Carbohydrate Metabolism B: Di-, Oligo-, and Polysaccharide Synthesis and Degradation

2011 ◽  
pp. 239-256
Author(s):  
Herbert J. Fromm ◽  
Mark S. Hargrove
BMC Genomics ◽  
2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Ming Gong ◽  
Henan Zhang ◽  
Di Wu ◽  
Zhong Zhang ◽  
Jinsong Zhang ◽  
...  

Abstract Background Hericium erinaceus, a rare edible and medicine fungus, is widely used in the food and medical field. Polysaccharides from H. erinaceus are the main bioactive compound that exert high bioactive value in the medical and healthcare industries. Results The genome of H. erinaceus original strain HEA was reported 38.16 Mb, encoding 9780 predicted genes by single-molecule, real-time sequencing technology. The phylogenomic analysis showed that H. erinaceus had the closest evolutionary affinity with Dentipellis sp. The polysaccharide content in the fermented mycelia of mutated strains HEB and HEC, which obtained by ARTP mutagenesis in our previous study, was improved by 23.25 and 47.45%, and a new β-glucan fraction with molecular weight 1.056 × 106 Da was produced in HEC. Integrative analysis of transcriptome and proteomics showed the upregulation of the carbohydrate metabolism pathway modules in HEB and HEC might lead to the increased production of glucose-6P and promote the repeating units synthesis of polysaccharides. qPCR and PRM analysis confirmed that most of the co-enriched and differentially co-expressed genes involved in carbohydrate metabolism shared a similar expression trend with the transcriptome and proteome data in HEB and HEC. Heatmap analysis showed a noticeably decreased protein expression profile of the RAS-cAMP-PKA pathway in HEC with a highly increased 47.45% of polysaccharide content. The S phase progression blocking experiment further verified that the RAS-cAMP-PKA pathway’s dysfunction might promote high polysaccharide and β-glucan production in the mutant strain HEC. Conclusions The study revealed the primary mechanism of the increased polysaccharide synthesis induced by ARTP mutagenesis and explored the essential genes and pathways of polysaccharide synthesis.


1971 ◽  
Vol 76 (3) ◽  
pp. 423-432 ◽  
Author(s):  
J. K. Thompson ◽  
P. N. Hobson

SUMMARYMicro-organisms from the rumen of a hay-fed sheep rapidly synthesized an intracellular polysaccharide (starch) when growing or resting suspensions of cells were incubatedin vitrowith easily metabolized sugars.In 30 min incubation periods the optimum pH for the synthesis of starch by resting cultures was about 6·0 when glucose or fructose were substrates. Relative to glucose (as 100%) in ability to form the polysaccharide were, fructose, 75%; sucrose, 80%; soluble starch, 18·6%; maltose, 6·9%; cellobiose, 4%; and xylose, 2·1%. No starch was formed from galacturonic, acetic, propionic, butyric, lactic or succinic acids. A bacterial fraction of the microbes was reponsible for about 80% of the starch formed from glucose, fructose or sucrose.In incubations of 24 h, resting cultures formed more starch per unit of microbial protein than growing cultures. The utilization of microbial starch and lactic acid, formation of which often accompanied starch synthesis, gave rise to volatile fatty acids. Acid production was maintained from these substrates at rates similar to those obtained from the fermentation of glucose. The acids were in molar proportions of 65–70% acetic, 20–27% propionic and 8–15% butyric. The maximum starch calculated to be synthesized by the microbes from 100 ml of rumen liquor, in media containing excess sugar, amounted to over 250 mg from glucose, 200 mg from fructose, 200 mg from cellobiose and 50 mg from xylose. It is calculated that under optimum conditions for synthesis about 25 g of starch would pass daily from the rumen of a sheep.


PEDIATRICS ◽  
1953 ◽  
Vol 12 (3) ◽  
pp. 338-338

The pediatrician will find a precise presentation of much valuable information on the physiologic, biochemical and clinical aspects of carbohydrate metabolism. Enzymatic synthesis and degradation of glycogen and the influence of hormones on carbohydrate metabolism and electrolyte balance are discussed by Drs. Carl F. Cori, Earl W. Sutherland, C. R. Park, A. Baird Hastings and Evan Calkins. The clinical application of these physiologic and biochemical aspects to glycogen storage disease, hypoglycemia and diabetic acidosis are discussed by Drs. Dorothy H. Andersen, Irvine McQuarrie and Allan M. Butler.


1991 ◽  
Vol 80 (3) ◽  
pp. 213-217 ◽  
Author(s):  
Jeff Arnold ◽  
Marcus J. Hamer ◽  
Miles Irving

1. In sepsis various processes of carbohydrate metabolism, such as hepatic gluconeogenesis and glycolysis, are altered. Phosphofructokinase-1, a key glycolytic enzyme, is controlled in the long term via regulation of synthesis and degradation of the protein itself, while in the short term it is regulated by allosteric effectors, such as fructose 2,6-bisphosphate (the most potent). In the present study hepatic phosphofructokinase-1 activity as well as phosphofructokinase-2 activity and the concentration of fructose 2,6-bisphosphate were assayed to determine if they might contribute to the derangement of carbohydrate metabolism seen commonly in sepsis. 2. The levels of glycogen and fructose 2,6-bisphosphate and the activity of phosphofructokinase-1 and phosphofructokinase-2 were determined in hepatic biopsies obtained at laparotomy from six patients with and seven patients without abdominal septic foci. 3. A significant increase in plasma lactate concentration was observed in the septic patients, whereas no significant differences in tissue glycogen content or plasma glucose concentration were seen between the groups. 4. No significant change in plasma insulin concentration was observed. However, levels of the counter-regulatory hormones (glucagon, cortisol and adrenaline) were elevated in the septic patients. 5. A 60% decrease in hepatic phosphofructokinase-1 activity was seen in the septic patients. However, no significant changes in hepatic phosphofructokinase-2 activity and fructose 2,6-bisphosphate content were observed in the septic patients. 6. The present results demonstrate that the decrease in hepatic phosphofructokinase-1 activity occurring in sepsis does not appear to reflect alterations in the concentration of fructose 2,6-bisphosphate.


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