Leptin and tumor growth in rats

López‐Soriano, Joaquín; Carbó, Neus; Tessitore, Luciana; López‐Soriano, Francisco J.; Argilés, Josep Μ.

doi:10.1002/(sici)1097-0215(19990531)81:5<726::aid-ijc10>3.0.co;2-q

Cited by 49 publications

(21 citation statements)

References 23 publications

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“…However, in the present study, leptin mRNA level was greatly decreased in WAT of cachectic mice, which is in agreement with previous reports that leptin gene expression in white fat and circulating leptin levels are markedly lower in mice bearing the MAC16 tumor (25) and in cachectic rats with Yoshida hepatoma (33). The fall in leptin production by adipose tissue seems to be the consequence of significant fat loss, which argues against a role for leptin in mediating enhanced lipolysis in cachexia.…”

Section: Discussionsupporting

confidence: 93%

Zinc-α2-glycoprotein, a lipid mobilizing factor, is expressed in adipocytes and is up-regulated in mice with cancer cachexia

Chen

Bao

Jenkins

et al. 2004

Proc. Natl. Acad. Sci. U.S.A.

280

261

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Zinc-␣2-glycoprotein (ZAG), a 43-kDa protein, is overexpressed in certain human malignant tumors and acts as a lipid-mobilizing factor to stimulate lipolysis in adipocytes leading to cachexia in mice implanted with ZAG-producing tumors. Because white adipose tissue (WAT) is an endocrine organ secreting a wide range of protein factors, including those involved in lipid metabolism, we have investigated whether ZAG is produced locally by adipocytes. ZAG mRNA was detected by RT-PCR in the mouse WAT depots examined (epididymal, perirenal, s.c., and mammary gland) and in interscapular brown fat. In WAT, ZAG gene expression was evident in mature adipocytes and in stromal-vascular cells. Using a ZAG Ab, ZAG protein was located in WAT by Western blotting and immunohistochemistry. Mice bearing the MAC16-tumor displayed substantial losses of body weight and fat mass, which was accompanied by major increases in ZAG mRNA and protein levels in WAT and brown fat. ZAG mRNA was detected in 3T3-L1 cells, before and after the induction of differentiation, with the level increasing progressively after differentiation with a peak at days 8 -10. Both dexamethasone and a ␤3 agonist, BRL 37344, increased ZAG mRNA levels in 3T3-L1 adipocytes. ZAG gene expression and protein were also detected in human adipose tissue (visceral and s.c.). It is suggested that ZAG is a new adipose tissue protein factor, which may be involved in the modulation of lipolysis in adipocytes. Overexpression in WAT of tumor-bearing mice suggests a local role for adipocyte-derived ZAG in the substantial reduction of adiposity of cancer cachexia.

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Section: Discussionsupporting

confidence: 93%

Zinc-α2-glycoprotein, a lipid mobilizing factor, is expressed in adipocytes and is up-regulated in mice with cancer cachexia

Chen

Bao

Jenkins

et al. 2004

Proc. Natl. Acad. Sci. U.S.A.

280

261

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“…The involvement of leptin in lipid depletion during cachexia is unlikely. Leptin circulating levels and its expression in adipose tissue decrease in tumour-bearing animals and patients with gastric cancer, also in the absence of lipid depletion and anorexia [24,25].…”

Section: Alterations In Lipid Metabolismmentioning

confidence: 99%

The “parallel pathway”: a novel nutritional and metabolic approach to cancer patients

et al. 2010

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Cancer-associated malnutrition results from a deadly combination of anorexia, which leads to reduced food intake, and derangements of host metabolism inducing body weight loss, and hindering its reversal with nutrient supplementation. Cancer patients often experience both anorexia and weight loss, contributing to the onset of the clinical feature named as anorexia-cachexia syndrome. This condition has a negative impact upon patients' nutritional status. The pathogenesis of the anorexia-cachexia syndrome is multifactorial, and is related to: tumour-derived factors, host-derived factors inducing metabolic derangements, and side effects of anticancer therapies. In addition, the lack of awareness of cancer patients' nutritional issues and status by many oncologists, frequently results in progressive weight loss going undiagnosed until it becomes severe. The critical involvement of host inflammatory response in the development of weight loss, and, in particular, lean body mass depletion, limits the response to the provision of standard nutrition support. A novel nutritional and metabolic approach, named "parallel pathway", has been devised that may help maintain or improve nutritional status, and prevent or delay the onset of cancer cachexia. Such an approach may improve tolerance to aggressive anticancer therapies, and ameliorate the functional capacity and quality of life even in advanced disease stages. The "parallel pathway" implies a multiprofessional and multimodal approach aimed at ensuring early, appropriate and continuous nutritional and metabolic support to cancer patients in any phase of their cancer journey.

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“…CAT/GS mRNA ratio adipose tissue, which contains slightly less GS enzyme activity than BAT in the rat [10] and in the mouse (H. Lie-Venema and W. H. Lamers, unpublished work), the ratio of CAT to GS enzyme activity was 3-fold lower than in BAT, indicating that, in this tissue, the 5h upstream regulatory region is not active. The brain was also included in the group of organs in which the 5h enhancer element is not very active or efficiently used.…”

Section: Organmentioning

confidence: 99%

“…However, in a number of organs, GS is expressed at much higher levels to facilitate ammonia and\or glutamate detoxification [1][2][3][4][5]. In the rat, high to very high GS levels can be found in the epithelium lining the epididymal duct of the caput epididymis, in astrocytes, in pericentral hepatocytes and in adipocytes, whereas in myocytes of skeletal muscle, the epithelium lining the lung bronchioli and the small intestine, GS is expressed to a lesser extent [6][7][8][9][10][11]. Probably the best studied organ with respect to the regulation of GS expression is the liver.…”

Section: Introductionmentioning

confidence: 99%

Role of the 5′ enhancer of the glutamine synthetase gene in its organ-specific expression

Lie-Venema

Boer

Moorman

et al. 1997

Biochemical Journal

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In mammals, glutamine synthetase (GS) is expressed in a large number of organs, but the precise regulation of its expression is still obscure. Therefore a detailed analysis of the activity of the upstream regulatory element of the GS gene in the transcriptional regulation of its expression was carried out in transgenic mice carrying the chloramphenicol acetyltransferase (CAT) gene under the control of the upstream regulatory region of the GS gene. CAT and GS mRNA expression were compared in liver, epididymis, lung, adipocytes, testis, kidney, skeletal muscle and gastrointestinal tract, both quantitatively by ribonuclease-protection analysis and topographically by in situ hybridization. It was found that the upstream regulatory region is active with respect both to the level and to the topography of GS gene expression in liver, epididymis, gastrointestinal tract (stomach, small intestine and colon) and skeletal muscle. On the other hand, in the kidney, brain, adipocytes, spleen, lung and testis, GS gene expression is not or only partly regulated by the 5´ enhancer. A second enhancer, identified within the first intron, may regulate GS expression in the latter organs. Furthermore, CAT expression in the brain did not co-localize with that of GS, showing that the 5´ regulatory region of the GS gene does not direct its expression to the astrocytes.

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Leptin and tumor growth in rats

Cited by 49 publications

References 23 publications

Zinc-α2-glycoprotein, a lipid mobilizing factor, is expressed in adipocytes and is up-regulated in mice with cancer cachexia

Zinc-α2-glycoprotein, a lipid mobilizing factor, is expressed in adipocytes and is up-regulated in mice with cancer cachexia

The “parallel pathway”: a novel nutritional and metabolic approach to cancer patients

Role of the 5′ enhancer of the glutamine synthetase gene in its organ-specific expression

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