Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038187 (starvation)
 24,951 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Nuclear proteins soluble in 0.2 M sulphuric acid were isolated from the liver of three groups of hens subjected for 60 hours to starvation, immobilization or cold exposure. The obtained proteins were separated by means of one-dimensional and two-dimensional electrophoresis on polyacrylamide gel. It was observed that this exposure of the birds to stress caused no qualitative changes in liver nuclear proteins. Histones, histone-like proteins - M1, M2, M3, uM1, HMG 1 and 2 proteins, and a large group of non-histone protein fractions gave nearly identical patterns. However, several components of nuclear proteins were found whose quantity changed in the liver of the birds subjected to stress. These changes were observed in a protein with molecular weight about 27 000 daltons and two proteins weighing over 100 000 daltons.
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PMID:Effects of cold, starvation and immobilization on the composition of acid-soluble nuclear proteins in chicken liver. 667 31

Magnesium deficiency may complicate many diseases. The causes include the following: inadequate intake during starvation or increased requirement during early childhood, pregnancy, or lactation; excessive losses of magnesium as a result of malabsorption from the gastrointestinal tract or from the kidneys during use of diuretics; and to a combination of the two, as in alcoholism. Most often the etiological factors have been operative for a month or more. Acute hypomagnesemia can occur without previous Mg deficiency after epinephrine, cold stress and stress of serious injury or extensive surgery. The clinical manifestations depend on the age of the patient and may begin insidiously or with dramatic suddenness, or there may be no overt symptoms or signs. The manifestations can be divided into the following categories: totally non-specific symptoms and signs ascribable to the primary disease; neuromuscular hyperactivity including tremor, myoclonic jerks, convulsions, Chvostek sign, Trousseau sign (rarely), spontaneous carpopedal spasm (rarely), ataxia, nystagmus and dysphagia; psychiatric disturbances from apathy and coma to some of all facets of delirium; cardiac arrhythmias including ventricular fibrillation and sudden death; hypocalcemia which is responsive only to Mg therapy; and hypokalemia which is not easily nor completely corrected without Mg therapy. The diversity of etiologies and the multiplicity of manifestations result in confusion and controversy. The documentation of normal renal function is absolutely necessary for maximum doses. The order of magnitude of dose is 1.0 meq Mg/kg on day 1, and 0.3 to 0.5 mEq/kg per day for 3 to 5 days. In emergencies such as convulsions or ventricular arrhythmias, a bolus injection of 1.0 gm (8.1 meq) of MgSO4 is indicated. Therapy of Mg deficiency in the presence of renal insufficiency requires smaller doses and frequent monitoring. Complete repletion occurs slowly.
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PMID:Magnesium deficiency. Etiology and clinical spectrum. 702 Mar 47

Hypoglycemia is but one of a number of causes of hypothermia, but is important to keep in mind as a possible precipitating or concurrent event even in those cases in which there are other obvious explanations for decreased body temperature (exposure, alcoholism, starvation, sepsis or hypothyroidism). Hypoglycemia may occur in as many as 40 percent of very cold patients, and be clinically unrecognized because symptoms are masked by the hypothermia itself. Although serum glucose levels are depressed, a cold-induced renal tubular glycosuria may occur. Glucose in the urine, therefore, cannot be used as assurance of hyperglycemia in a hypothermic patient. And, although cold protects against serious end organ damage from hypoglycemia by decreasing tissue metabolic need for glucose, a serum specimen should be drawn for glucose determination in all hypothermic patients and a 50 percent glucose solution immediately given intravenously. If this is not done, serum glucose levels may plummet as the patient is rewarmed and begins to shiver.
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PMID:Hypoglycemia and accidental hypothermia in an alcoholic population. 723 90

Starvation for 2 days and a chronic mild cold stress prevented the rises in body temperature that normally occur in newborn rabbits that have been injected with pyrogen (Piromen, 5 mg/kg). Nevertheless, the stressed pups selected significantly warmer positions in a thermal gradient than did saline-injected littermates and thereby raised their body temperatures. Enhanced heat seeking and subsequent fever were also observed in normally fed pups that were incubated at 24 degrees C and had become hypothermic after pyrogen injection. The responses of the pups before they were allowed to thermoregulate behaviorally resemble the types of thermal responses to infection seen in human newborns. The temperature selection of these pups, and others, indicates that pyrogen elevates the set points of newborn rabbits when endothermic fever is attenuated or even absent.
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PMID:Behavioral responses to pyrogen in cold-stressed and starved newborn rabbits. 728 62

The effect of 2 days (55 h) of starvation on the functional state of the sympathetic nervous system (SNS) and adrenal medulla in male rats was evaluated in both normal (24 degrees C) and cold (4 degrees C) environments. Fasting (24 degrees C) significantly decreased NE turnover in heart and spleen, and the concentration of plasma epinephrine (E) and norepinephrine (NE). Cold exposure in the fed animals significantly increased NE turnover in the heart and plasma E, but had no effect on plasma NE or spleen NE turnover compared to normal (no stress) conditions. Cardiac NE turnover was 50% less in fasted cold-stressed animals than in fed cold-stressed animals. Plasma E remained at low levels. Plasma concentration of free fatty acids was significantly elevated in the fasted state in both warm and cold environments. These results suggest that 2 days of starvation in adult male rats suppresses the activity of the SNS and adrenal medulla and interferes with the normal adrenergic response to cold stress. Moreover, E appears not to be essential for mobilization of fat stores for energy metabolism in the fasted state in either warm or moderately cold environments.
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PMID:Starvation suppresses sympathoadrenal medullary response to cold exposure in rats. 731 57

Periportal and perivenous hepatocytes were isolated from rats subjected to different treatments that induce (starvation, cold exposure) or depress (refeeding after starvation) hepatic fatty acid oxidation. These experiments were designed to determine factors that may be involved in creating and maintaining the asymmetrical distribution of this metabolic pathway in the acinus of the liver. The uneven distribution of mitochondrial [14C]-palmitate oxidation within the acinus (i) was very flexible and changed markedly with the physiological status of the animal (periportal/perivenous ratio: 1.5, 2.0, 1.0 and 0.4 for fed, starved, refed and cold-exposed animals respectively), (ii) coincided with a similar zonation of carnitine palmitoyltransferase I activity in fed as well as in cold-exposed animals, (iii) was paralleled by a comparable zonation of mitochondrial 3-hydroxy-3-methyl-glutaryl-CoA synthase activity in starved animals, and (iv) was not determined by zonal differences in any of the following parameters: sensitivity of carnitine palmitoyltransferase I to malonyl-CoA, intracellular concentration of malonyl-CoA, fatty acid synthesizing capacity, acetyl-CoA carboxylase activity, fatty acid synthase activity or relative content of the two hepatic acetyl-CoA carboxylase isoforms. Unlike mitochondrial oxidation, peroxisomal [14C]palmitate oxidation was always zonated towards the perivenous zone of the liver irrespective of the physiological status of the animal. The data presented show that changes in the acinar distribution of mitochondrial long-chain fatty acid oxidation involve specific long-term mechanisms under different physiological conditions.
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PMID:Flexibility of zonation of fatty acid oxidation in rat liver. 748 41

Sequence was obtained from a cDNA clone, designated ERD1, isolated from a cDNA library of 1-hour-dehydrated plants of Arabidopsis thaliana L. The clone (3150 bp) contains an open reading frame of 946 amino acid residues with greater than 34% sequence identity to the regulatory subunit of the Clp ATP-dependent protease in Escherichia coli and contains a putative chloroplast-targeting signal at the N-terminus. Southern blot analysis suggested the presence of additional ERD1-related genes in A. thaliana. The expression of ERD1 gene was strongly induced by dehydration-stress but not by heat-, cold-, or heavy-metal-stress. In addition ERD1 gene-expression was not strongly affected by treatment with plant growth regulators, such as auxin, cytokinin, abscisic acid, and gibberellic acid, or by starvation-stress for 10 hours.
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PMID:Characterization of cDNA for a dehydration-inducible gene that encodes a CLP A, B-like protein in Arabidopsis thaliana L. 750 70

Data from recent studies suggest that donor fasting imparts a beneficial effect on the viability of transplanted hepatic allografts. Because starvation may temporarily inactivate Kupffer cells, and because these cells are the likely mediators of liver injury after prolonged preservation-reperfusion, the purpose of this study is to establish a link between improved organ viability and Kupffer cell inactivation caused by donor allograft fasting. In an in vivo rat liver transplant model, 48 hours of donor fasting (1) improved allograft viability, (2) significantly decreased Kupffer cell phagocytosis, and (3) significantly decreased cytokine (tumor necrosis factor [TNF]) production postrevascularization. These data validate work from previous studies demonstrating that donor fasting improves allograft viability and furthermore support our previous research implicating activation of Kupffer cells as a causative agent of cold ischemia-preservation injury.
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PMID:Inactivation of Kupffer cells after prolonged donor fasting improves viability of transplanted hepatic allografts. 755 76

The ob gene mRNA expression in rat brown adipose tissue (BAT) and epididymal white adipose tissue (WAT) was measured on Northern blots hybridized with a rat ob gene probe. The level of ob gene mRNA in BAT was about 40% of that in WAT. Fasting (36 h) or semi-starvation (10 days) decreased the ob gene mRNA level in both tissues by 62-68%, and cold exposure at 6 degrees C (24 h) decreased it in BAT (-84%) but not in WAT. Acute administration of the beta 3-adrenergic agonist Ro 16-8714 decreased the ob gene mRNA level in BAT (-51%) and WAT (-28%) of lean Zucker rats and only in BAT (-74%) of obese falfa rats. This study demonstrates that, in the rat, the ob gene is not only expressed in WAT but also in BAT, and suggests that in these two tissues, the modulation of the ob gene expression might be more closely associated with known alterations in cell lipid content than with changes in sympathetic activity.
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PMID:Modulation of obese gene expression in rat brown and white adipose tissues. 758 51

Ecotoxicologists and ecologists have examined the effects of pollutants on individuals and populations largely in terms of one or only a few effects. Yet the recent trend toward a holistic approach to ecological risk assessment suggests that a rigorous paradigm should be applied to toxicants, from hazard identification to risk characterization. Recent discussions have recognized that an up-front problem formulation phase is more critical in ecological risk assessment than it is for human health risk assessment. In this article a modified environmental health risk assessment paradigm is used to examine the risk of lead to birds. This risk analysis is largely conceptual, based on laboratory and field data, and incorporates information currently available. The model expands the hazard identification phase to create a target identification phase that includes the identification of receptors, endpoints, relationships, spatial and temporal scales, and indicators. The target identification phase is unique to the particular hazard, species, population, or community being examined. Lead can cause mortality, or can indirectly affect populations through effects on the food base, avian behavior, reproductive success, and recruitment. Lead can (1) decrease the abundance and availability of prey, (2) bioaccumulate in prey causing increased lead toxicosis in predators, or (3) increase prey availability by interfering with its hiding or escape behavior. Moreover, lower abundance of prey can lead to starvation or nutrient deficiencies, which amplify the absorption and retention of lead. Lead also causes decreases in clutch and egg size, mortality of embryos and nestlings, depression of growth, and deficits in behavior that affect survival. Lead decreases migratory behavior, and increases vulnerability to cold stress, hunters, and other predators. Research needs for evaluating the risk of lead in birds include obtaining data on (1) metal dynamics within various tissues as a function of dose and time since initial exposure, (2) low-level effects on embryos, (3) effects on chicks following fledging and in the period prior to recruitment, (4) effects on adult foraging skills and reproductive behavior, and (5) the relationship between effects from exposure in the laboratory and those from exposure in the wild. This latter point is extremely important, particularly if wild birds have other means of ridding the body of lead not available or less apparent to laboratory birds.
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PMID:A risk assessment for lead in birds. 764 27


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