Numerous carbohydrates, including glucose, meet their catabolic end in $ycolysis after being transformed into glycolytic intermediates. Most significant are glycogen and starch, which are storage polysaccharides that are either in cell walls (endogenous) or in the diet. The disaccharides are maltose. Lactose, trehalose. and sucrose, and the monosaccharides fructose and mannose and galactose.
Dietary Polysaccharides and Disaccharides Undergo Hydrolysis to Monosaccharides
For the majority of humans it is the primary carbohydrate source in the diet. Digestion begins in the mouth is in which salivary amylase hydrolyzes inside (alpha1–>4) glycosidic linkages in starch, resulting in small polysaccharide fragments, or Oligosaccharides. (Note that in this hydrolysis process water and not Pi is the attacking species.)
The stomach’s salivary d’amylase is inhibited by the low pH however, the second form of a-amylase, released through the pancreas and absorbed into the small intestine is able to continue the process of breakdown. Pancreatic amylase is primarily produced by maltose as well as maltotriose (the trisaccharides and disaccharides from sugar) and oligosaccharides, also known as limit dextrins, which are fragments of amylopectin that contain (alpha1–>6) branches. Dextrins and maltose are converted to glucose by enzymes in the border of the intestinal brush (the microvilli that resemble fingers of the epithelial cells in the intestinal tract, which dramatically increase the surface area of the surface of the intestine). Dietary glycogen is essentially the same structure as starch, and its digestion is facilitated by the same process.
Endogenous Glyeoqen ad Starch Are Degraded by Phosphorolysis
Glycogen that is stored in the tissues of animals (primarily the skeletal muscle and liver) or in microorganisms as well as in the plant tissue, can be used in the cell through a phosphorolytic reaction triggered by the glycogen-phosphorylase (starch the phosphorylase found in plant). These enzymes cause the attack of Pi at the (alpha1–>4) glycosidic linkage, which connects to Iast the two sugar residues on a non-reducing end, creating glucose 1-phosphate as well as the polymer, which is one that is a glucose unit smaller. PhosphoroLyses conserves a portion of the energy contained in the glycosidic bond within the phosphate ester of glucose 1-phosphate. Glycogen Phosphorrylase (or starch-phosphorylase) is a repetitive enzyme until it is near an (alpha1–>6) branching point when its activity ceases. Debranching enzymes remove branches.
The glycogen phosphorylase can be converted into glucose 6-phosphate via phosphoglucomutase which is responsible for catalyzing the reversible reaction.
Glucose 1-phosphate = glucose 6-phosphat
Phosphoglucomutase is essentially the same mechanism as phosphoglycerate Mutase (p. 537) Both involve an intermediate bisphosphate, as well as being transiently phosphorylated during every catalytic process. Mutase is the general term used to describe enzymes that facilitate an exchange of functional groups one location to another within an identical molecule. Mutases are a class of isomerases, enzymes that convert stereoisomers and the structural and positional isomers. The glucose 6-phosphate that is formed during the phosphoglucomutase process can be absorbed into glycolysis or a different pathway, such as the pentose phosphate pathway.
The breakdown of polysaccharides in food like glycogen and starch inside the intestinal tract through hydrolysis, rather than phosphorolysis, will not result in any energy gain Sugar phosphates cannot be transferred into the cells of the intestine, but they must first be dephosphorylated and converted to sugar free.
Disaccharides have to be hydrolyzed to monosaccharides prior to entering cells. Disaccharides in the intestine and dextrins are hydrolyzed through enzymes that attach to the surface of intestinal epithelial cells:
The monosaccharides that are produced are then actively transported into epithelial cells. They are then absorbed into blood, where they are transported to different tissues, which are then phosphorylated before being then absorbed into the glycolytic chain.
Other monosaccharides Enter the Glycolytic Pathway Several Point
In the majority of organisms, other hexoses than glucose are able to undergo glycolysis following transformation into the phosphorylated form. D-Fructose is found in the form of a free substance in many fruits , and created by the hydrolysis of sucrose in the small intestines of vertebrates, can be phosphorylated by the enzyme hexokinase.
This is the main route of fructose entering glycolysis in kidneys and muscles. The liver is where fructose is absorbed via a different channel. Its liver-specific enzyme, fructokinase facilitates the phosphorylation process of fructose at C-l instead of C-6
The fructose l-phosphate then transformed into dihydroxyacetone and glyceraldehyde the phosphate through fructose l-phosphate:
Dihydroxyacetone phosphate is converted into Glyceraldehyde-3-phosphate through the glycolytic enzyme triose-phosphate isomerase. Glyceraldehyde gets phosphorylated by ATP and triose-kinase to Glyceraldehyde 3 phosphate
The two products of fructose-l-phosphate hydrolysis get into the glycolltic system as the glyceraldehyde 3-phosphate
D-Galactose is a result of the hydrolysis process of lactose (milk sugar) and is absorbed by the bloodstream from the intestine to liver, where it’s first phosphorylated in C-1 to the detriment of ATP by the galactokinase enzyme:
The galactose L-phosphate is transformed into its epimer at C-4, glucose 1 phosphate by a sequence of reactions where Uridine diphosphate (UDP) serves as a coenzyme-like transporter of hexose group. The epimerization process begins with the reduction of the C-4-OH element to form a ketone and following which, the ketone is reduced to an OH with changing the configuration to C-4. The cofactor is NAD in both reduction and oxidation.
A defect in one or all three of these enzymes involved in this pathway results in galactosemia among humans. Galactokinase deficiency causes galactosemia. the galactose levels are high in urine and in blood. Patients with this condition develop cataracts early in the early years of life, due to accumulation of the galactose-metabolite gallactitol within the lens.
The other symptoms in the disorder are fairly moderate, and strict control of galactose intake drastically reduces the severity. Transferase-deficiency galactosemia is more serious; it is characterized by poor growth in childhood, speech abnormality, mental deficiency, and liver damage that may be fatal, even when galactose is withheld from the diet. Galactosemia with epimerase-deficiency can trigger similar symptoms, but it is less severe when the amount of galactose in the diet is managed carefully.
D-Mannose, which is released during the digestion of different glycoproteins and polysaccharides found in foods, can be phosphorylated on C-6 through Hexokinase.
Mannose 6-phosphate can be isomerized by the phosphomannose isomerase, which results in fructose 6-phosphate which is an intermediate of glycolysis.
- Starch and endogenous glycogen sugars, which are the forms that store glucose, undergo glycolysis in two steps. The phosphorolytic process of cleaving a glucose residue at the beginning of the polymer and forming Glucose L-phosphate, which is catalyzed by glycogen’s phosphorylase or starch-phosphorylase. The phosphoglucomutase transforms the glucose 1-phosphate into glucose 6-phosphate. This phosphate is able to be converted into glycolysis.
- Polysaccharides and disaccharides that are ingested are converted into monosaccharides through the enzymes that hydrolyze the intestinal tract, and the monosaccharides are then absorbed by intestinal cells and get transported to the liver , or other tissues.
- F-hexoses of various kinds such as galactose, fructose mannose, and galactose, can be used to create glycolysis. Each one is phosphorylated before being transformed into glucose 6-phosphate, fructose 6-phosphate or 1-phosphate.
- Conversion of galactose 1 phosphate to glucose 1-phosphate requires two nucleotide derivatives, namely UDP-galactose and UDP-glucose. Genetic deficiencies in one of three enzymes involved in the transformation process of galactose glucose 1-phosphate can cause galactosemias varying in intensity.