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

Metabolic and endocrine studies on a 7-year-old boy who presented with hypoglycaemic convulsions are reported in detail, proving the diagnosis of isolated ACTH deficiency--a rare cause of hypoglycaemia in childhood. Adrenaline secretion during insulin-induced hypoglycaemia was reduced. Low blood alanine levels occurred during starvation-induced hypoglycaemia, together with raised total blood ketone bodies; blood glucose did not increase adequately after oral alanine at this time. Hypoglycaemia in isolated ACTH deficiency appears to be due to a combination of impaired alanine mobilisation and a decreased rate of gluconeogenesis.
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PMID:Isolated ACTH deficiency. Metabolic and endocrine studies in a 7-year-old boy. 21 Jul 21

Twenty-two female big brown bats (Eptesicus fuscus) were collected in a house attic in Montgomery County, Maryland. Seventeen were fed mealworms (Tenebrio molitor larvae) that contained 166 ppm DDE; the other five were fed uncontaminated mealworms. After 54 days of feeding, six dosed bats were frozen and the remaining 16 were starved to death. In a second experiment, 21 female big brown bats were collected in a house attic in Prince Georges County, Maryland. Sixteen were fed mealworms that contained 9.4 ppm Aroclor 1254 (PCB). After 37 days, two bats had died, four dosed bats were frozen, ant the remaining 15 were starved to death. Starvation caused mobilization of stored residues. After the feeding periods, average weights of all four groups (DDE-dosed, DDE control, PCB-dosed, PCB control) had increased. However, weights of DDE-dosed bats had increased significantly more than those of their contols, whereas weights of PCB-dosed bats had increased significantly less than those of their controls. During starvation, PCB-dosed bats lost weight significantly more slowly than controls. Because PCB levels in dosed bats resembled levels found in some free-living big brown bats, PCBs may be slowing metabolic rates of some free-living bats. It is not known how various common organochlorine residues may affect metabolism in hibernating bats. DDE and PCB increased in brains of starving bats as carcass fat was metabolized. Because the tremors and/or convulsions characteristic of neurotoxicity were not observed, we think even the maximum brain levels attained (132 ppm DDE, 20 ppm PCB) were sublethal. However, extrapolation of our DDE data predicted lethal brain levels when fat reserves declined sufficiently. PCB-dosed bats were probably in no danger of neurotoxic poisoning. However, PCB can kill by a nonneurotoxic mode, and this could explain the deaths of two bats on PCB dosage.
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PMID:Experimental feeding of DDE and PCB to female big brown bats (Eptesicus fuscus). 40 35

Effect of starvation on tissue radioactivity of 14C-DDT was examined in mice 8 days after its single injection. Animals were completely fasted and given barium sulfate by gastric intubation for the last 3 days. The findings obtained from starved mice were as follows: 1) loss of body weight, 2) decrease in organ weight of epedidymal fat and liver, 3) reduction in lipid content of whole body as well as of epididymal fat, 4) a marked elevation of DDT levels in tissues except muscle, and 5) occasional neurotoxidc signs characterized by tremors and convulsions. Excretion of DDT-related metabolites was not changed by starvation. Analysis of metabolic producets of 14C-DDT using thin-layer radiochromatography revealed that there was little or no significant difference between control and starved mice in the metabolic pattern of DDT-related compounds in the tissues and excreta. It was assumed the DDT-ingested animals with dietary energy restriction had a subsequent risk of toxicity resulted from redistribution of DDT, but not from alteration in excretion or metabolism.
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PMID:Effect of starvation on excretion, distribution and metabolism of DDT in mice. 88 38

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

The purpose of this study was to determine if the ketone body beta-hydroxybutyrate (beta-HBA) is a useful positive marker for sudden deaths in chronic alcoholics, thought to be due to hypoglycemia. Beta-HBA can be reliably measured in postmortem samples of vitreous humour and urine. In fatalities where there is a history of chronic alcoholism and routine investigations, including autopsy and routine toxicology, yield only a fatty liver as positive findings, a raised level of beta-HBA can be used as an indicator for alcoholic ketosis. Alcoholic ketosis is often associated with antemortem hypoglycemia. Caution should be observed in attributing the significance of ketosis exclusively to alcohol in those conditions where it would otherwise be expected (i.e. diabetic ketoacidosis and chronic starvation). A measurement of this marker of alcoholic ketosis may also help in the investigation of cases where hypothermia or alcohol withdrawal fits are suspected.
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PMID:The investigation of beta-hydroxybutyrate as a marker for sudden death due to hypoglycemia in alcoholics. 830 32

Both depressive disorders and eating disorders are multidimensional and heterogeneous disorders. This paper examines the nature of their relationship by reviewing clinical descriptive, family-genetic, treatment, and biological studies that relate to the issue. The studies confirm the prominence of depressive symptoms and depressive disorders in eating disorders. Other psychiatric syndromes which occur with less frequency, such as anxiety disorders and obsessive-compulsive disorders in anorexia nervosa, or personality disorders, anxiety disorders, and substance abuse in bulimia nervosa, also play an important role in the development and maintenance of eating disorders. Since few studies have controlled for starvation-induced physical, endocrine, or psychological changes which mimic the symptoms considered diagnostic for depression, further research will be needed. The evidence for a shared etiology is not compelling for anorexia nervosa and is at most suggestive for bulimia nervosa. Since in contemporary cases dieting-induced weight loss is the principal trigger, women with self-critical or depressive features will be disproportionately recruited into eating disorders. The model that fits the data best would accommodate a relationship between eating disorders and the full spectrum of depressive disorders from no depression to severe depression, with somewhat higher rates of depression in bulimic anorectic and bulimia nervosa patients than in restricting anorexia nervosa patients, but the model would admit a specific pathophysiology and psychopathology in each eating disorder.
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PMID:Depression and eating disorders. 980 21

Nitrosomonas europaea and Nitrobacter winogradskyi (strain "Engel") were grown in ammonia-limited and nitrite-limited conditions, respectively, in a retentostat with complete biomass retention at 25 degrees C and pH 8. Fitting the retentostat biomass and oxygen consumption data of N. europaea and N. winogradskyi to the linear equation for substrate utilization resulted in up to eight-times-lower maintenance requirements compared to the maintenance energy demand (m) calculated from chemostat experiments. Independent of the growth rate at different stages of such a retention culture, the maximum specific oxygen consumption rate measured by mass spectrometric analysis of inlet and outlet gas oxygen content always amounted to approximately 45 micromol of O2 mg-1 of biomass-C x h-1 for both N. europaea and N. winogradskyi. When bacteria were starved for different time periods (up to 3 months), the spontaneous respiratory activity after an ammonia or nitrite pulse decreased with increasing duration of the previous starvation time period, but the observed decrease was many times faster for N. winogradskyi than for N. europaea. Likewise, the velocity of resuscitation decreased with extended time periods of starvation. The increase in oxygen consumption rates during resuscitation referred to the reviving population only, since in parallel no significant increase in the cell concentrations was detectable. N. europaea more readily recovers from starvation than N. winogradskyi, explaining the occasionally observed nitrite accumulation in the environment after ammonia becomes available. From chloramphenicol (100 microg x ml-1) inhibition experiments with N. winogradskyi, it has been concluded that energy-starved cells must have a lower protein turnover rate than nonstarved cells. As pointed out by Stein and Arp (L. Y. Stein and D. J. Arp, Appl. Environ. Microbiol. 64:1514-1521, 1998), nitrifying bacteria in soil have to cope with extremely low nutrient concentrations. Therefore, a chemostat is probably not a suitable tool for studying their physiological properties during a long-lasting nutrient shortage. In comparison with chemostats, retentostats offer a more realistic approach with respect to substrate provision and availability.
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PMID:Maintenance energy demand and starvation recovery dynamics of Nitrosomonas europaea and Nitrobacter winogradskyi cultivated in a retentostat with complete biomass retention. 1034 29

Severe seasickness could pose a serious problem in diving, and anti-seasickness medication should therefore be prescribed for the seasickness-susceptible diver. Cinnarizine may be used as a medication if it does not increase the risk of central nervous system (CNS) oxygen toxicity when diving with closed-circuit oxygen or O2-enriched gas mixtures. Twenty-six male, white Sprague-Dawley rats were exposed to high O2 pressures (507 and 608 kPa) before and after cinnarizine ingestion (3.3 mg.kg-1), until the appearance of the first electrical discharge (FED) in the electroencephalogram (EEG) which precedes the clinical convulsions. Each rat was tested on five exposure protocols (control and cinnarizine at 507 kPa O2, control, cinnarizine, and 15 h starvation as a control for cinnarizine at 608 kPa O2) at intervals of at least 2 days or until the EEG connector became detached (a mean of 3.1 exposures per rat). Latency to the FED increased after cinnarizine ingestion in 16 of the 17 pairs of measurements at 507 kPa O2 (by more than 61%, P < 0.002) and in 17 of the 19 pairs of measurements at 608 kPa O2 (by 36%, P < 0.002). There was no significant effect of 15 h starvation. Cinnarizine can be further considered for use in seasickness-susceptible divers as it does not increase the risk of CNS O2 toxicity.
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PMID:Effect of the anti-motion-sickness medication cinnarizine on central nervous system oxygen toxicity. 1037 30

The tragic life of Vincent van Gogh is summarized, emphasizing his early departure from formal education, failure as a successful salesman in the art world, attempt at religious studies, difficulty with female and family relationships, return to the art world, and tendencies toward extremes of poor nutrition or near self-starvation and excessive drinking and smoking. In Paris he joined the Impressionists, but drank very heavily both absinthe and cognac. Southward he went to Arles and was joined by Paul Gauguin, with whom he had major personality problems, causing van Gogh to cut off part of his left ear. He experienced paranoid ideation and confinement in mental institutions in Arles, and then returned to Paris and onto Auvers-sur-Oise, where he committed suicide at age 37. Possible physical diagnoses include glaucoma, Meniere's disease, acute intermittent porphyria, and chronic lead poisoning, but these diagnoses seem unlikely. Possible psychiatric diagnoses include borderline personality disorder, anxiety-depressive disorder with episodes of depression and hypomania, and also paranoid schizophrenia. Van Gogh did not have spontaneous seizures and, therefore, did not have epilepsy. Before he began to drink heavily, when he was near starvation, he had "fainting fits," and after drinking, especially absinthe, a convulsant drug, he continued to have similar attacks. His episodes of unconsciousness can be well explained by chronic malnutrition and alcohol abuse, only possibly exacerbated by drinking large quantities of absinthe. Although van Gogh is an excellent example of the Geschwind syndrome, at times associated with temporal lobe epilepsy, this fact does not establish such an epilepsy. Thus, the syndrome is an orphan without the parent condition.
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PMID:A reappraisal of the possible seizures of Vincent van Gogh. 1590 45

Leptin is a pluripotent regulatory protein secreted by fat and exerts many effects through the CNS. Interpretation of the characteristics by which it crosses the blood-brain barrier (BBB) supports the view that leptin most potently signals the brain at serum levels well below those associated with the current definition of ideal body weight. This fits with the perspective that low serum levels of leptin are a signal to brain that a sufficient store of calories are available for the organism to expend energy for efforts unrelated to acquisition of calories. This would explain why low serum levels of leptin are permissive in many of the non-feeding actions of leptin, such as enhancing CNS-mediated immune function, memory, bone growth, reproduction, breathing, and neurogenesis. Triglycerides inhibit the transport of leptin across the BBB and so could be key in the onset of the peripheral leptin resistance, which is a hallmark of obesity. These results explain the paradox of why obesity should induce resistance to an anorectic: hypertriglyceridemia also occurs with starvation and we postulate that triglyceride-induced resistance to leptin transport across the BBB initially evolved to limit the signal of an anorectic to the brain during starvation.
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PMID:The effects of high fat diets on the blood-brain barrier transport of leptin: failure or adaptation? 1678 41


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