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Difference between revisions of "Arruda 2010 Endocrinology"

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{{Publication
{{Publication
|title=Arruda AP, Milanski M, Romanatto T, Solon C, Coope A, Alberici LC, Festuccia WT, Hirabara SM, Ropelle E, Curi R, Carvalheira JB, Vercesi AE, Velloso LA (2010) Hypothalamic actions of tumor necrosis factor alpha provide the thermogenic core for the wastage syndrome in cachexia. Endocrinology 151(2):683-694.
|title=Arruda AP, Milanski M, Romanatto T, Solon C, Coope A, Alberici LC, Festuccia WT, Hirabara SM, Ropelle E, Curi R, Carvalheira JB, Vercesi AE, Velloso LA (2010) Hypothalamic actions of tumor necrosis factor alpha provide the thermogenic core for the wastage syndrome in cachexia. Endocrinology 151:683-94.
|info=[http://www.ncbi.nlm.nih.gov/pubmed/19996183 PMID:19996183]
|info=[http://www.ncbi.nlm.nih.gov/pubmed/19996183 PMID: 19996183], [http://endo.endojournals.org/content/151/2/683.full.pdf+html free pdf]
|authors=Arruda AP, Milanski M, Romanatto T, Solon C, Coope A, Alberici LC, Festuccia WT, Hirabara SM, Ropelle E, Curi R, Carvalheira JB, Vercesi AE, Velloso LA
|authors=Arruda AP, Milanski M, Romanatto T, Solon C, Coope A, Alberici Luciane Carla, Festuccia WT, Hirabara SM, Ropelle E, Curi R, Carvalheira JB, Vercesi AE, Velloso LA
|year=2010
|year=2010
|journal=Endocrinol.
|journal=Endocrinology
|abstract=TNFalpha is an important mediator of catabolism in cachexia. Most of its effects have been characterized in peripheral tissues, such as skeletal muscle and fat. However, by acting directly in the hypothalamus, TNFalpha can activate thermogenesis and modulate food intake. Here we show that high concentration TNFalpha in the hypothalamus leads to increased O<sub>2</sub> consumption/CO<sub>2</sub> production, increased body temperature, and reduced caloric intake, resulting in loss of body mass. Most of the thermogenic response is produced by beta 3-adrenergic signaling to the brown adipose tissue (BAT), leading to increased BAT relative mass, reduction in BAT lipid quantity, and increased BAT mitochondria density. The expression of proteins involved in BAT thermogenesis, such as beta 3-adrenergic receptor, peroxisomal proliferator-activated receptor-gamma coactivator-1 alpha, and uncoupling protein-1, are increased. In the hypothalamus, TNFalpha produces reductions in neuropeptide Y, agouti gene-related peptide, proopiomelanocortin, and melanin-concentrating hormone, and increases CRH and TRH. The activity of the AMP-activated protein kinase signaling pathway is also decreased in the hypothalamus of TNFalpha-treated rats. Upon intracerebroventricular infliximab treatment, tumor-bearing and septic rats present a significantly increased survival. In addition, the systemic inhibition of beta 3-adrenergic signaling results in a reduced body mass loss and increased survival in septic rats. These data suggest hypothalamic TNFalpha action to be important mediator of the wastage syndrome in cachexia.
|abstract=TNFalpha is an important mediator of catabolism in cachexia. Most of its effects have been characterized in peripheral tissues, such as skeletal muscle and fat. However, by acting directly in the hypothalamus, TNFalpha can activate thermogenesis and modulate food intake. Here we show that high concentration TNFalpha in the hypothalamus leads to increased O<sub>2</sub> consumption/CO<sub>2</sub> production, increased body temperature, and reduced caloric intake, resulting in loss of body mass. Most of the thermogenic response is produced by beta 3-adrenergic signaling to the brown adipose tissue (BAT), leading to increased BAT relative mass, reduction in BAT lipid quantity, and increased BAT mitochondria density. The expression of proteins involved in BAT thermogenesis, such as beta 3-adrenergic receptor, peroxisomal proliferator-activated receptor-gamma coactivator-1 alpha, and uncoupling protein-1, are increased. In the hypothalamus, TNFalpha produces reductions in neuropeptide Y, agouti gene-related peptide, proopiomelanocortin, and melanin-concentrating hormone, and increases CRH and TRH. The activity of the AMP-activated protein kinase signaling pathway is also decreased in the hypothalamus of TNFalpha-treated rats. Upon intracerebroventricular infliximab treatment, tumor-bearing and septic rats present a significantly increased survival. In addition, the systemic inhibition of beta 3-adrenergic signaling results in a reduced body mass loss and increased survival in septic rats. These data suggest hypothalamic TNFalpha action to be important mediator of the wastage syndrome in cachexia.
|mipnetlab=BR_Campinas_Vercesi AE
|keywords=TNFalpha, Cachexia, Wastage syndrome
|mipnetlab=BR Campinas Vercesi AE, BR Ribeirao Preto Alberici LC
}}
}}
{{Labeling
{{Labeling
|organism=Rat
|tissues=Nervous system
|preparations=Permeabilized tissue
|instruments=Oxygraph-2k
|instruments=Oxygraph-2k
|organism=Rat
|tissues=Skeletal Muscle
|preparations=Permeabilized Cell or Tissue; Homogenate
}}
}}

Latest revision as of 10:17, 7 March 2020

Publications in the MiPMap
Arruda AP, Milanski M, Romanatto T, Solon C, Coope A, Alberici LC, Festuccia WT, Hirabara SM, Ropelle E, Curi R, Carvalheira JB, Vercesi AE, Velloso LA (2010) Hypothalamic actions of tumor necrosis factor alpha provide the thermogenic core for the wastage syndrome in cachexia. Endocrinology 151:683-94.

Β» PMID: 19996183, free pdf

Arruda AP, Milanski M, Romanatto T, Solon C, Coope A, Alberici Luciane Carla, Festuccia WT, Hirabara SM, Ropelle E, Curi R, Carvalheira JB, Vercesi AE, Velloso LA (2010) Endocrinology

Abstract: TNFalpha is an important mediator of catabolism in cachexia. Most of its effects have been characterized in peripheral tissues, such as skeletal muscle and fat. However, by acting directly in the hypothalamus, TNFalpha can activate thermogenesis and modulate food intake. Here we show that high concentration TNFalpha in the hypothalamus leads to increased O2 consumption/CO2 production, increased body temperature, and reduced caloric intake, resulting in loss of body mass. Most of the thermogenic response is produced by beta 3-adrenergic signaling to the brown adipose tissue (BAT), leading to increased BAT relative mass, reduction in BAT lipid quantity, and increased BAT mitochondria density. The expression of proteins involved in BAT thermogenesis, such as beta 3-adrenergic receptor, peroxisomal proliferator-activated receptor-gamma coactivator-1 alpha, and uncoupling protein-1, are increased. In the hypothalamus, TNFalpha produces reductions in neuropeptide Y, agouti gene-related peptide, proopiomelanocortin, and melanin-concentrating hormone, and increases CRH and TRH. The activity of the AMP-activated protein kinase signaling pathway is also decreased in the hypothalamus of TNFalpha-treated rats. Upon intracerebroventricular infliximab treatment, tumor-bearing and septic rats present a significantly increased survival. In addition, the systemic inhibition of beta 3-adrenergic signaling results in a reduced body mass loss and increased survival in septic rats. These data suggest hypothalamic TNFalpha action to be important mediator of the wastage syndrome in cachexia. β€’ Keywords: TNFalpha, Cachexia, Wastage syndrome

β€’ O2k-Network Lab: BR Campinas Vercesi AE, BR Ribeirao Preto Alberici LC


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Organism: Rat  Tissue;cell: Nervous system  Preparation: Permeabilized tissue 



HRR: Oxygraph-2k