Fatty acid synthesis diagram

Figure 11.4 Condensation, dehydration and reduction reactions in fatty add synthesis. These reactions constitute the major components of the pathway of fatty acid synthesis and are all catalysed by fatty acid synthase. The reduction reactions, indicated by addition of 2H in the diagram, involve the conversion of NADPH to NADP . (The re-conversion of NADP back to NADPH occurs in the pentose phosphate pathway.) The condensation reaction results in an increase in size of acyl-ACP by two carbon units in each step. The two carbons for each extension are each provided by malonyl-CoA. ACP - acyl carrier protein.

The malic enzyme/citrate lyase pathway is shown in Figure 5.10. The 2-carbon units acetyl groups) for fatty acid synthesis are supplied by the activity of citrate lyase, which may be considered an enzyme of fatty acid biosynthesis. The reduced NADP is Supplied at the point of malic enzyme. Figure 5.10 reveals no net production or utilization of NAD in the cytoplasm. The NADPH + H generated in the cytoplasm is used for fatly acid synthesis, which regenerates NADP. One molecule of CO is produced in the cytoplasm. The diagram reveals no net production or utilization of CO in the mitochondrion. One molecule of NAD is... 

Relationship between fattyacid synthesis and degradation. This diagram shows that malonyl CoA inhibits CPTI and thereby b-oxidation, avoiding the oxidation of newly synthesized fatty acids. Fatty-acyl CoA inhibits acetyl CoA carboxylase and thereby fatty-acid synthesis. When fatty-acyl CoAs are converted to triacylglycerols or phospholipids, they are effectively removed and will no longer be inhibitory. 

Fig. 38. Diagram of the multi-enzyme complex of fatty acid synthesis.

Figure 11.7 Synthesis of triaq/lglyceroL The precursors are glycerol 3-phosphate and long-chain acyl-CoA. R, is a saturated fatty acid, R2 is an unsaturated fatty acid (one or two doubte bonds) and R3 is either saturated or unsaturated. The activity of GPAT-1 regulates triacylglycerol synthesis. In all reactions involving RCO.SCoA, the CoASH is released but is not shown in this diagram. P,- - phosphate.

Figure 26-3. Schematic diagram of the interplay of fatty acid breakdown and ketone body formation with the synthesis (gluconeogenesis) and degradation of glucose (glycolysis). The P-oxidation of fatty acids provides the energy that drives the formation of glucose.

Refer to Fig. 11-24 Starting with one acetyl-CoA molecule to fill the XXX site (left side of the diagram) and a malonyl-CoA to fill the YYY site (right side of the diagram), a 4-carbon fatty acyl chain will be formed by also using two molecules of NADPH. Each subsequent addition of two carbon atoms requires a molecule of malonyl-CoA and two more molecules of NADPH. Thus a 16-carbon fatty acid molecule, palmitic acid, requires 1 acetyl-CoA, 7 malonyl-CoA, and 16 NADPH molecules for its synthesis. 

Figure 1. An abbreviated scheme for glycerollpld synthesis In Arabldopsls leaves showing the proposed locations of the enzymatic deficiencies In four mutants with altered fatty acid composition. The lesions are Indicated by a break In the diagram adjacent to the gene symbol (le., fadA, fadB, fadC and fadD).

The synthesis of phosphatides proceeds for some distance over the same pathway as that of the neutral fats. Glycerophosphate is esterified by long-chain activated fatty acids (i.e. by acyl-CoA compounds) to form phosphatidic acids. A monophosphodiesterase then frees the a-hydroxyl group to make room for the phospho-choline residue (see diagram Chapt. XII-6). 

Figure 2. Diagram representing anaplerotic (solid lines and shapes) and cataplerotic (dashed lines and shapes) sequences connecting the Krebs cycle to gluconeogenesis, fatty acid metabolism, and dispensible AA synthesis. Some sequences can serve both anaplerotic and cataplerotic roles, thus linked metabolites (bold) can be catabolized or synthesized. a-KG, a-ketoglutarate OAA, oxaloacetate PEP, phosphoenolpyruvate.

Figure 29.3 Summary diagram of major impacts of ethanol on metabolic pathways. An influx of ethanol disturbs the balance of carbohydrate and fatty acid metabolism. As a result of the oxidation of ethanol, concentrations of NADH and acetyl CoA are increased. Steps in the tricarboxylic acid cycle (TCA) and the mitochondrial pathway for p-oxidatlon of free fatty acids (FFA) which produce these species are inhibited (blue). At the same time, the excess amounts of NADH and acetyl CoA create conditions in which the fatty add synthesis and acidosis are favoured (red). The abundance of acetyl CoA means alcohol precursor metabolites accumulate. See text for a detailed explanation. Abbreviations ADH, alcohol dehydrogenase MEOS, microsomal endoplasmic oxidising system ALD, aldehyde dehydrogenase TG, triglycerides TCA, tricarboxylic acid cycle FFA, free fatty adds.

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