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

Rats were given daily injections of protamine-zinc insulin (PZI) that increased food intake and body weight. Termination of insulin treatment resulted in transient hypophagia and weight loss. Simultaneously with the weight loss, plasma levels of glycerol, free fatty acids, glucose, and ketones increased, whereas adipose tissue lipoprotein lipase activity and liver glycogen decreased. These changes in food intake and metabolism after termination of PZI treatment were accentuated in streptozotocin-diabetic rats. Two antilipolytic drugs (nicotinic acid and 3,5-dimethylpyrazole) blocked the elevation in plasma glycerol while having no effect on food intake. A 1-day fast after termination of insulin treatment equalized insulin-treated and control groups for plasma glycerol and ketones and reversed group differences in free fatty acids; the elevation in plasma glucose persisted despite starvation. Following starvation, previously PZI-treated rats ate less than controls on refeeding. The results show that enhanced lipolysis does not invariably accompany hypophagia during excess weight loss and suggest that a disturbance in carbohydrate metabolism or an increase in hepatic fatty acid oxidation may underlie this decrease in food intake.
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PMID:Metabolic concomitants of hypophagia during recovery from insulin-induced obesity in rats. 635 32

We have previously shown that [125I]insulin binding to medial hypothalamic receptors is attenuated following 14 days of food restriction. Such rats are characterized by considerably reduced circulating insulin levels with unchanged hypothalamic insulin concentration. The present data demonstrate that, in contrast to the effects of starvation, [125I]insulin binding to hypothalamic receptors from rats made hyperinsulinaemic by daily injections of protamine zinc insulin (4-6 U/rat/day for 14 days) is unaffected by this manipulation, even though hypothalamic insulin concentration in insulin-injected animals was significantly higher than in saline-injected controls. Insulin binding to partially purified membranes from the medial hypothalamic region was significantly greater than that from the lateral area, confirming a finding in our earlier study. Insulin treatment was associated with slight reductions in maximal insulin-binding capacity of medial hypothalamic receptors, a tendency which appeared to be compensated by reciprocal changes in receptor affinity for this hormone. The data indicate that hypothalamic insulin receptors are not regulated by peripheral or even central insulin levels per se; it appears, rather, that some other, as yet unidentified, correlate(s) of significantly altered food intake and/or body weight can modify hypothalamic insulin receptor function. Perhaps such modifications could, in turn, participate in the activation of regulatory mechanisms involved in correcting energy imbalance.
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PMID:Failure of chronic experimental hyperinsulinism to alter insulin binding to hypothalamic receptors in the rat. 638 95

Kwashiorkor kills millions of young children in the tropical Third World. It was believed to be a disease of protein starvation. The medical team headed by Professor Ralph Henrickse of the Liverpool School of Tropical Medicine has discovered that aflatoxin, a fungus toxin, may be the triggering factor in this disease which also impairs liver function. In New Zealand, we have a pasture fungus, the spores of which produce a liver toxin that has killed millions of animals this century and impaired the performance of millions more. New Zealand is a pastoral farming country with 70 million sheep and several million cattle. We now protect the animal with zinc medication. This paper describes the similarities between Kwashiorkor and the mycotoxic liver disease in New Zealand livestock, known locally as Facial Eczema. It describes briefly my discovery that pharmacological doses of zinc protected farm animals from pasture contaminated with the spores of the fungus Pithomyces chartarum, which contains the toxin sporidesmin. This paper proposes that Kwashiorkor and Facial Eczema are diseases with similar beginnings and a common end.
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PMID:Kwashiorkor. 649 86

Plasma and urine electrolytes were measured in five healthy non-obese young adults before, during and after a four-day period of total starvation (distilled water only). Plasma sodium, chloride and bicarbonate concentrations decreased in all subjects by a mean value of 4 mmol/l, whereas the sum of acetoacetate and hydroxybutyrate concentrations increased by 4-6 mmol/l. These changes occurred without alterations in the state of hydration or vascular volume. Hydroxybutyrate and ammonium ions became the main urinary ions during starvation, whereas sodium and chloride, which were quantitatively the most important urinary electrolytes before starvation, decreased four-fold, and potassium two-fold. Plasma zinc concentrations rapidly increased in all subjects by a mean of 4 mumol/1 (25%) and returned to normal on refeeding. The excretion of zinc in urine trebled and continued to rise on refeeding. There were no major changes in the excretion of calcium, magnesium, phosphate or sulphate during the starvation period. From knowledge of the intracellular concentrations of various minerals and extent of breakdown of lean tissues (N excretion), it is suggested that most of the urinary calcium, magnesium and phosphate probably originates from bone, and that the amount of zinc in urine is only a small fraction of that which is likely to be released from the breakdown of lean tissues. It is also suggested that the continued excretion of zinc on refeeding is due to release of zinc from tissues which 'buffered' it during the starvation period. This study provides useful data in non-obese individuals with which to compare changes which occur in post-traumatic and post-infective starvation.
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PMID:Mineral metabolism during short-term starvation in man. 672 71

When Candida albicans is grown at 25 degrees C in suspension in defined medium, cells accumulate at stationary phase as singlets in G1 of the deoxyribonucleic acid replication cycle and acquire the capacity to form mycelia. When cells were removed from a stationary-phase culture and a low concentration of fresh cells was inoculated into the cell-free, stationary-phase medium, the fresh cells grew to approximately the same cell density as the original culture. We demonstrated that in the accompanying decrease in pH, nor due to a depletion of O2, an accumulation of CO2, a physical crowding effect, or accumulation of the putative autoinhibitors tryptophol and 2-phenylethyl alcohol. Rather, cells stop multiplying at stationary phase due to the depletion of zinc from the culture medium. The manipulation of cultures with glassware to remove stationary-phase cells and to add fresh cells led to the addition of zinc to the medium and hence a new round of culture growth. The same manipulations with plasticware did not result in zinc supplementation and hence in now new round of culture growth. When cells enter stationary phase in excess zinc, they do not accumulate as singlets; rather, they accumulate as budded cells. When these cells were induced to form mycelia, they did so in half the time it took zinc-starved cells. The usefulness of employing zinc starvation as a method for obtaining a uniform stationary-phase phenotype and for synchronizing induced mycelium or bud formation is discussed.
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PMID:Zinc and regulation of growth and phenotype in the infectious yeast Candida albicans. 701 88

Triacylglycerol lipase activities of homogenates and subcellular fractions of rat liver were measured under optimal conditions at pH 7.5 using emulsified tri[1-14C]oleoylglycerol as substrate. Twenty-four hr after administration of streptozotocin, hepatic alkaline lipase activity was 39% of normal, and this lower level of activity was observed at 72 hr and 7 days, after streptozotocin injection. After 24 hr of starvation, lipase activity also was significantly lower (35%) than normal. Insulin (35 U regular/kg body weight) had no acute (90 min) effect on the hepatic lipase activity of either normal or diabetic rats. Chronic insulin administration (4 subcutaneous injections of 10 U protamine zinc insulin/kg at 16-hr intervals) to normal rats provoked a 40% increase in hepatic lipase activity. Diabetic rats given the same insulin treatment showed lipase activity that was significantly higher (155%) than normal. Lipase activity fell to 65% of normal when insulin was withheld (32 hr) from diabetic rats given chronic insulin therapy. Intracardial injection of glucagon (1 mg/kg) into normal rats had no acute (30 min) effect on hepatic alkaline lipase activity. Hepatic alkaline lipase activity varied independently from the concentrations of either glucose or triacylglycerol in the plasma. However, there was an apparent negative correlation between this lipase activity and the concentration of fatty acids in the plasma; lipase activity was highest when fatty acid concentrations were lowest, and lowest when fatty acid concentrations were elevated. From these data we conclude: 1) changes in hepatic alkaline lipase activity ware provoked by chronic, but not acute, alteration of the hormonal and metabolic status of the rat, and 2) changes in hepatic alkaline lipase activity may be mediated through changes in the levels of circulating fatty acids presented to the liver, but the effect is not an immediate one.
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PMID:Hepatic triacylglycerol lipase activities after induction of diabetes and administration of insulin or glucagon. 704 62

Parenchymal and non-parenchymal cells were isolated from the livers of control, starved, Zn2+-injected and Cd2+-injected rats. Parenchymal cells were prepared by differential centrifugation after perfusion of the liver with collagenase. Non-parenchymal cells were separated from parenchymal cells by unit-gravity sedimentation and differential centrifugation. Yields of 2 x 10(8) non-parenchymal cells with greater than 95% viability and less than 0.2% contamination with parenchymal cells were obtained without exposing cells to Pronase. Metallothioneins-I and -II were identified in parenchymal cells and non-parenchymal cells from Zn2+-treated rats. The metallothionein contents of parenchymal cells, non-parenchymal cells and intact liver were quantified by a competitive 203Hg-binding assay. Administration of heavy-metal salts significantly increased the metallothionein content of both cell populations, although the concentration of the protein was approx. 2.5-fold greater in parenchymal cells than in non-parenchymal cells. Overnight starvation increased the metallothionein content of parenchymal cells without altering that of non-parenchymal cells. The potential significance of this differential response by different liver cell types with regard to the influence of Zn2+ on stress-mediated alterations in hepatic metabolism is discussed.
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PMID:Identification of metallothionein in parenchymal and non-parenchymal liver cells of the adult rat. 711 46

Infection-induced malnutrition, the most common form of cytokine-induced malnutrition, results from the actions of proinflammatory cytokines, ie, tumor necrosis factor (TNF) and interleukins 1,6, and 8 (IL-1, IL-6, and IL-8). During acute generalized infections, these cytokines initiate the acute-phase reaction. This reaction is quite stereotyped, and includes fever, malaise, myalgia, headaches, cellular hypermetabolism, and multiple endocrine and enzyme responses. In addition, there is heightened catabolism of muscle proteins and many amino acids; flux of free amino acids into the liver; hepatic synthesis of acute-phase plasma proteins; sequestration of iron and zinc; gluconeo-genesis; insulin resistance; impaired cellular uptake of fatty acids from plasma triglycerides; sizable losses of body nitrogen, potassium, magnesium, phosphate, and zinc; retention of body salt and water; heightened metabolic degradation and/or loss of vitamins; and an activation of the immune system. The pathogenesis of cytokine-induced malnutrition is thus vastly different from the malnutrition caused by uncomplicated starvation. Cytokine-induced malnutrition can have a devastating effect on the immune system and its functions. Although proinflammatory cytokines are found in mucosal fluids, where they contribute to the pathogenesis of inflammatory bowel diseases, it is not known whether cytokines play a role in toxigenic, secretory diarrheas such as cholera, which cause huge losses of body water, electrolytes, and bicarbonate while exhibiting no systemic manifestations of an acute-phase reaction.
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PMID:Herman Award Lecture, 1995: infection-induced malnutrition--from cholera to cytokines. 757 15

Manganese superoxide dismutase (MnSOD) levels were monitored as a function of time in culture to determine whether these levels were altered at logarithmic growth versus when the cells exhibited density limitation of growth. For comparison, activities of the antioxidant enzymes copper, zinc superoxide dismutase (CuZnSOD), catalase, and glutathione peroxidase were also evaluated. Four cell lines were studied, two of which exhibited density limitation of growth and two of which did not. Each cell line showed a unique antioxidant enzyme profile. The two cell lines that showed density limitation of growth also demonstrated induction of MnSOD at the time when the cells stopped proliferating in culture, whereas the other two cell lines did not show induction of MnSOD. There was no strict correlation between density limitation of growth and activities of the other antioxidant enzymes. To determine whether SOD varied with various phases of the cell cycle, NIH/3T3 cells were synchronized using serum starvation, and then SOD activities were measured during quiescence (G0) and the phase of DNA synthesis (S-phase). MnSOD was decreased during S-phase compared with G0, whereas CuZnSOD was increased during S-phase compared with G0, demonstrating alteration of SOD activities with varying phases of the cell cycle. This study suggests the possibility that increased MnSOD may correlate with decreased cell proliferation and suggests significant alterations in SOD activities during the cell cycle.
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PMID:Antioxidant enzyme levels as a function of growth state in cell culture. 763 59

This report describes the identification, cloning, and molecular analysis of UME6 (CAR80/CARGRI), a key transcriptional regulator of early meiotic gene expression. Loss of UME6 function results in the accumulation of fully derepressed levels (70- to 100-fold increase above basal level) of early meiotic transcripts during vegetative growth. In contrast, mutations in five previously identified UME loci (UME1 to UME5), result in low to moderate derepression (2- to 10-fold increase) of early meiotic genes. The behavior of insertion and deletion alleles indicates that UME6 is dispensable for mitotic division but is required for meiosis and spore germination. Despite the high level of meiotic gene expression during vegetative growth, the generation times of ume6 mutant haploid and diploid cells are only slightly reduced. However, both ascus formation and spore viability are affected more severely. The UME6 gene encodes a 91-kD protein that contains a C6 zinc cluster motif similar to the DNA-binding domain of GAL4. The integrity of this domain is required for UME6 function. It has been reported recently that a mutation in CAR80 fails to complement an insertion allele of UME6. CAR80 is a gene required for nitrogen repression of the arginine catabolic enzymes. Here, through sequence analysis, we demonstrate that UME6 and CAR80 are identical. Analyses of UME6 mRNA during both nitrogen starvation and meiotic development indicate that its transcription is constitutive, suggesting that regulation of UME6 activity occurs at a post-transcriptional level.
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PMID:UME6 is a key regulator of nitrogen repression and meiotic development. 792 68


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