Carb_Metabolism.csv

net synthesis of glucose from noncarbohydrate sources

mostly liver; some in kidney; enzymes not expressed in all tissues

reciprocal regulation as compared to glycolysis; pyruvate -> oxaloacetic acid (pyruvate carboxylase - activated by acetyl CoA) ->PEP (PEP carboxykinase - in liver but not muscle; requires hydrolysis of GTP) -> fructose 1 6 bisphosphate -> fructose 6-phosphate (fructose 1 6 bisphosphatase; regulated by PFK-2) -> glucose 6-phosphate -> glucose (glucose 6-phosphatase; found only in liver)

alpha-ketoacids enter the citric acid cycle to form oxaloacetate -> PEP -> glucose

oxidation of odd-number fatty acid chains ->intermediates -> succinyl CoA -> 0.5 glucose; uses 2 ATP

glycerol -> glycerol-3-phosphate (glycerol kinase = catalyst; uses ATP) -> dihydroxyacetone phosphoate (glycerol -3-phosphate dehydrogenase = catalyst; uses NADH) -> 1/2 glucose or lactate

glucagon increases gluconeogenesis and decreases glycolysis; insulin decreases gluconeogenesis and increases glycolysis; regulation occurs @ level of F26BP (action of PFK-1 or FBPase-1)

supports glycolysis in tissues that lack mitochondria; release of lactate from exercising skeletal muscle/cells lacking mitochondria -> diffusion into blood -> uptake by liver -> conversion of lactate to glucose in liver -> re-release into bloodstream; net loss of 4 ATP from 2 lactate

supports glycolysis in tissues with partial oxygen deprivation; release of lactate from oxygen-deprived muscles -> liver -> glucose and urea; requires presence of alanine aminotransferase (found only in liver & muscle & intestine); transports ammonia to the liver; net loss of 3-5 ATP from 2 alanine

mobilized more quickly than fat stores; can be metabolized without oxygen (unlike fat stores); difficult to make glucose for brain from fat; osmotic pressure issues with storge as glucose

occurs in cytosol; requires ATP and UTP; steps = initiation; elongation; branching

accounts for less total glycogen storage than muscles; about 10% of liver devoted to glycogen; glycogen maintains blood glucose levels to provides energy for other tissues

accounts for most total glycogen storage; about 1-2% of muscles devoted to glycogen; glycogen provides energy for muscles only

glucose-6-phosphatase deficiency in liver -> Von Gierke's (type I); alpha 1->4 glucosidase deficiency in lysosomes -> Pompe's (type II); muscle phosphorylase deficiency in muscle -> McArdle's (type V)

provides building blocks for nucleic acid synthesis; occurs in cytosol in the absence of oxygen; involves two non-reversible steps; step 1: glucose-6-phosphate+ NADP+ -> 6-phosphogluconate + NADPH (via glucose-6-phosphate dehydrogenase); step 2: 6-phosphogluconate + NADP+ -> CO2 + ribose-5-phosphate + NADPH

functions as a biological reductant

branched-chain homopolysaccharide made up of alpha D-glucose; primarily alpha (1->4) glycosidic bonds; branch with with alpha (1->6) glycosidic bonds every 8-10 glucosyl residues

UTP + glucose-1-phosphate ->UDP-glucose via action of UDP-glucose-phosphorylase; glycogenin or glycogen fragments act as primers by accepting glucose residues from UDP-glucose; glycogenin continues to catalyze addition of glucose residues until glycogen synthase takes over

glycogen synthase catalyzes the transfer of glucose from UDP-glucose to the nonreducing end of the growing chain - forms bonds between C1 of the activated glucose and C4 of the accepting glycosyl residue

"branching increases solubility of glycogen and speeds up the processes of glycogen synthesis and degradation; ""branching enzyme"" breaks an alpha 1->4 bond and transfers a chain of 6 to 8 glucosyl residues to another residue; chain is attached by alpha 1->6 linkages"

glycogen phosphorylase cleaves 1->4 bonds at nonreducing ends of glycogen chains until 4 residues remain on each chain before a branch point; 4-D-glucotransferase transfers 3 residues from a branch to the end of another chain; A 1->6 glucosidase removes the last remaining glucose

insulin -> stimulation of glycogen synthesis; glucagon & beta-agonists (no glucagon receptors in muscles) -> stimulation of cAMP-mediated glycogen degradation; alpha-agonists -> stimulation of IP3- and calcium-mediated glycogen degradation

fructose entry -> cells is not insulin-dependent; fructose does not raise glycemic index as much as sucrose; fructose is more efficiently converted to fat than sucrose and may contribute to insulin resistance/obesity

galactose -> galactose-1-phosphate (via actions of galactokinase); galactose-1-phosphate + UDP-glucose -> glucose-1-phosphate + UPD-galactose (via galactose-1-phosphate uridylyl transferase); UDP-galactose recycled to UDP-glucose via UDP-galactose-4-epimerase; G1P -> G6P -> glycolysis

mannose -> mannose-6-phosphate (via actions of hexokinase) -> fructose-6-kinase (via actions of phosphomannose isomerase) -> glycolysis

fructose -> fructose-6-phosphate via actions of hexokinase -> glycolysis; hexokinase has low affinity for fructose and so is less important than the fructokinase-mediated pathway in the liver

fructose -> fructose-1-phosphate (via actions of fructokinase) -> glyceraldehyde (via actions of fructose-1-phosphate aldolase); glyceraldehyde can be phosphorylated by glyceraldehyde kinase to make glyceraldehyde-3-phosphate -> glycolysis; glyceraldehyde can also be converted to glycerol using alcohol dehydrogenase and from there can follow a number of pathways (-> phosphoglyceride synthesis; -> triacylglyceride synthesis; -> glycolysis)

X-linked recessive hereditary disease; results in loss of NADPH production; increases oxidative stress & membrane damage & red blood cell lysis