Cancer and malnutrition—A critical interaction: A review

Balducci, Lodovico; Hardy, Cheryl L.

doi:10.1002/ajh.2830180112

Cited by 23 publications

(10 citation statements)

References 59 publications

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“…In patients with malignant tumours, anorexia, weight loss, emaciation and progressive alterations of vital functions are common features associated with cancer cachexia (De Wys, 1985). Although in some cases anorexia, gastrointestinal obstruction or malabsorption are responsible for the weight loss of cachectic patients (Balducci and Hardy, 1985), it cannot be wholely attributed to these causes and therefore it has been postulated to be due to a decrease in the energetic efficiency of the cancer patient. Among the factors involved in decreasing the energetic efficiency, skeletal muscle protein turnover seems to have a very significant role as we have previously shown (see Argilés et al, 1997, for review).…”

Section: Discussionmentioning

confidence: 99%

TNF-α is involved in activating DNA fragmentation in skeletal muscle

et al. 2002

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Intraperitoneal administration of 100 mg kg 71 (body weight) of tumour necrosis factor-a to rats for 8 consecutive days resulted in a significant decrease in protein content, which was concomitant with a reduction in DNA content. Interestingly, the protein/DNA ratio was unchanged in the skeletal muscle of the tumour necrosis factor-a-treated animals as compared with the non-treated controls. Analysis of muscle DNA fragmentation clearly showed enhanced laddering in the skeletal muscle of tumour necrosis factor-a-treated animals, suggesting an apoptotic phenomenon. In a different set of experiments, mice bearing a cachexia-inducing tumour (the Lewis lung carcinoma) showed an increase in muscle DNA fragmentation (9.8-fold) as compared with their non-tumour-bearing control counterparts as previously described. When gene-deficient mice for tumour necrosis factor-a receptor protein I were inoculated with Lewis lung carcinoma, they were also affected by DNA fragmentation; however the increase was only 2.1-fold. These results suggest that tumour necrosis factor-a partly mediates DNA fragmentation during experimental cancer-associated cachexia.

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Section: Discussionmentioning

confidence: 99%

TNF-α is involved in activating DNA fragmentation in skeletal muscle

et al. 2002

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“…Although in many cases anorexia seems to be the cause of this syndrome [17], malabsorption or metabolic changes are often responsible for the weight loss of cachectic patients [11,18]. During cancer cachexia, the expression of both UCP2 and UCP3 is upregulated in skeletal muscle [19], this increase being related to a rise in the circulating levels of free fatty acids (FFA) [20].…”

Section: Introductionmentioning

confidence: 99%

Activation of UCPs gene expression in skeletal muscle can be independent on both circulating fatty acids and food intake

et al. 2005

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Implantation of a fast growing tumour to mice (Lewis lung carcinoma) resulted in a clear cachectic state characterized by a profound muscle wasting. This was accompanied by a significant increase in both UCP2 and UCP3 gene expression in skeletal muscle and heart. Interestingly, this increase in gene expression was not linked to a rise in circulating fatty acids or in a decrease in food intake, as previously reported in other pathophysiological states. These results question the concept that hyperlipaemia is the only factor controlling UCP gene expression in different pathophysiological conditions. In addition, the present work suggests that UCPs might participate in a counter-regulatory mechanism to lower the production of ROS.

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“…Weight loss, emaciation and progressive alterations of vital functions are common features associated with cancer cachexia. Although in many cases malabsorption or metabolic changes are responsible for the weight loss of cachectic patients (Argilés et al, 1992, 1997), in other cases this cannot be completely attributed to such causes and, therefore, it has been postulated to be related to anorexia (Balducci and Hardy, 1985). Therefore, understanding the mechanism by which anorexia occurs during tumor growth might allow for the development of treatments to prevent or improve the weight loss associated with cancer cachexia.…”

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confidence: 99%

Leptin and tumor growth in rats

et al. 1999

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We have examined the role of leptin in tumor‐induced anorexia in 2 different tumor models. In rats bearing the Yoshida AH‐130 ascites hepatoma, the reduction in food intake becomes important from day 6 after tumor inoculation. Interestingly, at day 4, when the animals do not show any anorectic behavior, circulating leptin levels were already reduced. Indeed, in all the tumor‐bearing groups studied the levels of leptin were lower than in control animals. Moreover, the changes in the circulating levels paralleled changes in adipose tissue leptin mRNA expression, even at early stages following tumor inoculation when neither food intake nor fat stores were modified by the presence of a tumor. Interestingly, 7‐day pair‐fed controls showed changes similar to those present in tumor‐bearing rats. These results agree with previous observations relating fasting to decreased leptin expression. Similar results were observed in another tumor model, the mouse Lewis lung carcinoma; i.e., at day 8 after tumor inoculation (when the animals did not show anorexia) both the circulating levels and the adipose leptin mRNA expression were also reduced. Our results suggest that experimental cancer‐induced anorexia is not related to leptin changes. Int. J. Cancer 81:726–729, 1999. © 1999 Wiley‐Liss, Inc.

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Cancer and malnutrition—A critical interaction: A review

Cited by 23 publications

References 59 publications

TNF-α is involved in activating DNA fragmentation in skeletal muscle

TNF-α is involved in activating DNA fragmentation in skeletal muscle

Activation of UCPs gene expression in skeletal muscle can be independent on both circulating fatty acids and food intake

Leptin and tumor growth in rats

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