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

Because critical illness often creates a vigorous metabolic response to permit the repair of injured tissues, nutritional considerations are essential in the medical management of the critically ill patient. Individuals with seemingly adequate endogenous nutritional reserves may rapidly develop complications of starvation. Nutritional supplementation is essential; however, critically ill patients may not readily tolerate nutritional support. Calories may need to be withheld until the patient is able to tolerate and utilize nutritional support. Once the decision to initiate nutritional support is made, nutritional status, level of stress, metabolic condition, and vital organ function influence the patient's nutritional requirements. An assessment of the patient's metabolic condition provides data useful in determining the need for supplemental electrolytes or macronutrients. These data also provide information regarding vital organ function, which is necessary for utilization of the fuel and substrate. Aggressive monitoring and judicious nutritional supplementation will afford the critically ill patient the best chance of recovery.
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PMID:Assessing the nutritional needs of the critically ill patient. 227 Jun 94

Exocrine and endocrine release of rat submandibular gland kallikrein has been shown to be low after parasympathetic and beta-adrenergic stimulation but greatly increased after alpha-adrenergic stimulation. In the present study, release of glandular kallikrein was investigated under conditions known to give a reflex-induced salivary gland response. Heat stress induced a rich flow of saliva originating in the submandibular glands. Salivary kallikrein secretory rate was higher than after parasympathetic stimulation but lower than after sympathetic stimulation (P less than 0.005). Only heat stress increased circulating glandular kallikrein (12.7 +/- 0.8 ng ml-1 before heat exposure and 53.3 +/- 14.1 ng ml-1 40 min afterwards, P less than 0.005). There were no indications that the endocrine release of kallikrein was due to non-specific leakage. Atropine abolished heat-induced salivation and endocrine kallikrein secretion, possibly through interference with central pathways (P less than 0.05). However, phentolamine did not, which may indicate as an yet unidentified mediator of endogenous kallikrein release. The salivary gland response to acid and ether was comparable to that observed after parasympathetic nerve stimulation and was abolished by atropine (P less than 0.005). Stimuli known to influence other salivary gland ductal cells, such as aggression and starvation followed by drinking, also did not increase the plasma concentration of glandular kallikrein. The fact that various conditions which induce salivation did not increase circulating glandular kallikrein, coupled with the fact that kallikrein concentration was the highest in animals that died from heat stress, may suggest that the increase in circulating glandular kallikrein seen after heat stress may be pathological and could contribute to the development of heat shock.
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PMID:Exocrine and endocrine release of kallikrein after reflex-induced salivary secretion. 235 56

We conclude that population fluctuations in Microtus in southern Indiana are produced by a syndrome of changes in birth and death rates similar to that found in other species of voles and lemmings. The mechanisms which cause the changes in birth and death rates are demolished by fencing the population so that no dispersal can occur. Dispersal thus seems critical for population regulation in Microtus. Because most dispersal occurs during the increase phase of the population cycle and there is little dispersal during the decline phase, dispersal is not directly related to population density. Hence the quality of dispersing animals must be important, and we have found one case of increased dispersal tendency by one genotype. The failure of population regulation of Microtus in enclosed areas requires an explanation by any hypothesis attempting to explain population cycles in small rodents. It might be suggested that the fence changed the predation pressure on the enclosed populations. However, the fence was only 2 feet (0.6 meter) high and did not stop the entrance of foxes, weasels, shrews, or avian predators. A striking feature was that the habitat in the enclosures quickly recovered from complete devastation by the start of the spring growing season. Obviously the habitat and food quality were sufficient to support Microtus populations of abnormally high densities, and recovery of the habitat was sufficiently quick that the introduction of new animals to these enclosed areas resulted in another population explosion. Finally, hypotheses of population regulation by social stress must account for the finding that Microtus can exist at densities several times greater than normal without "stress" taking an obvious toll. We hypothesize that the prevention of dispersal changes the quality of the populations in the enclosures in comparison to those outside the fence. Voles forced to remain in an overcrowded fenced population do not suffer high mortality rates and continue to reproduce at abnormally high densities until starvation overtakes them. The initial behavioral interactions associated with crowding do not seem sufficient to cause voles to die in situ. What happens to animals during the population decline? Our studies have not answered this question. The animals did not appear to disperse, but it is possible that the method we used to measure dispersal (movement into a vacant habitat) missed a large segment of dispersing voles which did not remain in the vacant area but kept on moving. Perhaps the dispersal during the increase phase of the population cycle is a colonization type of dispersal, and the animals taking part in it are likely to stay in a new habitat, while during the population decline dispersal is a pathological response to high density, and the animals are not attracted to settling even in a vacant habitat. The alternative to this suggestion is that animals are dying in situ during the decline because of physiological or genetically determined behavioral stress. Thus the fencing of a population prevents the change in rates of survival and reproduction, from high rates in the increase phase to low rates in the decline phase, and the fenced populations resemble "mouse plagues." A possible explanation is that the differential dispersal of animals during the phase of increase causes the quality of the voles remaining at peak densities in wild populations to be different from the quality of voles at much higher densities in enclosures. Increased sensitivity to density in Microtus could cause the decline of wild populations at densities lower than those reached by fenced populations in which selection through dispersal has been prevented. Fencing might also alter the social interactions among Microtus in other ways that are not understood. The analysis of colonizing species by MacArthur and Wilson (27) can be applied to our studies of dispersal in populations of Microtus. Groups of organisms with good dispersal and colonizing ability are called r strategists because they have high reproductive potential and are able to exploit a new environment rapidly. Dispersing voles seem to be r strategists. Young females in breeding condition were over-represented in dispersing female Microtus (17). The Tf(C)/Tf(E) females, which were more common among dispersers during the phase of population increase (Fig. 6), also have a slight reproductive advantage over the other Tf genotypes (19). Thus in Microtus populations the animals with the highest reproductive potential, the r strategists, are dispersing. The segment of the population which remains behind after the selection-via-dispersal are those individuals which are less influenced by increasing population densities. These are the individuals which maximize use of the habitat, the K strategists in MacArthur and Wilson's terminology, or voles selected for spacing behavior. Thus we can describe population cycles in Microtus in the same theoretical framework as colonizing species on islands. Our work on Microtus is consistent with the hypothesis of genetic and behavioral effects proposed by Chitty (6) (Fig. 7) in that it shows both behavioral differences in males during the phases of population fluctuation and periods of strong genetic selection. The greatest gaps in our knowledge are in the area of genetic-behavioral interactions which are most difficult to measure. We have no information on the heritability of aggressive behavior in voles. The pathways by which behavioral events are translated into physiological changes which affect reproduction and growth have been carefully analyzed by Christian and his associates (28) for rodents in laboratory situations, but the application of these findings to the complex field events described above remains to be done. Several experiments are suggested by our work. First, other populations of other rodent species should increase to abnormal densities if enclosed in a large fenced area (29). We need to find situations in which this prediction is not fulfilled. Island populations may be an important source of material for such an experiment (30). Second, if one-way exit doors were provided from a fenced area, normal population regulation through dispersal should occur. This experiment would provide another method by which dispersers could be identified. Third, if dispersal were prevented after a population reached peak densities, a normal decline phase should occur. This prediction is based on the assumption that dispersal during the increase phase is sufficient to ensure the decline phase 1 or 2 years later. All these experiments are concerned with the dispersal factor, and our work on Microtus can be summarized by the admonition: study dispersal.
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PMID:Population cycles in small rodents. 473 49

1. Aggressive behaviour was elicited in rats that had been deprived of food for 20 h daily (starved), by chronic administration of Cannabis sativa extract or (-)-Delta(9)-trans-tetrahydrocannabinol.2. The influence of intraperitoneal (i.p.) or oral glucose administration, cold environment, acidosis, and corn, and protein-free diets on this aggressiveness was studied.3. Intraperitoneal injections of glucose (100-1,600 mg/kg) did not alter the aggressiveness induced by marihuana in starved rats; glucose given orally, however, blocked this behaviour.4. Low temperature (14 degrees C) strongly potentiated the aggressive behaviour induced by marihuana in the starved rats.5. Lactic acid in doses capable of potentiating thiopental anaesthesia, failed to alter the marihuana-aggressiveness of starved rats or to facilitate this effect of marihuana in rats fed ad libitum. The same negative results were obtained with ammonium chloride.6. In rats fed ad libitum with protein-free or corn diets, marihuana administered chronically did not elicit aggressive behaviour. However, aggressiveness appeared when rats were fed for only 2 h daily on those diets.7. The results suggest that the stress of hunger (and not hypoglycaemia, acidosis or lack of specific nutrients due to starvation) is the factor that facilitates the development of aggressive behaviour by chronic administration of marihuana.
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PMID:Factors influencing the aggressiveness elicited by marihuana in food-deprived rats. 506 30

The successful treatment by behavioral methods of self-starvation and self-injury in a 35-year-old psychiatric in-patient, with a diagnosis of borderline personality disorder, is described. An individualized program using positive and negative reinforcers to increase food and fluid intake was used, while a token economy therapeutic milieu with time out was used to decrease acts of self-injury and aggression. Progress in treatment generalized to a non-secure treatment environment, and was maintained at an 8-month follow-up. The study illustrates the differential response of active and passive self injurious behaviors to group-based and individual treatments, respectively.
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PMID:The behavioral treatment of self-starvation and severe self-injury in a patient with borderline personality disorder. 818 51

Hepatic lipidosis occurs when lipid mobilized to the liver exceeds lipid leaving the liver via formation of very-low-density lipoproteins or by oxidation. Hepatic lipidosis in cats is associated with overt liver dysfunction. In affected cats, excess lipid is mobilized to the liver because of starvation. Removal of hepatic lipid may be impaired because of protein malnutrition, a relative carnitine deficiency, or oxidative damage to peroxisomes and other hepatic organelles. Hepatic lipidosis occurs in adult cats, and is manifest by signs of weight loss, depression, vomiting, and icterus. Diagnosis is achieved by evaluating laboratory and diagnostic imaging data, in conjunction with a liver biopsy. Aggressive tube feeding is the treatment of choice. With this treatment, survival rates are 60% to 80%.
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PMID:Feline hepatic lipidosis. 905 87

The development of malnutrition is often rapid in critically ill patients with sepsis and severe trauma. In such patients, a wide array of hormonal and nonhormonal mediators are released, inducing complex metabolic changes. Hypermetabolism, associated with protein and fat catabolism, negative nitrogen balance, hyperglycemia, and resistance to insulin, constitute the hallmark of this response. Critically ill patients demonstrate a marked alteration in the adaptation to prolonged starvation: resting metabolic rate and tissue catabolism stay elevated, while ketogenesis remains suppressed. The response to nutrition support is impaired. Substrate use is modified in septic and traumatized patients. Glucose administration during severe aggression does not suppress the enhanced hepatic glucose production and the lipolysis. This phenomenon, related to tissue insulin resistance, ensures a high flow of glucose to the predominantly glucose-consuming cells, such as the wound, the inflammatory, and immune cells, all insulin-independent cells. In addition, the elevated protein catabolism is difficult to abolish, even during aggressive nutrition support. Thus, in patients with prolonged aggression, these alterations produce a progressive loss of body cell mass and foster the development of malnutrition and it dire complications. In this review, the relevant physiologic data and the nutritional implications related to energy metabolism in septic and injured patients are discussed, while potential therapeutic strategies are proposed.
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PMID:Energy metabolism in sepsis and injury. 929 Jan 9

Prospects for future development in the field of gastrointestinal pharmacology were briefly discussed on the base of the present progress in our own research on animal models of gastric ulcer and the mechanism of gastric acid secretion. We established a few novel methods to induce extensive ulceration restricted to the gastric antral area in rats by a combination of drug-induced vagal stimulation with necrotizing agents or anti-inflammatory drugs, as well as with ammonia in relation to the etiological role of Helicobacter pilori. In these models, it was found that the gastric antral area become sensitive to mucosal aggression under vagal stimulation and refeeding after starvation and that the mucosal primary afferent nervous system was involved in the integration of gastric mucosal defense mechanisms. Among many experimental gastric ulcer models, the gastric antral ulcer is important for future study because of its unique analogy with human ulcer in its location of incidence and pathology. We also established methods to measure gastric acid secretion in the isolated gastric mucosa or whole stomach of rat or mouse, as well as acid secretion in anesthetized rats. By using these methods, the signal transduction route of vagus nerve stimulation to parietal cells was studied. The importance of mediation of enterochromaffin cells in gastric acid secretion was clearly confirmed. In the studies on receptor mechanisms in the central nervous system regulating gastric acid secretion, critical roles of GABA, barbiturate, glutamate, neurosteroids and opioid receptors were clarified. From these results, several remaining problems were suggested and these must be resolved in future research.
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PMID:[Prospects for future development in the pharmacology of gastric ulcer models and of gastric acid secretion in experimental animals]. 1055 77

Long-term cultures of telomerase-transduced adult human mesenchymal stem cells (hMSC) may evolve spontaneous genetic changes leading to tumorigenicity in immunodeficient mice (e.g., hMSC-TERT20). We wished to clarify whether this unusual phenotype reflected a rare but dominant subpopulation or if the stem cell origin allowed most cells to behave as cancer stem cells. Cultures of the hMSC-TERT20 strain at population doubling 440 were highly clonogenic (94%). From 110 single-cell clones expanded by 20 population doublings, 6 underwent detailed comparison. Like the parental population, each clone had approximately 1.2 days doubling time with loss of contact inhibition. All retained 1,25-(OH)(2) vitamin D(3)-induced expression of osteoblastic markers: collagen type I, alkaline phosphatase, and osteocalcin. All shared INK4a/ARF gene locus deletion and epigenetic silencing of the DBCCR1 tumor suppressor gene. Despite in vitro commonality, only four of six clones shared the growth kinetics and 100% tumorigenicity of the parental population. In contrast, one clone consistently formed latent tumors and the other established tumors with only 30% penetrance. Changing the in vitro microenvironment to mimic in vivo growth aspects revealed concordant clonal heterogeneity. Latent tumor growth correlated with extracellular matrix entrapment of multicellular spheroids and high procollagen type III expression. Poor tumorigenicity correlated with in vitro serum dependence and high p27(Kip1) expression. Aggressive tumorigenicity correlated with good viability plus capillary morphogenesis on serum starvation and high cyclin D1 expression. Thus, hMSC-TERT20 clones represent cancer stem cells with hierarchical tumorigenicity, providing new models to explore the stem cell hypothesis for cancer.
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PMID:Tumorigenic heterogeneity in cancer stem cells evolved from long-term cultures of telomerase-immortalized human mesenchymal stem cells. 1583 42

Aggressive androgen-independent (also termed as hormone-refractory) prostate cancer is a major clinical obstacle because there is no means to cure. Previous studies have shown that Akt activation is associated with prostate cancer progression from androgen-dependent to androgen-independent stage. However, its causative role in this process has not been established. One of the major limitations is the lack of a well-controlled inducible system to study Akt involvement. Recently, we developed a novel inducible Akt (iAKT) system based on a chemically induced dimerization (CID) approach. This system allows for conditional activation of Akt in a physiological setting. Utilizing this iAKT system, we found that Akt activation prevented cell death after serum withdrawal and promoted cell proliferation in the absence of androgen in vitro in human prostate cancer LNCaP cells, which should stop growing after androgen withdrawal or even die after serum starvation. The iAKT-induced death protection and growth promotion were further demonstrated in vivo using a transgenic mouse model that expresses the iAKT system conditionally in the prostate epithelium. Most importantly, in a mouse xenograft model derived from LNCaP cells, iAKT activation promoted tumor growth in castrated animals by enhancing cell proliferation and inhibiting apoptosis. Taken together, our data suggest that Akt activation is playing a causative role in androgen-independent progression of prostate cancer. This study provides a significant relevance of Akt-targeted therapy for hormone-refractory prostate cancers.
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PMID:Conditional Akt activation promotes androgen-independent progression of prostate cancer. 1703 58


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