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Oxaloacetate synthesis from

In common with cholesterol synthesis described in the next section, fatty acids are derived from glucose-derived acetyl-CoA. In the fed state when glucose is plentiful and more than sufficient acetyl-CoA is available to supply the TCA cycle, carbon atoms are transported out of the mitochondrion as citrate (Figure 6.8). Once in the cytosol, citrate lyase forms acetyl-CoA and oxaloacetate (OAA) from the citrate. The OAA cannot re-enter the mitochondrion but is converted into malate by cytosolic malate dehydrogenase (cMDH) and then back into OAA by mitochondrial MDH (mMDH) Acetyl-CoA remains in the cytosol and is available for fatty acid synthesis. [Pg.180]

Biotin (5) is the coenzyme of the carboxylases. Like pyridoxal phosphate, it has an amide-type bond via the carboxyl group with a lysine residue of the carboxylase. This bond is catalyzed by a specific enzyme. Using ATP, biotin reacts with hydrogen carbonate (HCOa ) to form N-carboxybiotin. From this activated form, carbon dioxide (CO2) is then transferred to other molecules, into which a carboxyl group is introduced in this way. Examples of biotindependent reactions of this type include the formation of oxaloacetic acid from pyruvate (see p. 154) and the synthesis of malonyl-CoA from acetyl-CoA (see p. 162). [Pg.108]

High acetyl CoA levels from 3-oxidation of fatty acids in liver cells inhibit the pyruvate dehydrogenase complex and activate pyruvate carboxylase, which increases oxaloacetate synthesis. [Pg.114]

Synthesis from oxaloacetate and a-ketoglutarate would deplete the citric acid cycle, which would decrease ATP production. Anapleurotic reactions would be required to replenish the citric acid cycle. [Pg.1492]

Thus, citrate not only modulates the rate of fatty acid synthesis but also provides carbon atoms for the synthesis. The oxaloacetate formed from pyruvate may eventually be converted (via malate) to glucose by the gluconeogenic pathway. The glucose oxidized via the pentose phosphate pathway augments fatty acid synthesis by providing NADPH. Pyruvate generated from oxaloacetate can enter mitochondria and be converted to oxaloacetate, which is required for the formation of citrate. [Pg.384]

When the regenerative pathway from acetate to oxaloacetate is included, the rTCA cycle develops the possibility of self-production, increasing the density of catalytic oxaloacetate molecules and hence the bulk rate of acetate synthesis from CO2. The gain in this cycle enables an exponentially growing relaxation process to... [Pg.398]

Synthesis of PEP. PEP synthesis from pyruvate requires two enzymes pyruvate carboxylase and PEP carboxykinase. Pyruvate carboxylase, found within mitochondria, converts pyruvate to oxaloacetate (OAA) ... [Pg.252]

Since Corynebacterium glutamicum does not possess a PEPsynthetase, no [3- CjPEP isotopomers can be formed from pyruvate. Thus, any [3- C]oxaloac-etate isotopomers must result from the action of PyrCx in vivo and their relative abundance allows to quantitate the relative contributions of PEPCx and PyrCx to oxaloacetate synthesis. In the aspartate derived from oxaloacetate a content of isotopomers labelled in C-3 but not in C-2 similarly high as that in pyruvate was found (Fig. 8 c), suggesting synthesis of oxaloacetate from pym-... [Pg.18]

In mammals, acetyl CoA from fatty acid oxidation cannot be used for the net synthesis of pyruvate or oxaloacetate, which in turn means that net glucose synthesis from acetyl CoA is impossible. However, glucose can be radioactively labeled when C-labeled acetate is introduced into human tissue culture cells and converted to acetyl CoA by acetyl CoA synthetase. Radioactive fatty acids can also be used to label glucose. Why If the methyl carbon of acetate is labeled, where will glucose be labeled ... [Pg.395]

Radioactive acetyl CoA can be generated by direct synthesis from C-acetate or from (3 oxidation of radioactive fatty acids, such as uniformly labeled palmitate. Examination of the reactions of the citric acid cycle reveals that neither of the two carbons that enter citrate horn acetate is removed as carbon dioxide during the first pass through the cycle. Labeled carbon from C-methyl-labeled acetate appears in C-2 and C-3 of oxaloacetate, because succinate is symmetrical, with either methylene carbon in that molecule labeling C-2 or C-3 of oxaloacetate. The conversion of oxaloacetate to phosphoenolpyruvate yields PEP labeled at C-2 or C-3 as well. Formation of glyceraldehyde 3-phosphate and its isomer dihydroxyacetone phosphate gives molecules, both labeled at carbons 2 and... [Pg.403]

Kraeva NI and Vorobjeva LI (1981b) Superoxide dismutase, catalase, and peroxidase of propionic acid bacteria. Mikrobiologiya 50 813-817 Krebs flA and Eggleston LV (1941) Biological synthesis of oxaloacetic acid from pyruvic acid and carbon dioxide. II. The mechanism of carbon dioxide fixation in propionic acid bacteria. Biochem J 35 676-687... [Pg.263]

This is a typical example of substrate-level phosphorylation. The GTP generated in this reaction undergoes different fates (a) transphosphorylation with ADP to give ATP and GDP (b) transphosphorylation with AMP to give ADP and GDP (c) direct activation of fatty acids (d) phosphoenol-pyruvate synthesis from oxaloacetate. [Pg.174]

As noted above the operation of the TCA cycle results in the conversion of acetyl-CoA to carbon dioxide and reduced co-enzymes, the oxidation of which may be coupled to the synthesis of ATP (see terminal oxidation below). However the TCA cycle must not be thought of simply as an incinerator—it is also important as a means whereby acetyl-Co A from a variety of sources is converted to compounds involved in a number of biosynthetic pathways. For example oxoglutarate is involved in amino acid synthesis and succinyl-CoA is a precursor of porphyrins. These and other intermediates are withdrawn from the cycle—however, a moment s thought will indicate that the carbon withdrawn must be replaced if the rate of utilization of acetyl-Co A by the cycle is not to be reduced. The reactions shown below result in the replenishment of the cycle with malic or oxaloacetic acid from phosphoenolpyruvate (PEP) or pyruvate and are sometimes referred to as anaplerotic reactions. [Pg.101]

In 1937 Krebs found that citrate could be formed in muscle suspensions if oxaloacetate and either pyruvate or acetate were added. He saw that he now had a cycle, not a simple pathway, and that addition of any of the intermediates could generate all of the others. The existence of a cycle, together with the entry of pyruvate into the cycle in the synthesis of citrate, provided a clear explanation for the accelerating properties of succinate, fumarate, and malate. If all these intermediates led to oxaloacetate, which combined with pyruvate from glycolysis, they could stimulate the oxidation of many substances besides themselves. (Kreb s conceptual leap to a cycle was not his first. Together with medical student Kurt Henseleit, he had already elucidated the details of the urea cycle in 1932.) The complete tricarboxylic acid (Krebs) cycle, as it is now understood, is shown in Figure 20.4. [Pg.642]

FIGURE 20.23 Export of citrate from mitochondria and cytosolic breakdown produces oxaloacetate and acetyl-CoA. Oxaloacetate is recycled to malate or pyruvate, which re-enters the mitochondria. This cycle provides acetyl-CoA for fatty acid synthesis in the cytosol. [Pg.663]

Succinyl-CoA derived from propionyl-CoA can enter the TCA cycle. Oxidation of succinate to oxaloacetate provides a substrate for glucose synthesis. Thus, although the acetate units produced in /3-oxidation cannot be utilized in glu-coneogenesis by animals, the occasional propionate produced from oxidation of odd-carbon fatty acids can be used for sugar synthesis. Alternatively, succinate introduced to the TCA cycle from odd-carbon fatty acid oxidation may be oxidized to COg. However, all of the 4-carbon intermediates in the TCA cycle are regenerated in the cycle and thus should be viewed as catalytic species. Net consumption of succinyl-CoA thus does not occur directly in the TCA cycle. Rather, the succinyl-CoA generated from /3-oxidation of odd-carbon fatty acids must be converted to pyruvate and then to acetyl-CoA (which is completely oxidized in the TCA cycle). To follow this latter route, succinyl-CoA entering the TCA cycle must be first converted to malate in the usual way, and then transported from the mitochondrial matrix to the cytosol, where it is oxida-... [Pg.793]

The acetyl-CoA derived from amino acid degradation is normally insufficient for fatty acid biosynthesis, and the acetyl-CoA produced by pyruvate dehydrogenase and by fatty acid oxidation cannot cross the mitochondrial membrane to participate directly in fatty acid synthesis. Instead, acetyl-CoA is linked with oxaloacetate to form citrate, which is transported from the mitochondrial matrix to the cytosol (Figure 25.1). Here it can be converted back into acetyl-CoA and oxaloacetate by ATP-citrate lyase. In this manner, mitochondrial acetyl-CoA becomes the substrate for cytosolic fatty acid synthesis. (Oxaloacetate returns to the mitochondria in the form of either pyruvate or malate, which is then reconverted to acetyl-CoA and oxaloacetate, respectively.)... [Pg.804]

Citrate is isomerized to isocitrate by the enzyme aconitase (aconitate hydratase) the reaction occurs in two steps dehydration to r-aconitate, some of which remains bound to the enzyme and rehydration to isocitrate. Although citrate is a symmetric molecule, aconitase reacts with citrate asymmetrically, so that the two carbon atoms that are lost in subsequent reactions of the cycle are not those that were added from acetyl-CoA. This asymmetric behavior is due to channeling— transfer of the product of citrate synthase directly onto the active site of aconitase without entering free solution. This provides integration of citric acid cycle activity and the provision of citrate in the cytosol as a source of acetyl-CoA for fatty acid synthesis. The poison fluo-roacetate is toxic because fluoroacetyl-CoA condenses with oxaloacetate to form fluorocitrate, which inhibits aconitase, causing citrate to accumulate. [Pg.130]

Aminotransferase (transaminase) reactions form pymvate from alanine, oxaloacetate from aspartate, and a-ketoglutarate from glutamate. Because these reactions are reversible, the cycle also serves as a source of carbon skeletons for the synthesis of these amino acids. Other amino acids contribute to gluconeogenesis because their carbon skeletons give rise to citric acid cycle... [Pg.133]

The synthesis of this aminoquinoline starts with one of the standard sequences for preparation of 4-hydroxyquinolines, i.e., with the formation of the Shiff base (5) from the appropriately substituted aniline and diethyl oxaloacetate. Thermal cycliza-tion gives the quinolone (6) this then spontaneously tautomerizes to the enol form (7). Saponification followed by decarboxylation gives the desired quinolol... [Pg.363]

The Jirst indirect route in glucose synthesis involves the formation of phosphoenolpyruvate from pyruvate without the intervention of pyruvate kinase. This route is catalyzed by two enzymes. At first, pyruvate is converted into oxaloacetate. This reaction occurs in the mitochondria as the pyruvate molecules enter them, and is catalyzed by pyruvate carboxylase according to the scheme... [Pg.186]

It was observed that glutamate and aspartate are diverted predominantly to the synthesis of cell substance rather than to the formation of oxalate. It is not inconsistent to see oc-ketoglutarate being formed from glutamate, while no oxaloacetic acid can be detected in the medium containing aspartate, as the oxaloacetic acid is known to be extremely unstable (2), (62), (Hi). The relatively low yields of oxalic acid, derived... [Pg.75]

There are two unusual aspects to the regulation of gluconeogenesis. The first step in the reaction, the formation of oxaloacetate from pyruvate, requires the presence of acetyl-CoA. This is a check to make sure that the TCA cycle is adequately fueled. If there s not enough acetyl-CoA around, the pyruvate is needed for energy and gluconeogenesis won t happen. However, if there s sufficient acetyl-CoA, the pyruvate is shifted toward the synthesis of glucose. [Pg.159]

Calculating energy costs for the synthesis of a CK, fatty acid from acetyl-CoA is not as simple as you might first think. The major complication is that acetyl-CoA is made in the mitochondria, but fatty acid synthesis occurs in the cytosol—acetyl-CoA can t cross the mitochondrial membrane. Acetyl-CoA gets out of the mitochondria disguised as citrate. The acetyl-CoA is condensed with oxaloacetate to give citrate, and the citrate leaves the mitochondria. In the cytosol, the citrate is cleaved by an ATP-dependent citrate lyase into acetyl-CoA and oxaloacetate ... [Pg.170]


See other pages where Oxaloacetate synthesis from is mentioned: [Pg.213]    [Pg.200]    [Pg.370]    [Pg.213]    [Pg.200]    [Pg.370]    [Pg.104]    [Pg.1266]    [Pg.773]    [Pg.890]    [Pg.331]    [Pg.308]    [Pg.925]    [Pg.148]    [Pg.106]    [Pg.253]    [Pg.669]    [Pg.157]    [Pg.177]    [Pg.231]    [Pg.316]    [Pg.214]    [Pg.213]    [Pg.269]    [Pg.545]    [Pg.136]   


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