1,721,044 research outputs found
Malnutrition, outcome, and nutritional support: Time to revisit the issues
No full text[No abstract available
Basics in clinical nutrition: Appetite and its control
No full textFood intake is modulated mainly within the hypothalamus, which continuously regulates the energy status of the body by directly sensing the presence of nutrients in the blood stream and by receiving afferent input from the periphery (oronasal, gut, liver, adipose tissue). Also, monoamines and neuropeptides produced in the brain and the gastrointestinal tract during a meal can directly or indirectly activate vagal afferents and mediate many of the nutrients' effects on appetite, gut functions, anabolism, and catabolism. In the hypothalamus, specific neuronal populations transduce these inputs into neuronal responses and, via second order neuronal signaling pathways and efferent output, into behavioral responses. © 2008 European Society for Clinical Nutrition and Metabolism
MUSCLE PERFORMANCE AND ADENINE-NUCLEOTIDES STATUS IN MCA-SARCOMA TUMOR-BEARING RATS
No full textThe reduction in DNA, RNA, amino acid, and total protein in muscle tissue of tumor-bearing rats may influence muscle function. The effects of MCA-sarcoma tumor burden on muscle performance and adenine nucleotides was evaluated in three fiber types of skeletal muscle. Twenty-one days after MCA-sarcoma tumor inoculation, the gastrocnemius-soleus muscle group of Fischer 344 rats was stimulated using an in situ preparation; tetanic stimulation for 10 min at 7.5, 15, or 30 tetani per min (TPM) or 60 TPM for 5 min (n = 6 control and six tumor-bearing rats/group). ATP, ADP, AMP, IMP, phosphocreatine, and creatine content in white and red gastrocnemius muscle and soleus muscle was measured. There were no differences among controls and tumor-bearing rats in force output; however, ATP content in the soleus muscle of tumor-bearing rats was significantly reduced after 30 TPM for 10 min or 60 TPM for 5 min. The performance of skeletal muscle, over a wide range of stimulation frequency, in tumor-bearing rats does not appear to be influenced by changes in adenine nucleotide content
Oxidative stress and wasting in cancer
No full textPurpose of review Cancer anorexia-cachexia syndrome is becoming a critical component in the comprehensive approach to cancer patients because it influences morbidity, mortality and quality of life. Consequently, pathogenic mechanisms have been elucidated to facilitate development of better therapies. Reported findings indicate that increased production of reactive oxygen species and reduced activity of antioxidant enzymes contribute to development of anorexia and cachexia in cancer. Recent findings Systemic inflammation impairs tryptophan handling promoting oxidative stress, which appears to mimic hypothalamic negative feedback signalling. Thus, trytophan contributes to cancer anorexia by stimulating hypothalamic serotonergic activity and promoting oxidative stress, because neuroinflammation facilitates tryptophan degradation into free radical generators via the kynurenine pathway. Upregulation of protein degradation by increased oxidative stress has been documented in cancer. Also, hypothalamic, cytokine-mediated suppression of fatty acid oxidation reduces food intake, and triggers mitochondrial biogenesis and oxidative gene expression in skeletal muscle, thus potentially increasing oxidative stress. Summary Increased oxidative stress contributes to cancer anorexia and cachexia. Preliminary clinical data on the efficacy of antioxidant therapy in cancer patients are encouraging, but uncertainly persists regarding the optimal dose and timing of administration. Also, better biological/genetic characterization of those cancer patients who are more likely to obtain significant clinical benifits appears necessary
Cancer anorexia: Clinical implications, pathogenesis, and therapeutic strategies
No full textAnorexia and reduced food intake are important issues in the management of patients with cancer because they contribute to the development of malnutrition, increase morbidity and mortality, and impinge on quality of life. Accumulating evidence indicates that cancer anorexia is multifactorial in its pathogenesis, and most of the hypothalamic neuronal signalling pathways modulating energy intake are likely to be involved. Several factors are considered to be putative mediators of cancer anorexia, including hormones (eg, leptin), neuropeptides (eg, neuropeptide Y), cytokines (eg, interleukin 1 and 6, and tumour necrosis factor), and neurotransmitters (eg, serotonin and dopamine). These pathways are not isolated and distinct pathogenic mechanisms but are closely inter-related. However, convincing evidence suggests that cytokines have a vital role, triggering the complex neurochemical cascade which leads to the onset of cancer anorexia. Increased expression of cytokines during tumour growth prevents the hypothalamus from responding appropriately to peripheral signals, by persistently activating anorexigenic systems and inhibiting prophagic pathways. Hypothalamic monoaminergic neurotransmission may contribute to these effects. Thus, the optimum therapeutic approach to anorectic cancer patients should include changes in dietary habits, achieved via nutritional counselling, and drug therapy, aimed at interfering with cytokine expression or hypothalamic monoaminergic neurotransmission
Nutritional care: from the dark ages to the renaissance, to the age of enlightenment
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Intracellular energy signals and dietary calcium: A milky way to the physiologic control of hyperphagia and obesity?
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An analysis of temporal changes in meal number and meal size at onset of anorexia in male tumor-bearing rats
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