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Metabolism Leading (metabolism + leading)
Selected AbstractsRole of biohydrogenation intermediates in milk fat depressionEUROPEAN JOURNAL OF LIPID SCIENCE AND TECHNOLOGY, Issue 8 2007Kevin J. Shingfield Abstract Fat is the most variable constituent in milk and is reduced on low-fiber/high-concentrate diets or on rations containing lipid supplements rich in polyunsaturated fatty acids. The biohydrogenation theory attributes the causal mechanism underlying diet-induced milk fat depression (MFD) to changes in ruminal lipid metabolism leading to increased formation of specific biohydrogenation intermediates that exert anti-lipogenic effects. Trans -10, cis -12 conjugated linoleic acid (CLA) is the only intermediate shown unequivocally to inhibit milk fat synthesis. However, increases in ruminal trans -10, cis -12 CLA formation do not provide a universal explanation for the reductions in milk fat during diet-induced MFD, suggesting that other biohydrogenation intermediates may also be involved. Post-ruminal infusion experiments have provided tentative evidence that cis -10, trans -12 CLA and trans -9, cis -11 CLA also exert anti-lipogenic effects. Diet-induced MFD is consistently associated with an increase in milk fat trans -10 18:1 concentrations, but recent direct evidence offers little support for a role of this intermediate in the regulation of milk fat synthesis. Further research is required to characterize the structure and function of other biohydrogenation intermediates, as well as considering the contribution of more global changes in ruminal lipid metabolism to provide a more universal explanation of diet-induced MFD. [source] Diagnosis and phenotypic classification of Wilson disease,LIVER INTERNATIONAL, Issue 3 2003Peter Ferenci Wilson disease is an inherited autosomal recessive disorder of hepatic copper metabolism leading to copper accumulation in hepatocytes and in extrahepatic organs such as the brain and the cornea. Originally Wilson disease was described as a neurodegerative disorder associated with cirrhosis of the liver. Later, Wilson disease was observed in children and adolescents presenting with acute or chronic liver disease without any neurologic symptoms. While diagnosis of neurologic Wilson disease is straightforward, it may be quite difficult in non-neurologic cases. Up to now, no single diagnostic test can exclude or confirm Wilson disease with 100% certainty. In 1993, the gene responsible for Wilson disease was cloned and localized on chromosome 13q14.3 (MIM277900) (1, 2). The Wilson disease gene ATP7B encodes a P-type ATPase. More than 200 disease causing mutations of this gene have been described so far (3). Most of these mutations occur in single families, only a few are more frequent (like H1069Q, 3400delC and 2299insC in Caucasian (4,6) or R778L in Japanese (7), Chinese and Korean patients). Studies of phenotype-genotype relations are hampered by the lack of standard diagnostic criteria and phenotypic classifications. To overcome this problem, a working party discussed these problems in depth at the 8th International Meeting on Wilson disease and Menkes disease in Leipzig/Germany (April 16,18, 2001),. After the meeting, a preliminary draft of a consensus report was mailed to all active participants and their comments were incorporated in the final text. [source] Whole Plant Regulation of Sulfur Nutrition of Deciduous Trees-Influences of the EnvironmentPLANT BIOLOGY, Issue 3 2003C. Herschbach Abstract: The current view of sulfur nutrition is based on the source-to-sink relationship of carbohydrates. SO42- reduction is thought to occur mainly in leaves. Surplus reduced sulfur must be transported out of the leaves, loaded into the phloem and transported to other tissues, in particular tissues assumed to be sink organs. However, it has not been proved that tissues which are sinks for carbohydrates are also sink organs for reduced sulfur. It is evident that sinks must communicate with sources, and vice versa, to signal demand and to transport the surplus of reduced sulfur that is produced. The demand-driven control model of sulfur nutrition proposes that the tripeptide glutathione is the signal which regulates S nutrition of the whole plant at the level of SO42- uptake. Acclimatization to environmental changes has been shown to result in several changes in S nutrition of deciduous trees: (i) Drought stress diminished SO42- transport into the xylem, although the GSH content in lateral roots remained unaffected, possibly due to an overall reduction in water status. (ii) Flooding decreased APS reductase activity in the anoxic roots. This may be due to enhanced GSH transport to the roots, but it is more likely to be the result of a change in metabolism leading to diminished energy gain in the roots. (iii) Mycorrhization enhanced the GSH content in the phloem, while SO42- uptake was not affected. This clearly goes against the demand-driven control model. (iv) Under both short- and long-term exposure to elevated pCO2, the APS reductase activity in leaves and lateral roots did not correlate with the GSH contents therein. Therefore, it must be assumed that, under these conditions, regulation of S nutrition goes beyond the demand-driven control model, and occurs within the network of other nutrient metabolism. (v) Atmospheric S in the form of H2S enhanced the reduced sulfur content of the phloem and lateral roots. Under these conditions, the SO42- loaded into the xylem decreased. It would appear that the demand-driven control model of sulfur nutrition is not always valid in the case of deciduous trees. [source] Plant virus infection-induced persistent host gene downregulation in systemically infected leavesTHE PLANT JOURNAL, Issue 2 2008Zoltán Havelda Summary Understanding of virus infection-induced alterations in host plant gene expression and metabolism leading to the development of virus disease symptoms is both scientifically and economically important. Here, we show that viruses belonging to various RNA virus families are able to induce efficient host gene mRNA downregulation (shut-off) in systemically infected leaves. We demonstrate that the host gene mRNA shut-off overlaps spatially with virus-occupied sectors, indicating the direct role of virus accumulation in this phenomenon. The establishment of shut-off was not directly connected to active viral replication or the RNA-silencing machinery. Importantly, the induced shut-off phenomenon persisted for several weeks, resulting in severe deficiency of mRNA for important housekeeping genes in the infected plants. Interestingly, we found that some other RNA viruses do not induce or only slightly induce the shut-off phenomenon for the same set of genes, implicating genetic determination in this process. Nuclear run-on experiments suggest that plant viruses, similarly to animal viruses, mediate suppression of host mRNA synthesis in the nucleus. By investigating various host,virus interactions, we revealed a correlation between the intensity of the shut-off phenomenon and the severity of disease symptoms. Our data suggest that efficient and persistent downregulation of host genes may be an important component of symptom development in certain host,virus interactions. [source] Metabolism of PER.C6TM cells cultivated under fed-batch conditions at low glucose and glutamine levelsBIOTECHNOLOGY & BIOENGINEERING, Issue 1 2006Luis Maranga Abstract This is the first study to examine PER.C6TM cell glucose/energy and glutamine metabolism with fed-batch cultures at controlled low glutamine, low glucose, and simultaneous low glucose and low glutamine levels. PER.C6TM cell metabolism was investigated in serum-free suspension bioreactors at two-liter scale. Control of glucose and/or glutamine concentrations had a significant effect on cellular metabolism leading to an increased efficiency of nutrient utilization, altered byproduct synthesis, while having no effect on cell growth rate. Cultivating cells at a controlled glutamine concentration of 0.25 mM reduced qGln and q by approximately 30%, qAla 85%, and qNEAA 50%. The fed-batch control of glutamine also reduced the overall accumulation of ammonium ion by approximately 50% by minimizing the spontaneous chemical degradation of glutamine. No major impact upon glucose/energy metabolism was observed. Cultivating cells at a glucose concentration of 0.5 mM reduced qGlc about 50% and eliminated lactate accumulation. Cells exhibited a fully oxidative metabolism with Y of approximately 6 mol/mol. However, despite no increase in qGln, an increased ammonium ion accumulation and Y were also observed. Effective control of lactate and ammonium ion accumulation by PER.C6TM cells was achieved using fed-batch with simultaneously controlled glucose and glutamine. A fully oxidative glucose metabolism and a complete elimination of lactate production were obtained. The qGln value was again reduced and, despite an increased q compared with batch culture, ammonium ion levels were typically lower than corresponding ones in batch cultures, and the accumulation of non-essential amino acids (NEAA) was reduced about 50%. In conclusion, this study shows that PER.C6TM cell metabolism can be confined to a state with improved efficiencies of nutrient utilization by cultivating cells in fed-batch at millimolar controlled levels of glucose and glutamine. In addition, PER.C6TM cells fall into a minority category of mammalian cell lines for which glutamine plays a minor role in energy metabolism. © 2006 Wiley Periodicals, Inc. [source] | ||||||||||