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Biochemical Pathways for the Biofuel Production
Published in Debabrata Das, Jhansi L. Varanasi, Fundamentals of Biofuel Production Processes, 2019
Debabrata Das, Jhansi L. Varanasi
TAGs are the predominant component of the oils extracted from the seeds or fruits of oleaginous plants like sunflower, oilseed rape, maize, and soybean. TAGs of higher plants contain acyl groups of palmitic acid (16:0), stearic acid (18:0), oleic acid (18:1), linolenic acid (18:2), and α-linolenic acid (18:3). In these organisms, the fatty acid biosynthesis occurs in the stroma of plastids. The subsequent incorporation of fatty acids into the glycerol backbone leads to the biosynthesis of TAGs in the endoplasmic reticulum (ER) (Figure 4.1a). During fatty acid synthesis, the acetyl-CoA carboxylases (ACC) catalyze the irreversible carboxylation of acetyl-CoA to form malonyl-CoA. The malonyl group is then transferred to the acyl carrier protein (ACP), giving rise to malonyl-ACP, which is the primary substrate for fatty acid synthase complex. Repeated condensation of malonyl-ACP by the action of fatty acid synthase complex with the subsequent addition of two carbon units after each elongation leads to the formation of fatty acid-ACP complexes (like 16:0 ACP, 18:0 ACP, and 18:1 ACP). The type of acyl chain bound to ACP depends upon the type of enzyme present (mostly ketoacyl synthases I, II, and III) and varies in different plant species. The termination of fatty acid elongation is catalyzed by ACP thioesterases, which catalysis the hydrolysis of acyl-ACP to produce free fatty acids that are able to cross the plastidial envelope. These free fatty acids are then reactivated as acyl-CoAs in the cytosol and form the acyl-CoA pool, which provides the acyl donor for the acyl transferase reactions of the TAG assembly in the ER.
Processes for Overproduction of Microbial Metabolites for Industrial Applications
Published in Nduka Okafor, Benedict C. Okeke, Modern Industrial Microbiology and Biotechnology, 2017
Nduka Okafor, Benedict C. Okeke
Ease of permeability is important in industrial microorganisms not only because it facilitates the isolation of the product, but more importantly because of the removal of the product from the site of feedback regulation. If the product did not diffuse out of the cell but remained cell-bound, then the cell would have to be disrupted to enable the isolation of the product, thereby increasing costs. The importance of permeability is most easily demonstrated in glutamic acid producing bacteria. In these bacteria, the permeability barrier must be altered so that a high level of amino acid is accumulated in the broth. This increased permeability can be induced by several methods:Biotin deficiency: Biotin is a coenzyme in carboxylation and trans-carboxylation reactions, including the fixation of CO2 to acetate to form malonate. The enzyme which catalyzes this is rich in biotin. The formation of malonyl COA by this enzyme (acetyl-CoA carboxylase) is the limiting factor in the synthesis of long chain fatty acids. Therefore, biotin deficiency would cause aberrations in the fatty acid produced and hence in the lipid fraction of the cell membrane, resulting in leaks in the membrane. Biotin deficiency has been shown also to cause aberrant forms in Bacillus polymax, B. megaterium, and in yeasts.Use of fatty acid derivatives: Fatty acid derivatives which are surface-acting agents, e.g. tween 60 (polyoxyethylene-sorbitan monostearate) and tween 40 (polyoxyethylene-sorbitan monopalmitate), have actions similar to biotin and must be added to the medium before or during the log phase of growth. These additives seem to cause changes in the quantity and quality of the lipid components of the cell membrane. For example, they cause a relative increase in saturated fatty acids as compared to unsaturated fatty acids.Penicillin: Penicillin inhibits cell wall formation in susceptible bacteria by interfering with the crosslinking of acetyl-muramic-polypeptide units in the mucopeptide. The cell wall is thus deranged causing glutamate excretion, probably due to damage to the membrane which is the site of synthesis of the wall.
High yield production of lipid and carotenoids in a newly isolated Rhodotorula mucilaginosa by adapting process optimization approach
Published in Biofuels, 2023
Ravi Gedela, Ashish Prabhu, Venkata Dasu Veeranki, Pakshirajan Kannan
In oleaginous yeast, the hydrophilic substrate is consumed via the de novo pathway, and the lipid accumulation proceeds with the depletion of nitrogen compound, which in turns activate AMP deaminase. This activity leads toa series of cascade reactions, which disturbs the TCA cycle in mitochondria and splits the ATP-citrate lyase and acetyl-CoA and oxaloacetate. Further, the acetyl CoA is carboxylated in to malonyl CoA which is the first step of lipid synthesis, and then followed a by series of enzymatic reactions catalyzed by a complex of fatty acid synthases, which ultimately leads to the synthesis of triacyl glycerol. Further in yeast such as Rhodoturula sp that is capable of synthesizing carotenoids, which initiates by the conversion of acetyl CoA to 3 hydroxyl-3 methylglutaryl-CoA catalyzed by 3 hydroxyl-3 methylglutaryl-CoA synthase. Consequently, the HMG- CoA is reduced to mevalonic acid by HMG-CoA reductase and the cascade of reaction takes place for the production of isopentenyl diphosphate (IPP), which is further subjected to an isomerization reaction to form dimethylallyl pyrophosphate (DMAPP), and the addition of 3 molecules of IPP to DMAPP results in geranylgeranyl pyrophosphate (GGPP). The GGPP undergoes a condensation reaction catalyzed by phytoene synthase to form phytoene and finally converted to β-carotene [18]. The biochemical pathway for the formation of lipids and carotenoids in Rhodotorula sp is depicted in Figure S1 (Supplementary Material).
Effects of mixotrophic cultivation on antioxidation and lipid accumulation of Chlorella vulgaris in wastewater treatment
Published in International Journal of Phytoremediation, 2020
Ran Li, Jie Pan, Minmin Yan, Jiang Yang, Wenlong Qin
The fatty acid synthesis pathway of mixotrophic C. vulgaris in wastewater is illustrated in Figure 5. Specifically, CO2 enters the chloroplast to produce glyceraldehyde triphosphate through the Calvin cycle. After that, the glycolytic pathway forms pyruvate, which releases a CO2 molecule and produces acetyl-CoA under the action of pyruvate dehydrogenase (PDH) (Avidan et al.2015). The first key reaction in fatty acid synthesis is the acetyl-CoA conversion to malonyl-CoA catalyzed by ACCase. Our results showed the ACCase activity was enhanced and contributed to the fatty acid accumulation of C. vulgaris cultured in wastewater. During heterotrophic metabolism, after a small molecule of organic matter (e.g., glucose) enters the cell, it is first converted to pyruvic acid by the glycolysis pathway and then by the fatty acid metabolism pathway (Gao et al.2014). Glucose can also be converted into ADPGlc and then into starch under the catalysis by AGPase. However, the activity of ACCase in mixotrophic C. vulgaris in wastewater was weakened, indicating more glucose molecules participate in fatty acid synthesis, causing lipid accumulation.
Mechanisms of beneficial effects of exercise training on non-alcoholic fatty liver disease (NAFLD): Roles of oxidative stress and inflammation
Published in European Journal of Sport Science, 2019
Parvin Farzanegi, Amir Dana, Zeynab Ebrahimpoor, Mahdieh Asadi, Mohammad Ali Azarbayjani
Numerous studies showed that exercise training significantly decreases intrahepatic fat contents. The underlying mechanism involves β-oxidation and lipogenesis (Figure 1). Recent investigations have indicated that exercise activity can regulate hepatic lipid metabolism by regulating hepatic β-oxidation and lipogenesis (Jeppesen & Kiens, 2012). Rector et al. (2008) indicated that exercise training increases hepatic fatty acid oxidation in NAFLD rats by increasing acetyl-coenzyme A carboxylase (ACC) phosphorylation and cytochrome c contents, indicating a possible enhancement of the final steps of oxidative phosphorylation. They also showed that exercise training decreases hepatic lipogenesis by reducing fatty acid synthase (FAS) and ACC contents (Rector et al., 2008). ACC is the committed step in fatty acid synthesis, catalysing the carboxylation of acetyl-CoA to form malonyl-CoA. ACC phosphorylation inhibits its activity and reduces formation of malonyl-CoA. Reduced content of malonyl-CoA is associated with increase in fatty acid oxidation and decrease in available substrate for FAS. Koves et al. (2005) found that exercise training increased the flux of both β-oxidation and tricarboxylic acid (TCA) cycle in the skeletal muscle. These data suggest that exercise training can enhance the complete oxidation of lipids in both the liver and the skeletal muscle.