I started this thread to show there are many roads to Glycogen Storage Depletion
Glycogen Storage Diseases (Glycogenosis)
Glucose derived from glycogen breakdown is an important source of energy for the body. It provides energy for muscle contraction, and serves as the primary source of energy for the brain. Healthy people maintain a relatively constant 5 mM blood glucose concentration to support tissues and organs.
http://www.uic.edu/classes/phar/phar332/Clinical_Cases/carbo metab cases/glycogen metab/Glycogen metabolism.htm
Glycogen Breakdown
http://oregonstate.edu/instruct/bb450/summer09/lecture/glycogennotes.html
10 Steps of Glycolysis
http://biology.about.com/od/cellularprocesses/a/aa082704a.htm
Debranching enzyme is a molecule that helps facilitate the breakdown of glycogen, which serves as a store of glucose in the body, through glucosyltransferase and glucosidase activity. Together with phosphorylases, debranching enzymes mobilize glucose reserves from glycogen deposits in the muscles and liver. This constitutes a major source of energy reserves in most organisms. Glycogen breakdown is highly regulated in the body, especially in the liver, by various hormones including insulin and glucagon, to maintain a homeostatic balance of blood-glucose levels.[1] When glycogen breakdown is compromised by mutations in the glycogen debranching enzyme, metabolic diseases such as Glycogen storage disease type III can result.
http://oregonstate.edu/instruct/bb450/summer09/lecture/glycogennotes.html
Gluconeogenesis
http://en.wikipedia.org/wiki/Gluconeogenesis
Kynurenine Pathway
Viruses and mineral depletion can affect the NAD Synthesis in the Kynurenine pathway. We know quinolinic is elevated in CFS/ME subgroups.The main concern is the NADH recycling anaerobic metabolism (ADP to ATP) imbalance. If we have a metabolic imbalance of NAD+ NADH, this can impact the metabolism of glycogen and possibly cause Glycogenosis storage depletion.
Glycogen Storage Metabolic Syndrome?
There is a consistently high Methylhistidine on OAT testing in the chronic fatigue community, could this contribute to a glycogen storage problem?
Chronic-Infection-H-Pylori-Manganese-Connection?
http://forums.phoenixrising.me/inde...nfection-h-pylori-manganese-connection.27569/
Glycogen Storage Diseases (Glycogenosis)
Glucose derived from glycogen breakdown is an important source of energy for the body. It provides energy for muscle contraction, and serves as the primary source of energy for the brain. Healthy people maintain a relatively constant 5 mM blood glucose concentration to support tissues and organs.
http://www.uic.edu/classes/phar/phar332/Clinical_Cases/carbo metab cases/glycogen metab/Glycogen metabolism.htm
Glycogen Breakdown
http://oregonstate.edu/instruct/bb450/summer09/lecture/glycogennotes.html
10 Steps of Glycolysis
http://biology.about.com/od/cellularprocesses/a/aa082704a.htm
Debranching enzyme is a molecule that helps facilitate the breakdown of glycogen, which serves as a store of glucose in the body, through glucosyltransferase and glucosidase activity. Together with phosphorylases, debranching enzymes mobilize glucose reserves from glycogen deposits in the muscles and liver. This constitutes a major source of energy reserves in most organisms. Glycogen breakdown is highly regulated in the body, especially in the liver, by various hormones including insulin and glucagon, to maintain a homeostatic balance of blood-glucose levels.[1] When glycogen breakdown is compromised by mutations in the glycogen debranching enzyme, metabolic diseases such as Glycogen storage disease type III can result.
http://oregonstate.edu/instruct/bb450/summer09/lecture/glycogennotes.html
Gluconeogenesis
http://en.wikipedia.org/wiki/Gluconeogenesis
Kynurenine Pathway
Viruses and mineral depletion can affect the NAD Synthesis in the Kynurenine pathway. We know quinolinic is elevated in CFS/ME subgroups.The main concern is the NADH recycling anaerobic metabolism (ADP to ATP) imbalance. If we have a metabolic imbalance of NAD+ NADH, this can impact the metabolism of glycogen and possibly cause Glycogenosis storage depletion.
- Gluconeogenesis begins in the mitochondria with the formation of oxaloacetate by the carboxylation of pyruvate. This reaction also requires one molecule of ATP, and is catalyzed by pyruvate carboxylase. This enzyme is stimulated by high levels of acetyl-CoA (produced in β-oxidation in the liver) and inhibited by high levels of ADP.
- Oxaloacetate is reduced to malate using NADH, a step required for its transportation out of the mitochondria.
Glycogen Storage Metabolic Syndrome?
There is a consistently high Methylhistidine on OAT testing in the chronic fatigue community, could this contribute to a glycogen storage problem?
Chronic-Infection-H-Pylori-Manganese-Connection?
http://forums.phoenixrising.me/inde...nfection-h-pylori-manganese-connection.27569/
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