF, promoted increase of tumor lipid peroxidation. In conclusion, SLO supplemented chronically, alone or associated with CF, was able to reduce tumor growth and cachexia.

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“…These data suggest that tumor-borne factors promote cardiac dysfunction in cachexia. Besides heart atrophy, cachexia was able to suppress the expression of CYP in liver of mice [40] and increase ROS production ~12-fold in liver of cancer bearing rats [21]. Therefore, tumor-derived factors are mainly responsible for the deregulation of body redox homeostasis and the development of OS that might lead to multiorgan failure and enhance cachexia progression (Figure 1).…”

Section: Multiorgan Presence Of Oxidative Stress Markers During Camentioning

confidence: 99%

“…Unfortunately, the obtained results were not always positives but sometimes without any significant effect or even deleterious [12–19]. Indeed, if the use of antioxidants appears to be complicated in cancer, it could be even more problematical in cancer cachexia given the intricate tissue crosstalk and the disruption of redox balance that takes place in many organs, including skeletal muscle, heart, liver, and blood [17, 20, 21]. In other words, high levels of ROS could be present at different sites, at the same time, and exert distinct roles in an organ-dependent manner.…”

Section: Introductionmentioning

confidence: 99%

The Janus‐Faced Role of Antioxidants in Cancer Cachexia: New Insights on the Established Concepts

Assi

Rebillard

2016

Oxidative Medicine and Cellular Longevity

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Chronic inflammation and excessive loss of skeletal muscle usually occur during cancer cachexia, leading to functional impairment and delaying the cure of cancer. The release of cytokines by tumor promotes the formation of reactive oxygen species (ROS), which in turn regulate catabolic pathways involved in muscle atrophy. ROS also exert a dual role within tumor itself, as they can either promote proliferation and vascularization or induce senescence and apoptosis. Accordingly, previous studies that used antioxidants to modulate these ROS-dependent mechanisms, in cancer and cancer cachexia, have obtained contradictory results, hence the need to gather the main findings of these studies and draw global conclusions in order to stimulate more oriented research in this field. Based on the literature reviewed in this paper, it appears that antioxidant supplementation is (1) beneficial in cancer cachectic patients with antioxidant deficiencies, (2) most likely harmful in cancer patients with adequate antioxidant status (i.e., lung, gastrointestinal, head and neck, and esophageal), and (3) not recommended when undergoing radiotherapy. At the moment, measuring the blood levels of antioxidants may help to identify patients with systemic deficiencies. This approach is simple to realize but could not be a gold standard method for cachexia, as it does not necessarily reflect the redox state in other organs, like muscle.

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Efficiency of oxidative phosphorylation in liver mitochondria is decreased in a rat model of peritoneal carcinosis

Cited by 45 publications

References 43 publications

Mechanisms of metabolic dysfunction in cancer-associated cachexia

Mechanisms of metabolic dysfunction in cancer-associated cachexia

Chronic Supplementation With Shark Liver Oil for Reducing Tumor Growth and Cachexia in Walker 256 Tumor-Bearing Rats

The Janus‐Faced Role of Antioxidants in Cancer Cachexia: New Insights on the Established Concepts

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