Hexose Pentose Pathway and Uronic Acid Pathway

( Hexose Pentose Pathway) (Pentose Phosphate Pathway)

$**HMP**$ : pathway by which glucose is converted to @@pentose phosphate@@ with production of @@NADPH@@

Site: ==cytosol== of many cells (e.g. liver, adipose tissue, adrenal, ovaries, testis, red blood cells, and retina)

Oxidative Phase:
- %%irreversible%%
- glucose-6-phosphate converted to @@6 molecules of ribulose-5-phosphate@@
- @@2 NADPH produced@@
Nonoxidative Phase:
- reversible
- 6 molecules of pentoses into @@5 molecules of glucose-6-phosphate@@

can account for complete oxidation of glucose, where it is converted to 6 molecules of CO2 and 12 molecules of NADPH
provides the body with ribose-5-phosphate, which forms %%phosphoribosyl pyrophosphate (PRPP)%% for the synthesis of nucleotides and nucleic acids
==main source of NADPH==
in red blood cells: protects these cells from ==oxidative damage== by providing reduced glutathione for removal of H2O2

induces synthesis of glucose-6-phosphate dehydrogenase and 6-phosphogluconate dehydrogenase: insulin
inhibits glucose-6-phosphate dehydrogenase: NADPH

$Uronic acid pathway$ : minor pathway that produces @@uronic acids@@

UDP-glucuronate utilized for:

synthesis of @@Glycosaminoglycans (GAGs)@@
for conjugation with compounds to make them ^^more soluble^^ before excretion:
- steroid hormones and their metabolites
- bilirubin
- detoxification reactions e.g. phenols
in many mammals (not in primates and guinea pigs) glucuronate is converted to vitamin C (L-ascorbic acid)

In HMP:

$Favism$

glucose-6-phosphate dehydrogenase (G6PD) deficiency
red blood cell capacity to protect itself from oxidative damage is decreased (due to decreased concentration of NAPDH)

$NADPH oxidase deficiency$

genetic deficiency
produces chronic granulomatosis
- severe and persistent chronic pyogenic infections

In Uronic acid pathway:

$Essential Pentosuria$