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Energy Deficiency (energy + deficiency)
Selected AbstractsA comparative proteomic approach to understand the adaptations of an H+ -ATPase-defective mutant of Corynebacterium glutamicum ATCC14067 to energy deficienciesPROTEINS: STRUCTURE, FUNCTION AND BIOINFORMATICS, Issue 18 2007Liyuan Li Abstract F172-8, an H+ -ATPase-defective mutant of the glutamic acid-producing bacterium Corynebacterium glutamicum ATCC 14067, exhibits enhanced rates of glucose consumption and respiration compared to the parental strain when cultured in a biotin-rich medium with glucose as the carbon source. We conducted a comparative proteomic analysis to clarify the mechanism by which the enhanced glucose metabolism in this mutant is established using a proteome reference map for strain ATCC 14067. A comparison of the proteomes of the two strains revealed the up-regulated expression of the several important enzymes such as pyruvate kinase (Pyk), malate:quinone oxidoreductase (Mqo), and malate dehydrogenase (Mdh) in the mutant. Because Pyk activates glycolysis in response to cellular energy shortages in this bacterium, its increased expression may contribute to the enhanced glucose metabolism of the mutant. A unique reoxidation system has been suggested for NADH in C. glutamicum consisting of coupled reactions between Mqo and Mdh, together with the respiratory chain; therefore, the enhanced expression of both enzymes might contribute to the reoxidation of NADH during increased respiration. The proteomic analysis allowed the identification of unique physiological changes associated with the H+ -ATPase defect in F172-8 and contributed to the understanding of the adaptations of C. glutamicum to energy deficiencies. [source] Grazing impact and phenology of the freshwater sponge Ephydatia muelleri and the bryozoans Plumatella emarginata and Fredericella sultana under experimental warmingFRESHWATER BIOLOGY, Issue 5 2009ANDREAS VOHMANN Summary 1.,Both the clearance rates (CR) and abundances of the freshwater sponge Ephydatia muelleri and the bryozoans Plumatella emarginata and Fredericella sultana were investigated from autumn to spring under different temperature regimes. The experiments were performed in bypass channels of the River Rhine (Cologne, Germany) in which temperature could be manipulated. 2.,The impact of temperature increase on CRs depends upon the grazer: E. muelleri showed a clear increase in CRs with increasing temperature whereas P. emarginata was not significantly affected by experimental warming. 3.,Distinct differences in food preference were found for the sponge (which is an efficient grazer of bacteria and small algae) and for the bryozoan P. emarginata (which feeds primarily on large algae, and with no significant grazing on bacteria). 4.,In contrast to their temperature-related patterns in CR, respiration of both P. emarginata and E. muelleri increased with temperature between 19 and 32 °C, suggesting that the risk of experiencing energy deficiency at high temperatures due to increased metabolic rates is particularly high for the bryozoan. 5.,A temperature elevation of 3 °C above the natural Rhine temperature resulted in a delay in the disappearance of active tissue and formation of resting stages for E. muelleri in autumn. This delay ranged from 8 (beginning of gemmulation) to 22 days (termination of gemmulation). In contrast, there was no distinct effect of warming on the disappearance of active zooids of the two bryozoan species in autumn. However, warming can positively affect the maintenance of active zooids during winter in F. sultana. In spring, the appearance of active zooids of P. emarginata was clearly stimulated by temperature elevations, whereas the hatching of both F. sultana and E. muelleri was hardly affected by warming. 6.,The study demonstrated different patterns in the thermal ecology of the two freshwater bryozoans and the sponge in comparison to other filter feeders, particularly mussels. Such patterns need to be considered when predicting the impact of temperature on pelagic-benthic coupling in aquatic habitats. [source] Sulphide-induced energy deficiency in colonic cells is prevented by glucose but not by butyrateALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 2 2002S. J. Hulin Background: In ulcerative colitis, hydrogen sulphide is postulated to impair colonocyte butyrate metabolism, leading to cellular energy deficiency and dysfunction. Aims: To determine the effects of sulphide exposure on butyrate metabolism and adenosine triphosphate levels of HT29 colonic epithelial cancer cells, and to establish whether energy deficiency can be prevented by increased butyrate concentrations or the presence of glucose. Methods: HT29 cells were maintained in medium containing 3 mM butyrate, 5 mM glucose, or both substrates. Oxidation rates were measured by 14CO2 release from 14C-labelled substrates. Cellular adenosine triphosphate was assayed using the luciferin/luciferase chemiluminescent method. The effects of sulphide (0,5 mM) on substrate oxidation and adenosine triphosphate levels and of increasing butyrate concentration (0,30 mM) with sulphide were observed. Results: HT29 cells showed similar energy substrate usage to primary colonocyte cultures. Sulphide exposure inhibited butyrate oxidation and led to a reduction in cellular adenosine triphosphate. This fall was prevented by co-incubation with glucose, but not by increasing concentrations of butyrate. Conclusions: HT29 cells utilize butyrate as an energy substrate and represent a useful in vitro model of the effects of sulphide on colonocytes. Sulphide inhibits butyrate oxidation and leads to demonstrable energy deficiency, prevented by the presence of glucose but not by increased butyrate concentrations. [source] Proteomics analysis of hypothalamic response to energy restriction in dairy cowsPROTEINS: STRUCTURE, FUNCTION AND BIOINFORMATICS, Issue 19 2007Björn Kuhla Abstract The hypothalamus is the central regulatory unit that balances a number of body functions including metabolic rate, hunger, and satiety signals. Hypothalamic neurons monitor and respond to alterations of circulating nutrients and hormones that reflect the peripheral energy status. These extracellular signals are integrated within the cell at the ATP:AMP ratio and at the level of ROS, triggering gene expression associated with glucose and lipid metabolism. In order to identify new molecular factors potentially associated with the control of energy homeostasis, metabolic adaptation, and regulation of feed intake, hypothalami from ad libitum fed and energy restricted cows were characterized using 2-DE and MALDI-TOF-MS. Among 189 different protein spots identified, nine proteins were found to be differentially expressed between groups. Beside the 5-aminoimidazole-4-carboxamide ribonucleotide formyltransferase/IMP cyclohydrolase, stress-induced phosphoprotein-1, heat shock protein 70,kDa-protein-5, dihydropyrimidinase-related protein-2, [Cu-Zn]-superoxide dismutase, ubiquitin carboxy-terminal hydrolase-L1, and inorganic pyrophosphatase were found to be up-regulated, whereas glyceraldehyde 3-phosphate dehydrogenase and aconitase-2 were down-regulated in the restricted group. In conclusion, differentially expressed proteins are related to energy and nucleotide metabolism and cellular stress under conditions of dietary energy deficiency. These proteins may be new candidate molecules that are potentially involved in signaling for maintaining energy homeostasis. [source] How Palatable Food Disrupts Appetite RegulationBASIC AND CLINICAL PHARMACOLOGY & TOXICOLOGY, Issue 2 2005Charlotte Erlanson-Albertsson Hunger signals may be generated in peripheral organs (e.g. ghrelin) but most of them are expressed in the hypothalamus (neuropeptide Y, orexins, agouti-related peptide, melanin concentrating hormone, endogenous opiates and dopamine) and are expressed during situations of energy deficiency. Some satiety signals, such as cholecystokinin, glucagon-like peptide 1, peptide YY and enterostatin are released from the digestive tract in response to food intake. Others, such as leptin and insulin, are mobilized in response to perturbations in the nutritional state. Still others are generated in neurones of the hypothalamus (,-melanocyte-stimulating hormone and serotonin). Satiety signals act by inhibiting the expression of hunger signals and/or by blunting their effect. Palatable food, i.e. food rich in fat and sugar, up-regulates the expression of hunger signals and satiety signals, at the same time blunting the response to satiety signals and activating the reward system. Hence, palatable food offsets normal appetite regulation, which may explain the increasing problem of obesity worldwide. [source] Expanding roles for AMP-activated protein kinase in neuronal survival and autophagyBIOESSAYS, Issue 9 2009Jeroen Poels Abstract AMP-activated protein kinase (AMPK) is an evolutionarily conserved cellular switch that activates catabolic pathways and turns off anabolic processes. In this way, AMPK activation can restore the perturbation of cellular energy levels. In physiological situations, AMPK senses energy deficiency (in the form of an increased AMP/ATP ratio), but it is also activated by metabolic insults, such as glucose or oxygen deprivation. Metformin, one of the most widely prescribed anti-diabetic drugs, exerts its actions by AMPK activation. However, while the functions of AMPK as a metabolic regulator are fairly well understood, its actions in neuronal cells only recently gained attention. This review will discuss newly emerged functions of AMPK in neuroprotection and neurodegeneration. Additionally, recent views on the role of AMPK in autophagy, an important catabolic process that is also involved in neurodegeneration and cancer, will be highlighted. [source] | |||||||||||||