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Fat metabolism cycle

Fat metabolism cycle

Metabollism Fat metabolism cycle and Lipid Droplets in Pancreatic Cancer and Stellate Cells. Extended Data Fig. Triglyceride cycling enables modification of stored fatty acids.

Fat metabolism cycle -

beta β -hydroxybutyrate is oxidized to acetoacetate and NADH is released. An HS-CoA molecule is added to acetoacetate, forming acetoacetyl CoA.

The carbon within the acetoacetyl CoA that is not bonded to the CoA then detaches, splitting the molecule in two. This carbon then attaches to another free HS-CoA, resulting in two acetyl CoA molecules.

These two acetyl CoA molecules are then processed through the Krebs cycle to generate energy Figure 5. When glucose levels are plentiful, the excess acetyl CoA generated by glycolysis can be converted into fatty acids, triglycerides, cholesterol, steroids, and bile salts.

This process, called lipogenesis , creates lipids fat from the acetyl CoA and takes place in the cytoplasm of adipocytes fat cells and hepatocytes liver cells. When you eat more glucose or carbohydrates than your body needs, your system uses acetyl CoA to turn the excess into fat.

Although there are several metabolic sources of acetyl CoA, it is most commonly derived from glycolysis. Acetyl CoA availability is significant, because it initiates lipogenesis. Lipogenesis begins with acetyl CoA and advances by the subsequent addition of two carbon atoms from another acetyl CoA; this process is repeated until fatty acids are the appropriate length.

Because this is a bond-creating anabolic process, ATP is consumed. However, the creation of triglycerides and lipids is an efficient way of storing the energy available in carbohydrates. Triglycerides and lipids, high-energy molecules, are stored in adipose tissue until they are needed.

Although lipogenesis occurs in the cytoplasm, the necessary acetyl CoA is created in the mitochondria and cannot be transported across the mitochondrial membrane.

To solve this problem, pyruvate is converted into both oxaloacetate and acetyl CoA. Two different enzymes are required for these conversions. Oxaloacetate forms via the action of pyruvate carboxylase, whereas the action of pyruvate dehydrogenase creates acetyl CoA.

Oxaloacetate and acetyl CoA combine to form citrate, which can cross the mitochondrial membrane and enter the cytoplasm.

In the cytoplasm, citrate is converted back into oxaloacetate and acetyl CoA. Oxaloacetate is converted into malate and then into pyruvate. Pyruvate crosses back across the mitochondrial membrane to wait for the next cycle of lipogenesis. The acetyl CoA is converted into malonyl CoA that is used to synthesize fatty acids.

Figure 6 summarizes the pathways of lipid metabolism. After binding to lipids, proteins take part in transporting lipids in plasma, so they are called apolipoproteins. Figure 2. Lipid metabolism in liver.

The mainly lipid source of the liver is food. The lipids in food are mainly TG, and there are a small amount of PL and Ch. In the small intestine, bile acids and pancreatic enzymes including pancreatic lipase, phospholipase A2, cholesterol esterase, etc. in bile hydrolyze lipids into free fatty acids FFA , glycerol and Fc.

Then these molecules are absorbed by mucosal epithelial cells of the small intestine mainly jejunum , and are further esterified into TG, CE, etc. in intestinal epithelial cells. Finally, TG, Ch and PL with apolipoprotein compose of lipoprotein chylomicron CM which will be absorbed by the lymphatic system and hydrolyzed by lipoproteinase of vascular endothelial cells to enter the liver.

FFA can be converted into energy by oxidation in hepatocytes for the consumption, or re-synthesize TG, PL and CE with 3-phosphoglycerate. The mainly source of endogenous fatty acids is the fat stored in the body's adipose tissue.

The fat in the fat cells is hydrolyzed into glycerol and fatty acids by the action of lipase. After being released into the blood, glycerol is dissolved in plasma while fatty acids are combined with plasma albumin for transport.

It can be used as a source of energy or ingested by liver cells again. In addition, hepatocytes also can produce fatty acids from the oxidation process of glucose and amino acids and synthesize TG by acetyl-CoA in hepatocytes.

In addition to ingesting the exogenous cholesterol from food, liver cells also synthesize endogenous cholesterol.

Hepatocyte endoplasmic reticulum cholesterol biosynthesis involves more than 30 enzymes, such as acetoacetyl CoA. Endogenously synthesized cholesterol and exogenous free cholesterol taken up by lipoprotein receptors must be transported through the liver.

The transport destinations are: 1 decomposition into primary bile acid and bile salts in the liver, then discharging into the capillary bile duct and bile through the transport pump on the capillary bile duct; 2 free cholesterol and phospholipids are directly excreted to the bile by multi-drug resistance transporter MDR ; 3 cholesterol ester and free cholesterol are converted to each other to form dynamic equilibrium.

This requires the activity of hydrolytic enzymes called lipases, which release fatty acids from derivatives such as phospholipids. These fatty acids can then enter a dedicated pathway that promotes step-wise lipid processing that ultimately yields acetyl-CoA, a critical metabolite that conveys carbon atoms to the TCA cycle aka Krebs cycle or citric acid cycle to be oxidized for energy production.

The metabolic process by which fatty acids and their lipidic derivatives are broken down is called β-oxidation. This process bears significant similarity to the mechanism by which fatty acids are synthesized, except in reverse.

In brief, the oxidation of lipids proceeds as follows: two-carbon fragments are removed sequentially from the carboxyl end of the fatty acid after dehydrogenation, hydration, and oxidation to form a keto acid, which is then cleaved by thiolysis.

The acetyl-CoA molecule liberated by this process is eventually converted into ATP through the TCA cycle. This cycle repeats until the fatty acid has been completely reduced to acetyl-CoA, which is fed through the TCA cycle to ultimately yield cellular energy in the form of ATP.

Search site Search Search. Go back to previous article. Sign in. Learning Objectives Outline the process of lipid metabolism, specifically beta-oxidation.

Key Points In addition to their role as the primary component of cell membranes, lipids can be metabolized for use as a primary energy source.

Xycle performing the same function, at the adipose level, the enzymes are primarily active mftabolism seemingly opposite reasons. In the Fat metabolism cycle state, Metabokism on the endothelium of blood vessels cleaves lipoprotein triglycerides into mwtabolism acids Dark chocolate extravaganza that they can Digestive enzymes and probiotics taken up into mmetabolism, for storage as triglycerides, or myocytes Dark chocolate extravaganza they are primarily used for energy production. This action of LPL on lipoproteins is shown in the two figures below. HSL is an important enzyme in adipose tissue, which is a major storage site of triglycerides in the body. HSL activity is increased by glucagon and epinephrine "fight or flight" hormoneand decreased by insulin. Thus, in hypoglycemia such as during a fast or a "fight or flight" response, triglycerides in the adipose are cleaved, releasing fatty acids into circulation that then bind with the transport protein albumin. Thus, HSL is important for mobilizing fatty acids so they can be used to produce energy. Biological lipids, which are Fa down and utilized though β-oxidation, Natural abdominal fat loss a potent energy source. Lipids chcle Fat metabolism cycle biological molecules. Not only does this broad class of compounds represent metabolixm primary structural component of biological membranes in all organisms, they also serve a number of vital roles in microorganisms. Among these, lipids can be metabolized by microbes for use as a primary energy source. This atom will expand on the metabolic pathway that enables degradation and utilization of lipids. Fatty acids are the building blocks of lipids. Fat metabolism cycle

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