Endocrine system Video transcript - [Instructor] Now the ultimate goal in fat metabolism is to be able to deliver some triacylglycerides, which I'm gonna abbreviate here at TAG, which remember is the chemical name for a fat molecule, or free fatty acids, which I'll abbreviate here at FFA, which if you recall are the kind of monomer subunits of these fat molecules directly into the bloodstream where they can eventually reach capillary beds like the one that I've drawn here. So I'll go ahead and label this as a capillary bed, and it's important that they reach these capillary beds because it's at this point where they can diffuse to surrounding tissues such as muscle or heart tissue, for example, where they can be taken up by these tissues and oxidized to obtain cellular energy in the form of ATP. Now I want to remind you that there are three main sources of these triacylglycerides or free fatty acids that can enter the bloodstream, and so I'm gonna go ahead and scroll up here and show you kind of what I've already drawn out here and go ahead and explain it. Starting off here on the far left I've drawn a cheeseburger, perhaps not the best drawing in the world, but just to remind us that one of our sources of fat that ultimately reaches our bloodstream is directly from our diet.
NADPH is also formed by the pentose phosphate pathway which converts glucose into ribose, which can be used in synthesis of nucleotides and nucleic acidsor it can be catabolized to pyruvate.
The pyruvate produced by glycolysis is an important intermediary in the conversion of carbohydrates into fatty acids and cholesterol. However, this acetyl CoA needs to be transported into cytosol where the synthesis of fatty acids and cholesterol occurs.
This cannot occur directly. To obtain cytosolic acetyl-CoA, citrate produced by the condensation of acetyl CoA with oxaloacetate is removed from the citric acid cycle and carried across the inner mitochondrial membrane into the cytosol. The oxaloacetate can be used for gluconeogenesis in the liveror it can be returned into mitochondrion as malate.
The two pathways are distinct, not only in where they occur, but also in the reactions that occur, and the substrates that are used. The two pathways are mutually inhibitory, preventing the acetyl-CoA produced by beta-oxidation from entering the synthetic pathway via the acetyl-CoA carboxylase reaction.
During each turn of the cycle, two carbon atoms leave the cycle as CO2 in the decarboxylation reactions catalyzed by isocitrate dehydrogenase and alpha-ketoglutarate dehydrogenase.
Thus each turn of the citric acid cycle oxidizes an acetyl-CoA unit while regenerating the oxaloacetate molecule with which the acetyl-CoA had originally combined to form citric acid.
The decarboxylation reactions occur before malate is formed in the cycle. This is the only substance that can be removed from the mitochondrion to enter the gluconeogenic pathway to form glucose or glycogen in the liver or any other tissue.
Only plants possess the enzymes to convert acetyl-CoA into oxaloacetate from which malate can be formed to ultimately be converted to glucose. Acetyl-CoA carboxylase is the point of regulation in saturated straight-chain fatty acid synthesis, and is subject to both phosphorylation and allosteric regulation.
Regulation by phosphorylation occurs mostly in mammals, while allosteric regulation occurs in most organisms.
Allosteric control occurs as feedback inhibition by palmitoyl-CoA and activation by citrate. When there are high levels of palmitoyl-CoA, the final product of saturated fatty acid synthesis, it allosterically inactivates acetyl-CoA carboxylase to prevent a build-up of fatty acids in cells. Citrate acts to activate acetyl-CoA carboxylase under high levels, because high levels indicate that there is enough acetyl-CoA to feed into the Krebs cycle and conserve energy.
This pathway does not utilize oxygen and is dependent on enzymes to insert the double bond before elongation utilizing the normal fatty acid synthesis machinery.
In Escherichia coli, this pathway is well understood. This creates the transdecenoyl intermediate. Either the transdecenoyl intermediate can be shunted to the normal saturated fatty acid synthesis pathway by FabB, where the double bond will be hydrolyzed and the final product will be a saturated fatty acid, or FabA will catalyze the isomerization into the cisdecenoyl intermediate.
When FabB reacts with the cis-decenoyl intermediate, the final product after elongation will be an unsaturated fatty acid. FadR is the more extensively studied protein and has been attributed bifunctional characteristics.
In contrast, FabR acts as a repressor for the transcription of fabA and fabB. It is utilized in all eukaryotes and some prokaryotes. This pathway utilizes desaturases to synthesize unsaturated fatty acids from full-length saturated fatty acid substrates. Desaturases are specific for the double bond they induce in the substrate.
These enzymes allow molecular oxygen, O2, to interact with the saturated fatty acyl-CoA chain, forming a double bond and two molecules of water, H2O. These are all termed essential fatty acidsmeaning that they are required by the organism, but can only be supplied via the diet.
Arachidonic acid is the precursor the prostaglandins which fulfill a wide variety of functions as local hormones. DesK is a membrane-associated kinase and DesR is a transcriptional regulator of the des gene.
Unsaturated fatty acids increase the fluidity of the membrane and stabilize it under lower temperatures. DesK is the sensor protein that, when there is a decrease in temperature, will autophosphorylate.These results demonstrate that PES1 and PES2 are involved in the deposition of free phytol and free fatty acids in the form of phytyl esters in chloroplasts, a process involved in maintaining the integrity of the photosynthetic membrane .
Fatty acid Synthase complex- The Fatty Acid Synthase Complex is apolypeptide containing seven enzymeactivities In bacteria and plants, the individualenzymes of the fatty acid synthase systemare separate, and the acyl radicals are foundin combination with a protein called the acylcarrier protein (ACP).
In yeast, mammals, and birds, the. Fatty acid synthesis is the creation of fatty acids from acetyl-CoA and NADPH through the action of enzymes called fatty acid synthases. This process takes place in the cytoplasm of the cell.
Most of the acetyl-CoA which is converted into fatty acids is derived from carbohydrates via the glycolytic pathway. Sep 24, · The rate of fatty acid synthesis in leaves expressing OtsA was 29% higher than in leaves expressing EV (Fig. 2E). T6P specifically binds to Arabidopsis KIN10 and weakens its association with GRIK1.
Sep 28, · There has been a growing interest towards mitochondrial fatty acid synthesis (mtFAS) since the recent discovery of a neurodegenerative human disorder termed MEPAN (mitochondrial enoyl reductase protein associated neurodegeneration), caused by mutations in the mitochondrial enoyl-CoA/ACP (acyl carrier protein) .
Fatty acid synthesis occurs similarly to Beta-oxidation – acetyl groups are added to a growing chain, but the mechanism of the pathway is distinctly different from being simply the reverse of Beta-oxidation.
Fatty acid synthesis occurs in the cytosol (not mitochondria).