Regulation Of Amino Acid Catabolism Research Articles

Amino Acid Catabolism: An Overlooked Area of Metabolism.

Amino acids have been extensively studied in nutrition, mainly as key elements for maintaining optimal protein synthesis in the body as well as precursors of various nitrogen-containing compounds. However, it is now known that amino acid catabolism is an important element for the metabolic control of different biological processes, although it is still a developing field to have a deeper understanding of its biological implications. The mechanisms involved in the regulation of amino acid catabolism now include the contribution of the gut microbiota to amino acid oxidation and metabolite generation in the intestine, the molecular mechanisms of transcriptional control, and the participation of specific miRNAs involved in the regulation of amino acid degrading enzymes. In addition, molecules derived from amino acid catabolism play a role in metabolism as they are used in the epigenetic regulation of many genes. Thus, this review aims to examine the mechanisms of amino acid catabolism and to support the idea that this process is associated with the immune response, abnormalities during obesity, in particular insulin resistance, and the regulation of thermogenesis.

Glucagon regulates lipolysis and fatty acid oxidation through inositol triphosphate receptor1 in the liver.

Glucagon promotes hepatic glucose production, lipolysis and amino acid catabolism. Inhibition of glucagon activity, or glucagon resistance, not only lowers blood glucose levels, but also induces non-alcoholic fatty liver disease and hyperaminoacidemia.

Induction of a bZIP Type Transcription Factor and Amino Acid Catabolism-Related Genes in Soybean Seedling in Response to Starvation Stress

To address roles of bZIP transcription factors on regulation of amino acid catabolism under autophagy-induced plant cells, we examined the effect of nutrient starvation on the expression of low energy stress-related transcription factor homologs, GmbZIP53A and GmbZIP53B, and amino acid catabolism-related genes in soybean (Glycine max (L.) Merr.). Sucrose starvation treatment significantly enhanced the expressions of GmbZIP53A, but not GmbZIP53B asparagine synthase (GmASN1), proline dehydrogenase1 (GmProDH), and branched chain amino acid transaminase 3 (GmBCAT3). GmbZIP53-related immunoreactive signals were upregulated under severe starvation with sucrose starvation and protease inhibitors, while 3% sucrose and sucrose starvation had no or marginal effects on the signal. Profiles of induction of GmASN1, GmProDH and GmBCAT3 under various nutrient conditions were consistent with the profiles of GmbZIP53 protein levels but not with those of GmbZIP mRNA levels. These results indicate that GmbZIP53 proteins levels are regulated by posttranslational mechanism in response to severe starvation stress and that the increased protein of GmbZIP53 under severe starvation accelerates transcriptional induction of GmASN1, GmProDH, and GmBCAT3. Furthermore, it is conceivable that decrease of branched chain amino acid level by the BCAT-mediated degradation eventually enhances autophagy under severe starvation.

Amino Acid Catabolic Pathways of Lactic Acid Bacteria

Lactic acid bacteria (LAB) constitute a diverse group of Gram positive obligately fermentative microorganisms which include both beneficial and pathogenic strains. LAB generally have complex nutritional requirements and therefore they are usually associated with nutrient-rich environments such as animal bodies, plants and foodstuffs. Amino acids represent an important resource for LAB and their utilization serves a number of physiological roles such as intracellular pH control, generation of metabolic energy or redox power, and resistance to stress. As a consequence, the regulation of amino acid catabolism involves a wide set of both general and specific regulators and shows significant differences among LAB. Moreover, due to their fermentative metabolism, LAB amino acid catabolic pathways in some cases differ significantly from those described in best studied prokaryotic model organisms such as Escherichia coli or Bacillus subtilis. Thus, LAB amino acid catabolism constitutes an interesting case for the study of metabolic pathways. Furthermore, LAB are involved in the production of a great variety of fermented products so that the products of amino acid catabolism are also relevant for the safety and the quality of fermented products.

Nutrient metabolism and utilization in the liver

The role of ruminant liver in modifying the profile of absorbed nutrients before presented to peripheral tissues is illustrated with literature data on hepatic nutrient exchanges. These data are mainly from experiments with multicatheterized dairy cows enabling estimation of blood flow rates and nutrient balances across the liver. In cow liver there is net uptake of propionate, butyrate, valerate, long-chain fatty acids, lactate, amino acids, NH 4 + and O 2, while there is net release of acetate, ketone bodies, glucose, urea and CO 2. Approximately 55% of urea synthesized in the liver is recycled to portal drained viscera. More than 40% of amino acid net absorption is removed by the liver resulting in an amino acid deficit for milk protein synthesis. This could indicate an underestimation of amino acid absorption. Estimated negative carbon balances across the liver can be related to incomplete data concerning lipid exchange and also to carbon use in gluconeogenesis as hepatic uptake of gluconeogenic carbon is less than hepatic release of glucose-carbon. Within a range of glucose flux rates from 3 to 15 mol/d milk yield is linearly related to glucose flux rate. This relationship and published relationships between feed intake and hepatic glucose output are used to calculate regression estimates of basal glucose requirement in cows (2 mol/d) as well as glucose requirement for milk synthesis (0.4 mol/kg milk). Glucose synthesis in the liver is under both metabolic (stimulation by substrate availability; inhibition by glucose itself) and hormonal control (stimulation by glucagon and probably by somatotropin; inhibition by insulin). In early lactation with increased lipid mobilization and fatty acid oxidation in the liver a high rate of gluconeogenesis is ensured by regulation of metabolite transport across mitochondrial membranes. However, in severely underfed animals with excessive lipid mobilization and ketogenesis glucose synthesis is depressed. Reference is given to published mathematical models of liver metabolism in lactating cows. Simulation results obtained with such models have brought further attention to the need for more quantitative knowledge, both regarding hepatic nutrient exchanges (in particular lipids and proteins) and also inter-organ nutrient metabolism (eg. regulation of amino acid catabolism). It is concluded that future feed evaluation systems for ruminants should be based on dynamic, mechanistic whole animal models simulating feed intake, digestion and absorption as well as nutrient metabolism and utilization.

Nitrogen regulation of amino acid catabolism in Neurospora crassa.

Neurospora crassa can utilize numerous compounds including certain amino acids as a sole nitrogen source. Mutants of the nit-2 locus, a regulatory gene which is postulated to mediate nitrogen catabolite repression, are deficient in the ability to utilize several amino acids as well as other nitrogen sources used by wild type. Various enzymes involved in amino acid catabolism were found to be regulated in distinct ways. Arginase, ornithine transaminase, and pyrroline-5-carboxylate dehydrogenase are all inducible enzymes but are not subject to nitrogen catabolite repression. By contrast, proline oxidase and the amino acid transport system(s) are controlled by nitrogen repression and their synthesis is increased markedly when nitrogen source is limiting. Unlike wild type, the nit-2 mutant cannot derepress amino acid transport, although proline oxidase is regulated in a normal fashion.