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Cardiologist REVEALS Why LDL Cholesterol Is Actually Good for You (It DOESN’T Cause Heart Disease) The oxidation of fats is one of oxidatioon main Wholesome plant oils Joint health solutions deterioration mecbanisms food along with Joint health solutions action of microorganisms. It results in alterations of aroma and flavour, oxidztion, loss of Low glycemic index foods nutrients and the formation of potentially harmful substances, which leads to a reduction in the shelf life of the food. This process has important economic repercussions because the food becomes unfit for consumption. The oxidative process of fats causes a decrease in the nutritional capacity of the food by the destruction of fat-soluble vitamins and the degradation of polyunsaturated acids. Food safety can also be affected, since the products originating from the oxidation can present toxicity, some volatile products, peroxides, oxy acids etc.Fat oxidation mechanisms -
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Cell Metab 29 4 — Cui L, Mirza AH, Zhang S, Liang B, Liu P. Lipid droplets and mitochondria are anchored during brown adipocyte differentiation. Protein Cell 10 12 —6. In catabolism, fatty acids are metabolized to produce energy, mainly in the form of adenosine triphosphate ATP.
When compared to other macronutrient classes carbohydrates and protein , fatty acids yield the most ATP on an energy per gram basis, when they are completely oxidized to CO 2 and water by beta oxidation and the citric acid cycle. In anabolism, intact fatty acids are important precursors to triglycerides, phospholipids, second messengers, hormones and ketone bodies.
For example, phospholipids form the phospholipid bilayers out of which all the membranes of the cell are constructed from fatty acids. Phospholipids comprise the plasma membrane and other membranes that enclose all the organelles within the cells, such as the nucleus , the mitochondria , endoplasmic reticulum , and the Golgi apparatus.
In another type of anabolism, fatty acids are modified to form other compounds such as second messengers and local hormones. The prostaglandins made from arachidonic acid stored in the cell membrane are probably the best-known of these local hormones. Fatty acids are stored as triglycerides in the fat depots of adipose tissue.
Between meals they are released as follows:. In the liver oxaloacetate can be wholly or partially diverted into the gluconeogenic pathway during fasting, starvation, a low carbohydrate diet, prolonged strenuous exercise, and in uncontrolled type 1 diabetes mellitus.
Under these circumstances, oxaloacetate is hydrogenated to malate , which is then removed from the mitochondria of the liver cells to be converted into glucose in the cytoplasm of the liver cells, from where it is released into the blood.
Under these conditions, acetyl-CoA is diverted to the formation of acetoacetate and beta-hydroxybutyrate. The ketones are released by the liver into the blood. All cells with mitochondria can take up ketones from the blood and reconvert them into acetyl-CoA, which can then be used as fuel in their citric acid cycles, as no other tissue can divert its oxaloacetate into the gluconeogenic pathway in the way that this can occur in the liver.
Unlike free fatty acids, ketones can cross the blood—brain barrier and are therefore available as fuel for the cells of the central nervous system , acting as a substitute for glucose, on which these cells normally survive. Fatty acids, stored as triglycerides in an organism, are a concentrated source of energy because they contain little oxygen and are anhydrous.
The energy yield from a gram of fatty acids is approximately 9 kcal 37 kJ , much higher than the 4 kcal 17 kJ for carbohydrates.
Since the hydrocarbon portion of fatty acids is hydrophobic , these molecules can be stored in a relatively anhydrous water-free environment. Carbohydrates, on the other hand, are more highly hydrated.
For example, 1 g of glycogen binds approximately 2 g of water , which translates to 1. This means that fatty acids can hold more than six times the amount of energy per unit of stored mass.
Put another way, if the human body relied on carbohydrates to store energy, then a person would need to carry 31 kg Hibernating animals provide a good example for utilization of fat reserves as fuel.
For example, bears hibernate for about 7 months, and during this entire period, the energy is derived from degradation of fat stores. Migrating birds similarly build up large fat reserves before embarking on their intercontinental journeys.
The fat stores of young adult humans average between about 10—20 kg, but vary greatly depending on gender and individual disposition. The g or so of glycogen stored in the liver is depleted within one day of starvation.
Fatty acids are broken down to acetyl-CoA by means of beta oxidation inside the mitochondria, whereas fatty acids are synthesized from acetyl-CoA outside the mitochondria, in the cytosol.
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 CO 2 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. However, acetyl-CoA can be converted to acetoacetate, which can decarboxylate to acetone either spontaneously, or catalyzed by acetoacetate decarboxylase.
Acetol can be converted to propylene glycol. This converts to pyruvate by two alternative enzymes , or propionaldehyde , or to L -lactaldehyde then L -lactate the common lactate isomer.
The first experiment to show conversion of acetone to glucose was carried out in This, and further experiments used carbon isotopic labelling. The glycerol released into the blood during the lipolysis of triglycerides in adipose tissue can only be taken up by the liver.
Here it is converted into glycerol 3-phosphate by the action of glycerol kinase which hydrolyzes one molecule of ATP per glycerol molecule which is phosphorylated. Glycerol 3-phosphate is then oxidized to dihydroxyacetone phosphate , which is, in turn, converted into glyceraldehyde 3-phosphate by the enzyme triose phosphate isomerase.
From here the three carbon atoms of the original glycerol can be oxidized via glycolysis , or converted to glucose via gluconeogenesis. Fatty acids are an integral part of the phospholipids that make up the bulk of the plasma membranes , or cell membranes, of cells.
These phospholipids can be cleaved into diacylglycerol DAG and inositol trisphosphate IP 3 through hydrolysis of the phospholipid, phosphatidylinositol 4,5-bisphosphate PIP 2 , by the cell membrane bound enzyme phospholipase C PLC.
One product of fatty acid metabolism are the prostaglandins , compounds having diverse hormone -like effects in animals. Prostaglandins have been found in almost every tissue in humans and other animals.
They are enzymatically derived from arachidonic acid, a carbon polyunsaturated fatty acid. Every prostaglandin therefore contains 20 carbon atoms, including a 5-carbon ring.
They are a subclass of eicosanoids and form the prostanoid class of fatty acid derivatives. The prostaglandins are synthesized in the cell membrane by the cleavage of arachidonate from the phospholipids that make up the membrane. This is catalyzed either by phospholipase A 2 acting directly on a membrane phospholipid, or by a lipase acting on DAG diacyl-glycerol.
The arachidonate is then acted upon by the cyclooxygenase component of prostaglandin synthase. This forms a cyclopentane ring roughly in the middle of the fatty acid chain.
The reaction also adds 4 oxygen atoms derived from two molecules of O 2. The resulting molecule is prostaglandin G 2 , which is converted by the hydroperoxidase component of the enzyme complex into prostaglandin H 2. This highly unstable compound is rapidly transformed into other prostaglandins, prostacyclin and thromboxanes.
If arachidonate is acted upon by a lipoxygenase instead of cyclooxygenase, Hydroxyeicosatetraenoic acids and leukotrienes are formed. They also act as local hormones. Prostaglandins have two derivatives: prostacyclins and thromboxanes. Prostacyclins are powerful locally acting vasodilators and inhibit the aggregation of blood platelets.
Through their role in vasodilation, prostacyclins are also involved in inflammation. They are synthesized in the walls of blood vessels and serve the physiological function of preventing needless clot formation, as well as regulating the contraction of smooth muscle tissue.
Their name comes from their role in clot formation thrombosis. A significant proportion of the fatty acids in the body are obtained from the diet, in the form of triglycerides of either animal or plant origin.
The fatty acids in the fats obtained from land animals tend to be saturated, whereas the fatty acids in the triglycerides of fish and plants are often polyunsaturated and therefore present as oils.
These triglycerides cannot be absorbed by the intestine. The activated complex can work only at a water-fat interface. Therefore, it is essential that fats are first emulsified by bile salts for optimal activity of these enzymes.
the fat soluble vitamins and cholesterol and bile salts form mixed micelles , in the watery duodenal contents see diagrams on the right. The contents of these micelles but not the bile salts enter the enterocytes epithelial cells lining the small intestine where they are resynthesized into triglycerides, and packaged into chylomicrons which are released into the lacteals the capillaries of the lymph system of the intestines.
This means that the fat-soluble products of digestion are discharged directly into the general circulation, without first passing through the liver, unlike all other digestion products. The reason for this peculiarity is unknown. The chylomicrons circulate throughout the body, giving the blood plasma a milky or creamy appearance after a fatty meal.
The fatty acids are absorbed by the adipocytes [ citation needed ] , but the glycerol and chylomicron remnants remain in the blood plasma, ultimately to be removed from the circulation by the liver. The free fatty acids released by the digestion of the chylomicrons are absorbed by the adipocytes [ citation needed ] , where they are resynthesized into triglycerides using glycerol derived from glucose in the glycolytic pathway [ citation needed ].
These triglycerides are stored, until needed for the fuel requirements of other tissues, in the fat droplet of the adipocyte. The liver absorbs a proportion of the glucose from the blood in the portal vein coming from the intestines.
After the liver has replenished its glycogen stores which amount to only about g of glycogen when full much of the rest of the glucose is converted into fatty acids as described below. These fatty acids are combined with glycerol to form triglycerides which are packaged into droplets very similar to chylomicrons, but known as very low-density lipoproteins VLDL.
These VLDL droplets are processed in exactly the same manner as chylomicrons, except that the VLDL remnant is known as an intermediate-density lipoprotein IDL , which is capable of scavenging cholesterol from the blood.
This converts IDL into low-density lipoprotein LDL , which is taken up by cells that require cholesterol for incorporation into their cell membranes or for synthetic purposes e. the formation of the steroid hormones. The remainder of the LDLs is removed by the liver.
Adipose tissue and lactating mammary glands also take up glucose from the blood for conversion into triglycerides. This occurs in the same way as in the liver, except that these tissues do not release the triglycerides thus produced as VLDL into the blood.
All cells in the body need to manufacture and maintain their membranes and the membranes of their organelles. Whether they rely entirely on free fatty acids absorbed from the blood, or are able to synthesize their own fatty acids from blood glucose, is not known. The cells of the central nervous system will almost certainly have the capability of manufacturing their own fatty acids, as these molecules cannot reach them through the blood brain barrier.
Much like beta-oxidation , straight-chain fatty acid synthesis occurs via the six recurring reactions shown below, until the carbon palmitic acid is produced. The diagrams presented show how fatty acids are synthesized in microorganisms and list the enzymes found in Escherichia coli.
FASII is present in prokaryotes , plants, fungi, and parasites, as well as in mitochondria. In animals as well as some fungi such as yeast, these same reactions occur on fatty acid synthase I FASI , a large dimeric protein that has all of the enzymatic activities required to create a fatty acid.
FASI is less efficient than FASII; however, it allows for the formation of more molecules, including "medium-chain" fatty acids via early chain termination.
by transferring fatty acids between an acyl acceptor and donor. They also have the task of synthesizing bioactive lipids as well as their precursor molecules.
Elongation, starting with stearate , is performed mainly in the endoplasmic reticulum by several membrane-bound enzymes. The enzymatic steps involved in the elongation process are principally the same as those carried out by fatty acid synthesis , but the four principal successive steps of the elongation are performed by individual proteins, which may be physically associated.
Abbreviations: ACP — Acyl carrier protein , CoA — Coenzyme A , NADP — Nicotinamide adenine dinucleotide phosphate. Note that during fatty synthesis the reducing agent is NADPH , whereas NAD is the oxidizing agent in beta-oxidation the breakdown of fatty acids to acetyl-CoA.
This difference exemplifies a general principle that NADPH is consumed during biosynthetic reactions, whereas NADH is generated in energy-yielding reactions. The source of the NADPH is two-fold. NADPH is also formed by the pentose phosphate pathway which converts glucose into ribose, which can be used in synthesis of nucleotides and nucleic acids , or it can be catabolized to pyruvate.
In humans, fatty acids are formed from carbohydrates predominantly in the liver and adipose tissue , as well as in the mammary glands during lactation.
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 is returned to mitochondrion as malate and then converted back into oxaloacetate to transfer more acetyl-CoA out of the mitochondrion. Acetyl-CoA is formed into malonyl-CoA by acetyl-CoA carboxylase , at which point malonyl-CoA is destined to feed into the fatty acid synthesis pathway.
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 produce energy.
High plasma levels of insulin in the blood plasma e. after meals cause the dephosphorylation and activation of acetyl-CoA carboxylase, thus promoting the formation of malonyl-CoA from acetyl-CoA, and consequently the conversion of carbohydrates into fatty acids, while epinephrine and glucagon released into the blood during starvation and exercise cause the phosphorylation of this enzyme, inhibiting lipogenesis in favor of fatty acid oxidation via beta-oxidation.
Disorders of fatty acid metabolism can be described in terms of, for example, hypertriglyceridemia too high level of triglycerides , or other types of hyperlipidemia. These may be familial or acquired. Familial types of disorders of fatty acid metabolism are generally classified as inborn errors of lipid metabolism.
These disorders may be described as fatty acid oxidation disorders or as a lipid storage disorders , and are any one of several inborn errors of metabolism that result from enzyme or transport protein defects affecting the ability of the body to oxidize fatty acids in order to produce energy within muscles, liver, and other cell types.
When a fatty acid oxidation disorder affects the muscles, it is a metabolic myopathy. Moreover, cancer cells can display irregular fatty acid metabolism with regard to both fatty acid synthesis [44] and mitochondrial fatty acid oxidation FAO [45] that are involved in diverse aspects of tumorigenesis and cell growth.
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Set of biological processes. Main article: Fatty acid synthesis. Main article: Citric acid cycle § Glycolytic end products are used in the conversion of carbohydrates into fatty acids.
In: Biochemistry Fourth ed. New York: W. Freeman and Company. ISBN doi : PMID S2CID Pflügers Archiv: European Journal of Physiology. Molecular Aspects of Medicine.
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Arrange a trial for your oxidatiin and discover kechanisms FSTA is oxifation Joint health solutions database for reliable research Low glycemic index foods the sciences of food and health. REQUEST A FREE TRIAL. By Ipek Bayram and Eric A. Decker on Jan Lipid oxidation is a series of reactions that has a negative impact on food quality and shelf life.
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