Lipoproteins occur in various subtypes see slide The chylomicrons also transport dietary cholesterol; this is discussed in slide Like glucose and other solutes taken up from the gut, the chylomicrons are released into the extracellular space at the basolateral side of the intestinal epithelia.
However, unlike those solutes, the chylomicrons are not drained toward the liver via the portal vein, but instead are drained via the lymphatics. This is explained in the next two slides. This slide and the next one introduce a bit of background to explain how chylomicrons are transported from the intestine to the systemic circulation. The capillaries of the blood circulation are porous, and the hydrostatic pressure within them drives the filtration of plasma fluid into the interstitial space.
Since the pores in the capillary walls are small, filtration is limited to water and small solutes. Albumin and other plasma proteins are not filtrated and therefore maintain an osmotic pressure gradient that opposes and mostly compensates for hydrostatic filtration. The fraction of the filtrate that is not recovered through osmosis is drained by lymphatic vessels and then back to the venous side of the systemic circulation.
Just as plasma proteins are excluded from diffusing out of capillaries, the chylomicrons are excluded from diffusing into them. Chylomicrons thus cannot enter the circulation directly and must instead be drained through the lymphatic system. The thoracic duct , which is the major effluent of the entire lymphatic system, joins one of the major veins just a short distance upstream of the heart, but downstream of the liver.
Therefore, unlike glucose and other small molecules that are taken up in the intestines, chylomicrons bypass the portal circulation and the liver. They will, however, reach the liver via the systemic circulation at a later stage see next slide. Once the chylomicrons have entered the circulation, the capillary wall barrier must again be overcome in the delivery of triacylglycerol to extravascular cells.
This is accomplished with the help of lipoprotein lipase , which is located on the endothelial surface. It binds the chylomicrons and extracts triacylglycerol from them, which it then cleaves again to fatty acids and glycerol. These small molecules can cross the endothelial barrier by diffusion and reach the cells in the surrounding tissue. In adipose cells, the fatty acids are combined with glycerol yet again for storage.
In other cell types, most notably muscle cells, they may either be stored or degraded directly to acetyl-CoA, which is then consumed in the TCA cycle and the respiratory chain. The remnants of chylomicrons, depleted of most of their triacylglycerol, are captured by the liver, endocytosed, and degraded. The cholesterol and remaining fat released in the process is either utilized in the liver or repackaged into other lipoprotein particles.
Medium-chain fatty acids MCFA are not a major constituent of our regular diet, nor are they required; however, they can be useful in patients whose ability to digest or absorb regular fats is compromised. They are more readily hydrolyzed by enzymes, in particular by gastric lipase, which usually plays a minor role only in the digestion of triacylglycerol with regular, longer acyl chains. Gastric lipase continues to be secreted, even at increased levels [ 53 ] , when pancreatic lipase is lacking due to exocrine pancreas insufficiency.
Therefore, MCFA triglycerides can still be processed in this situation. They are used in the dietary treatment of such patients and also of those with other types of fat maldigestion and malabsorption. This pathway runs in the mitochondria, so the first task after cellular uptake of the fatty acid molecule is to get it into the mitochondrion. Fatty acids are initially activated to fatty acyl-CoA in the cytosol.
However, during transport, the CoA-moiety is transiently replaced by carnitine. This slide shows the structures of both the CoA- and the carnitine-activated forms; the entire transport process is outlined in the next one.
Fatty acids are activated in the cytosol to acyl-CoA by acyl thiokinase, also known as acyl-CoA synthetase. After transport across the outer mitochondrial membrane, the acyl group is transferred to carnitine by carnitine acyltransferase.
Exchange for free carnitine transports the acylcarnitine molecule into the mitochondrial matrix, where carnitine is replaced again with coenzyme A by a second acyl transferase. One unusual aspect of this transport process is that the energy of the thioester bond in acyl-CoA seems to be sufficiently well preserved in the ester bond of acylcarnitine to allow the exchange reaction to be reversed inside the mitochondrion. I once stumbled upon a theoretical paper explaining why carnitine is special in this regard, but it went straight over my head, and I therefore cannot give you an explanation.
The reactions are as follows:. The process is repeated until the fatty acid is completely broken down. In the case of acyl chains with even numbers of carbons, this will yield acetyl-CoA only, whereas those with odd numbers of carbons will yield one molecule of propionyl-CoA in the final thiolase step. There is a special pathway to take care of the propionyl-CoA, which is surprisingly complicated see slide You may have noticed the similarities of the enzyme reactions discussed above to some others we have seen before.
In the first three steps, the similarities to reactions from the citric acid cycle are quite straightforward. The thiolase mechanism does not have a closely analogous precedent among the reactions we have seen so far. However, if we look at the individual steps of the thiolase reaction, we can still recognize some familiar features:.
Fatty acids with odd numbers of carbon atoms yield one molecule of propionyl-CoA as the final degradation product.
This metabolite has a rather elaborate degradative pathway:. Note that succinyl-CoA is a citric acid cycle intermediate. 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, both 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 Lipids are available to the body from three sources. They can be ingested in the diet, stored in the adipose tissue of the body, or synthesized in the liver. Fats ingested in the diet are digested in the small intestine.
The triglycerides are broken down into monoglycerides and free fatty acids, then imported across the intestinal mucosa. Measure ad performance. Select basic ads.
Create a personalised ads profile. Select personalised ads. Apply market research to generate audience insights. Measure content performance. Develop and improve products. List of Partners vendors. Triglycerides are a form of fat that the body uses for energy storage and transporting.
Triglycerides account for the vast majority of fat stored in the human body. The different types of triglycerides are named according to the length of the glycerol chains they contain.
Some of the names for specific triglycerides you may have heard include oleic acid and palmitic acid. Triglycerides are best thought of as the means for storing and transporting the fatty acids we need for fuel. We get our triglycerides from two sources: from manufacturing them ourselves, and from the food we eat.
Triglycerides we make. Triglycerides are synthesized in our liver and by our fat cells at times when food is plentiful. For instance, when we eat a high-carbohydrate meal, any excess carbs carbs that are not needed right then for fuel are converted to triglycerides.
The liver releases these newly-made triglycerides into the bloodstream, in the form of VLDL very low-density lipoproteins.
The VLDL delivers the triglycerides to fat cells for long-term storage. Triglycerides we eat. Most of the fat we eat—whether from animals or from plants—consists of various triglycerides.
Our intestines cannot absorb the triglycerides in-tact since they are very large molecules , so during the digestive process, the triglycerides in our food are broken down into their glycerol and fatty acid components, which are then absorbed by the cells that line our intestines. The bonds between the glycerol molecules and fatty acids are covalent bonds called ester bonds.
They are formed from a condensation reaction which can be seen in the picture below. It's called condensation because water molecules are formed they condense during the reaction. You've probably heard of saturated and unsaturated fats on TV ads, nutrition labels, and billboards.
The difference between their structures is really small. Let's take a look:. Saturated fats have straight chains because the chain part of their structure contains only single carbon -carbon bonds. Saturated fats pack together closely and are solid at room temperature. Saturated fats are typically found in animal products.
Butter is a good example. Unsaturated fats have a kink in their chain caused by double or triple carbon-carbon bonds.
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