Propionate tca cycle

Table 1. Oxidative pathways of glycolysis employed by various bacteria. Bacterium Embden-Meyerhof pathway Phosphoketolase (heterolactic) pathway Entner Doudoroff pathway Acetobacter aceti - + - Agrobacterium tumefaciens - - + Azotobacter vinelandii - - + Bacillus subtilis major minor - Escherichia coli + - - Lactobacillus acidophilus + - - Leuconostoc mesenteroides - + - Pseudomonas aeruginosa - - + Vibrio cholerae minor - major Zymomonas mobilis - - +

Recently, a specific peptide inhibitor for ATGL was isolated from white blood cells, specifically mononuclear cells. This peptide was originally identifed as being involved in the regulation of the G 0 to G 1 transition of the cell cycle . This peptide was, therefore, called G0G1 switch protein 2 (G0S2). The protein is found in numerous tissues, with highest concentrations in adipose tissue and liver. In adipose tissue G0S2 expression is very low during fasting but increases after feeding. Conversely, fasting or PPARα-agonists increase hepatic G0S2 expression. The protein has been shown to localize to LDs, cytoplasm, ER, and mitochondria. These different subcellular localizations likely relate to multiple functions for G0S2 in regulating lipolysis, the cell cycle , and, possibly, apoptosis via its ability to interact with the mitochondrial antiapoptotic factor Bcl-2. With respect to ATGL regulation, the binding of the enzyme to LDs and subsequent is dependent on a physical interaction between the N-terminal region of G0S2 and the patatin domain of ATGL.

If OAA is converted to PEP by mitochondrial PEPCK, it is transported to the cytosol where it is a direct substrate for gluconeogenesis and nothing further is required. Transamination of OAA to aspartate allows the aspartate to be transported to the cytosol where the reverse transamination occurs yielding cytosolic OAA. This transamination reaction requires continuous transport of glutamate into, and 2-oxoglutatrate (α-ketoglutarate) out of, the mitochondrion. Therefore, this process is limited by the availability of these other substrates. Either of these latter two reactions will predominate when the substrate for gluconeogenesis is lactate. Whether mitochondrial decarboxylation or transamination occurs is a function of the availability of PEPCK or transamination intermediates.

Biotin is mainly required as a coenzyme for carboxylation reactions and the main examples are carboxylation of-i) pyruvate to oxaloacetate (first step of gluconeogenesis); ii) Acetyl co A to Malonyl co A (first step of fatty acid synthesis) and iii) Propionyl co A to D-Methyl malonyl co A (in the conversion of propionyl co A to Succinyl co A to gain entry to TCA cycle). In biotin deficiency, out of the given options, defective fatty acid synthesis is the most suited option because of the impaired conversion of acetyl co A to malonyl co A.

In 1904, the German chemist Franz Knoop elucidated the steps in beta-oxidation by feeding dogs odd- and even-chain ω-phenyl fatty acids, such as ω-phenylvaleric acid and ω-phenylbutyric acid, respectively. The mechanism of beta-oxidation, . successive removal of two carbons, was realized when it was discovered that the odd-chain ω-phenylvaleric acid was metabolized to hippuric acid , and that the even-chain ω-phenylbutyric acid was metabolized to phenaceturic acid . At this time, any reaction mechanism involving oxidation at the beta carbon was as yet unknown in organic chemistry . [10] [11]

Propionate tca cycle

propionate tca cycle

Biotin is mainly required as a coenzyme for carboxylation reactions and the main examples are carboxylation of-i) pyruvate to oxaloacetate (first step of gluconeogenesis); ii) Acetyl co A to Malonyl co A (first step of fatty acid synthesis) and iii) Propionyl co A to D-Methyl malonyl co A (in the conversion of propionyl co A to Succinyl co A to gain entry to TCA cycle). In biotin deficiency, out of the given options, defective fatty acid synthesis is the most suited option because of the impaired conversion of acetyl co A to malonyl co A.

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