Propionate kinase 2

DHEA is transformed into DHEA-S by sulfation at the C3β position via the sulfotransferase enzymes SULT2A1 and to a lesser extent SULT1E1 . [40] [50] [51] This occurs naturally in the adrenal cortex and during first-pass metabolism in the liver and intestines when exogenous DHEA is administered orally. [ citation needed ] Levels of DHEA-S in circulation are approximately 250 to 300 times those of DHEA. [19] DHEA-S in turn can be converted back into DHEA in peripheral tissues via steroid sulfatase (STS). [52] [53]

Lipids and amino acids can also be used as energy sources, but they enter the main pathways at different points. C. elegans has a functional methylmalonyl-CoA epimerase (racemase) that is involved in propionyl-CoA metabolism for the degradation of branched amino acids and odd-chain fatty acids ( Kühnl et al., 2005 ). Fatty acid moieties of lipids are broken down by β -oxidation into acetyl-CoA (which in turn can enter the TCA cycle). β -oxidation occurs in the mitochondrial matrix and also yields reduced electron carriers. Peroxisomal β -oxidation of long-chain fatty acids is not linked directly to energy metabolism because the reduced electron carrier is directly oxidized by molecular oxygen (yielding hydrogen peroxide). Amino acids can be broken down via distinct pathways and their carbon skeletons can be metabolized in the TCA cycle.

Initial dose based on previous asthma drug therapy and disease severity; 100 mcg via oral inhalation once daily is the usual recommended starting dose for patients not on an inhaled corticosteroid. After 2 weeks of therapy, if asthma symptoms are uncontrolled, increase dose to 200 mcg via oral inhalation once daily. Max: 200 mcg once daily. Administer at the same time each day. The maximum beneficial effect may not be achieved for up to 2 weeks or longer after starting treatment. Titrate to the lowest effective dose once asthma stability is achieved.

Propionate kinase 2

propionate kinase 2

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