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Query: UMLS:C0038187 (starvation)
 24,951 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

As a complex syndrome, cachexia has different clinical manifestations; anorexia appears to be one of the most frequent findings, together with weight loss. Anorexia is the cause and partly the consequence of metabolic changes and of progressive undernourishment. In cancer cachexia, weight loss is associated with a marked decrease of food intake and severe alteration of body composition. Malnourished cancer patients show a marked loss of adipose tissue and protein mass with BIA evidence of decreased body cell mass and expansion of extracellular water. The mechanisms of anorexia and cachexia are still a matter of debate, but the possible involvement of cytokines in the pathogenesis of this syndrome has opened up new possibilities for its understanding and treatment. As a result of the multifactorial etiology of cancer cachexia/anorexia, therapies that stimulate appetite and promote greater food intake, coupled with factors that influence metabolism and cytokine production may be an optimal therapeutic strategy. Of particular interest appears to be the possible role played by fish oil in antagonizing the negative effects of cytokines. Future research in this field will help clinicians develop new methods to treat patients who have disease-induced starvation and wasting.
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PMID:Food intake and body composition in cancer cachexia. 885 Feb 14

We test the hypothesis that human immunodeficiency virus (HIV)-related weight loss is accompanied by inappropriately large losses of fat-free mass (FFM). Our secondary aims were to examine whether FFM increases during weight gain and to compare several techniques for measuring FFM change. FFM was measured at intervals averaging 5 months in 21 AIDS patients by means of skinfold thickness (SF), dual-energy x-ray absorptiometry (DEXA), total body water (TBW), and bioelectrical impedance using the equation of the manufacturer of the equipment (BIA(EZComp)) and a published prediction equation (BIA(Segal)). The FFM content of weight loss was similar for SF (57%), DEXA (60%), TBW (55%) and BIA(EZComp) (65%), but the result from BIA(Segal) (78%) was higher. The results were close to predicted starvation values apart from the results with BIA(Segal), which were significantly higher than predicted values. Weight gain was also composed of a large proportion of FFM. There were large intermethod differences in measurements of absolute FFM, but for measuring changes in FFM, the bias between SF, DEXA, and TBW was minimal. The results of BIA vary with the prediction equation used. In this group of patients with the acquired immune deficiency syndrome (AIDS), weight loss was composed of a large proportion of FFM, but in general this is compatible with undernutrition as the underlying cause and does not support the hypothesis of excessive FFM catabolism in HIV disease. SF, DEXA, TBW, and BIA(Segal) show reasonable agreement for measuring body composition changes. This information should be considered in the design of future intervention studies for HIV-related wasting.
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PMID:Longitudinal changes in body composition measured with a variety of methods in patients with AIDS. 905 20

Progressive wasting is common in many types of cancer and is one of the most important factors leading to the early death of cancer patients. Although anorexia frequently accompanies cachexia it has been difficult to establish a simple cause-and-effect relationship, and nutritional supplementation is not able to effectively reverse the process of cachexia. An increased resting energy expenditure may contribute to weight loss in some cancer patients and may explain the increased oxidation of fat. Futile energy-consuming cycles, such as the Cori cycle, may contribute to the increased energy demand. Unlike starvation, weight loss in cancer arises equally from loss of muscle and fat, and the process is characterized by an increased catabolism of skeletal muscle and a decrease in protein synthesis. Several experimental studies have suggested a role for the cytokines tumor necrosis factor alpha, interleukins-1 and -6, and interferon gamma as mediators of the process of cachexia, although conclusive data supporting a role in human disease are often lacking. Catabolic factors capable of direct breakdown of muscle and adipose tissue appear to be secreted by cachexia-inducing human tumors and may play an active role in the process of tissue degeneration. Pharmacologic intervention using antagonists to cachexia factors may be capable of reversing the wasting process.
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PMID:Cancer cachexia: metabolic alterations and clinical manifestations. 905 39

The anorexia (anx) mutation causes reduced food intake in preweanling mice, resulting in death from starvation within 3-4 weeks. In wild-type rodents, starvation induces increased neuropeptide Y (NPY) mRNA levels in the arcuate nucleus that promotes compensatory hyperphagia. Despite severely decreased body weight and food intake at 3-weeks age, anx/anx mice do not show elevated NPY mRNA levels in the hypothalamic arcuate nucleus compared to wild-type/heterozygous littermates. The NPY mRNA levels can be upregulated in normal mice at this chronological age, because 24-h food deprivation increased arcuate NPY mRNA in wild-type littermates. The unresponsiveness of NPY expression in the arcuate of anx/anx mice was paralleled by serotonergic hyperinnervation of the arcuate nucleus, comparable to the serotonergic hyperinnervation previously reported in the rest of the anx/anx brain. This result is consistent with the hypothesis that wasting disorders are accompanied by disregulation of NPY mRNA expression in the arcuate nucleus, and suggests that reduced food intake, the primary behavioral phenotype of the anx/anx mouse, may be the result of altered hypothalamic mechanisms that normally regulate feeding.
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PMID:Neuropeptide Y mRNA and serotonin innervation in the arcuate nucleus of anorexia mutant mice. 959 28

Wasting is a debilitating complication of the human immunodeficiency virus/acquired immunodeficiency syndrome (HIV/AIDS) and is a major cause of morbidity and mortality. The etiology of wasting in HIV/AIDS is complex and its origins are multifactorial. Both patterns of simple starvation and the more complex metabolic and endocrine alterations associated with stress and trauma have been described in patients with the AIDS wasting syndrome. Observations suggest that the pathophysiology of the wasting in individual patients with HIV/AIDS may vary according to the primary cause of wasting and underlying disease activity. Optimal treatment of the AIDS wasting syndrome will depend on a thorough evaluation of all possible contributing factors. This review addresses the pathophysiologic basis of weight loss in HIV/AIDS, based on the current literature.
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PMID:The etiology of wasting in the human immunodeficiency virus and acquired immunodeficiency syndrome. 962 88

The aim of the study was to evaluate the possible contribution of changes in energy metabolism and substrate oxidation rates to malnutrition in Crohn's disease and to assess the effect of enteral nutrition on these parameters. Energy metabolism was evaluated by indirect calorimetry in 32 patients with active Crohn's disease and 19 age- and sex-matched healthy individuals. Measurements were done in the postabsorptive state. Seven out of 32 patients received enteral nutrition via a nasogastric tube. In these patients, resting energy metabolism was determined at d 0 (postabsorptive), 7, 14 (during full enteral nutrition) and 15 (postabsorptive). Resting energy expenditure was not significantly different between patients and controls, whereas the respiratory quotient (RQ) was lower in patients (0.78 +/- 0.05 vs. 0.86 +/- 0.05; P < 0.05). During enteral nutrition in 7 patients with Crohn's disease, the RQ increased on d 7 compared with d 0 and remained high even after cessation of enteral nutrition (d 0, 0.78 +/- 0.03; d 7, 0.91 +/- 0.04; d 15, 0. 84 +/- 0.05; P < 0.05; d 7 and 15 vs. d 0). No effects of enteral nutrition on resting energy expenditure were found. Active Crohn's disease is associated with changes in substrate metabolism that resemble a starvation pattern. These changes appear not to be specific to Crohn's disease but to malnutrition and are readily reversed by enteral nutrition. Enteral nutrition did not affect resting energy expenditure. Wasting is a consequence of malnutrition but not of hypermetabolism in Crohn's disease.
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PMID:Energy and substrate metabolism in patients with active Crohn's disease. 1020 59

Hepatocyte nuclear factors 3 (HNF-3) belong to an evolutionarily conserved family of transcription factors that are critical for diverse biological processes such as development, differentiation, and metabolism. To study the physiological role of HNF-3alpha, we generated mice that lack HNF-3alpha by homologous recombination in embryonic stem cells. Mice homozygous for a null mutation in the HNF-3alpha gene develop a complex phenotype that is characterized by abnormal feeding behavior, progressive starvation, persistent hypoglycemia, hypotriglyceridemia, wasting, and neonatal mortality between days 2 and 14. Hypoglycemia in HNF-3alpha-null mice leads to physiological counter-regulatory responses in glucocorticoid and growth hormone production and an inhibition of insulin secretion but fails to stimulate glucagon secretion. Glucagon-producing pancreatic alpha cells develop normally in HNF-3alpha-/- mice, but proglucagon mRNA levels are reduced 50%. Furthermore, the transcriptional levels of neuropeptide Y are also significantly reduced shortly after birth, implying a direct role of HNF-3alpha in the expression of these genes. In contrast, mRNA levels were increased in HNF-3 target genes phosphofructo-2-kinase/fructose-2,6-bisphophatase, insulin growth factor binding protein-1, and hexokinase I of HNF-3alpha-null mice. Mice lacking one or both HNF-3alpha alleles also show impaired insulin secretion and glucose intolerance after an intraperitoneal glucose challenge, indicating that pancreatic beta-cell function is also compromised. Our results indicate that HNF-3alpha plays a critical role in the regulation of glucose homeostasis and in pancreatic islet function.
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PMID:Impaired glucose homeostasis and neonatal mortality in hepatocyte nuclear factor 3alpha-deficient mice. 1046 78

Progressive wasting is common in many types of cancer and is one of the most important factors leading to early death in cancer patients. Weight loss is a potent stimulus to food intake in normal humans and animals. The persistence of anorexia in cancer patients, therefore, implies a failure of this adaptive feeding response, although the weight loss in the patients differs from that found in simple starvation. Tremendous progress has been made in the last 5 years with regard to the regulation of feeding and body weight. It has been demonstrated that leptin, a hormone secreted by adipose tissue, is an integral component of the homeostatic loop of body weight regulation. Leptin acts to control food intake and energy expenditure via neuropeptidergic effector molecules within the hypothalamus. Complex interactions among the nervous, endocrine, and immune systems affect the loop and induce behavioral and metabolic responses. A number of cytokines, including tumor necrosis factor-alpha, interleukins 1 and 6, IFN-gamma, leukemia inhibitory factor, and ciliary neurotrophic factor have been proposed as mediators of the cachectic process. Cytokines may play a pivotal role in long-term inhibition of feeding by mimicking the hypothalamic effect of excessive negative feedback signaling from leptin. This could be done by persistent stimulation of anorexigenic neuropeptides such as corticotropin-releasing factor, as well as by inhibition of the neuropeptide Y orexigenic network that consists of opioid peptides and galanin, in addition to the newly identified melanin-concentrating hormone, orexin, and agouti-related peptide. Information is being gathered, although it is still insufficient, on such abnormalities in the hypothalamic neuropeptide circuitry in tumor-bearing animals that coincide with the development of anorexia and cachexia. Characterization of the feeding-associated gene products have revealed new biochemical pathways and molecular targets for pharmacological intervention that will likely lead to new treatments. Although therapeutic intervention using neuropeptide agonists/antagonists is now directed at obesity treatment, it may also have an effect on treating cancer anorexia-cachexia, especially when combined with other agents that have effects on muscle and protein breakdown.
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PMID:Cancer anorexia-cachexia syndrome: are neuropeptides the key? 1049 94

Anorexia nervosa is one of the most common forms of malnutrition observed in Western society in individuals without physical diseases, with an average risk of mortality of 20% in a younger population aged between 15 and 25 years. It is characterised by an initial dramatic decrease in food intake that leads to profound depletion in muscle and fat mass. During the course of the disease, the resting energy expenditure decreases proportionally to the loss of lean body mass with a decrease in thyroid hormone secretion. The metabolic adaptation during anorexia nervosa is similar to that observed during starvation with a relative sparing of protein stores. After an initial weight loss, the total energy expenditure is similar to that in normal individuals, with a decrease in resting energy expenditure and an increased energy-related physical activity. At the end stage of wasting, however, physical activity dramatically decreases as well as energy intake. This metabolic adaptation of semi-starvation is impaired during refeeding with an increase in the thermic effect of food and a high risk of refeeding syndrome with severe hypophosphatemia.
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PMID:From malnutrition to refeeding during anorexia nervosa. 1056 98

Nutritional alterations are common in HIV infection. Early studies documented weight loss and protein depletion, a finding associated with body cell mass depletion in untreated patients. The application of highly active antiretroviral therapy has led to a decreased incidence of malnutrition, although altered body fat distribution and metabolic alterations, including hyperlipidemia and insulin resistance, are common sequelae. The development of malnutrition is multifactorial and occurs through changes in caloric intake, nutrient absorption, or energy expenditure. Clinically, malnutrition develops as a result of either starvation or cachexia. Other hormonal and endocrinologic alterations include hypercortisolemia and hypogonadism. The rationale for providing nutritional support to AIDS patients is based upon the assumptions that nutrition status can be improved and that such improvements have clinical benefits. The results of hypercaloric feeding studies, including the use of appetite stimulants, indicate that weight gain is possible but that the weight gained is predominantly fat. In contrast, anabolic agents and resistance training exercise have been shown to promote body cell mass repletion and skeletal muscle gain. Cytokine inhibitors also have been evaluated for the treatment of wasting in HIV infection. Development of combination therapies, preventive therapies, and efficient and cost-effective therapies are current tasks in the field.
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PMID:Nutritional alterations associated with HIV infection. 1112 32


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