Stored fat is the major source of energy during both short term and long term fasting. During fasting, the level of glucose in the blood drops, which causes the level of insulin to drop. This stimulates the release of fatty acids into the blood, as triglycerides are broken down. The fatty acids, bound to albumin, travel mainly to the liver which converts them in one of several ways: Beta-oxidation (energy producing), ketone formation (alternate route of energy production), or to VLDL. The pathway taken will depend on conditions and the body’s needs at the moment.
Ketones are produced as an alternate source of energy, especially for the muscles and the brain, when glucose levels in the cells are extremely low, i.e. during starvation. Ketone formation goes up as the level of fatty acids in the blood increases, or starvation continues. Once starvation has continued for 2-3 days, ketones can enter the brain to be used as its energy source (the brain’s preferred source, as with other cells, is glucose).
People with diabetes (especially type 1) are prone to ketone formation, since they don’t produce insulin. If someone with type 1 diabetes does not take their insulin, glucose cannot get into their cells to be used for energy. Therefore, their body adapts by using fat as an energy source, and goes toward ketone formation if the conditions continue. It can be very dangerous if ketone levels get too high, because ketones are acids. A very acidic blood pH can result in the body’s enzymes not functioning, and this condition is known as ketoacidosis.
Ketones are produced in the liver from the CoA that is made through Beta-oxidation. The ketones formed are acetoacetate and beta-hydroxybutyrate. Two acetyl CoA’s are needed to begin the process, which are the same two from the final cycle of beta-oxidation. Normally, these two would just go on to the TCA cycle to make energy, but when acetyl CoA is very high, due to such a large amount of fatty acid stores being used for energy, ketone formation will occur.
1.The first reaction is catalyzed by the enzyme thiolase, and causes the two molecules of acetyl CoA to join into one molecule of acetoacetyl CoA.
2.The second reaction uses the enzyme HMG CoA synthase and acetyl CoA to form 3-hydroxy-3-methylglutaryl CoA (HMG-CoA)
3.Next, HMG-CoA is cleaved by HMG-CoA lyase to form acetyl CoA and acetoacetate, while losing a hydrogen.
The acetoacetate may enter the blood directly, or form the other major ketone, Beta-hydroxybutyrate, with the enzyme Beta-hydroxybutyrate dehydrogenase which adds a hydrogen at the second carbonyl carbon. Or, as an alternate, acetoacetate may become acetone, which mainly gets expired by the lungs.
The ketones can go on to make energy in muscle and skeletal tissue. Nearly all cell and tissue types, aside from the liver and red blood cells, can use ketones. In the mitochondrial matrix, the beta-hydroxybutyrate is oxidized back to acetoacetate, with the help of the enzyme beta-hydroxybutyrate dehydrogenase, which produces NADH. Acetoacetate then accepts a CoA group from succinyl in a transferase reaction. This results in the formation of acetoacetyl CoA, which can then be broken into 2 acetyl CoA’s with a thiolase enzyme reaction. These acetyl CoA’s then enter the TCA cycle to make energy.
Even during prolonged fasting (30-40 days) levels of glucose and free fatty acids remain constant. A person can actually live this long without food by using their fat stores, and eventually their muscle protein stores. The use of ketones for energy is an adaptive measure taken by the body to spare muscle protein for as long as possible. The level of glucose can stay constant because, although it tries to keep it minimal, the body can make glucose from the amino acids being released from the muscle.
Friday, October 29, 2010
Thursday, October 28, 2010
More Fun with Fat: Fatty Acid Oxidation
This week is about how fat is used to make energy.
Beta-oxidation is the process that fat undergoes which produces large amounts of energy. This process occurs within the mitochondrial matrix of the cells. Between meals, during fasting, or during prolonged exercise, fatty acids are released from the adipose tissue in response to a drop in insulin and an increase in glucagon. The main type of fats released are the long-chain fatty acids palmitate (C-16), oleate (C-18), and stearate (C-18:1), since these encompass the highest proportion of fats consumed in the diet and also synthesized in the body.
When these fatty acids enter the blood, they cannot travel far without assistance because they are extremely hydrophobic. Therefore, they bind to albumin, which is the major protein in the blood. Once they reach the cells, they still need a lot of help to get inside. They are able to enter the cell by binding to a fatty acid binding protein located at the plasma membrane, which facilitates their transport through. Once in the cytosol, the fatty acid becomes activated by reacting with ATP and coenzyme A (CoA), making it into a fatty acyl CoA.
At this point, fatty acyl CoA may take several paths:
1. It can go on into the mitochondrial matrix to undergo Beta-oxidation or ketogenesis and create energy.
2. It can go to storage in the form of triglyceride
3. It can become part of phospholipids or sphingolipids
If fatty acyl CoA goes toward energy formation, it can pass through into the outer mitochondrial membrane alone. However, it still needs help to cross the inner membrane, again due to being hydrophobic. It goes through the inner mitochondrial membrane by binding with carnitine and becoming fatty acyl carnitine. Carnitine is made from the essential amino acids lysine and methionine. Therefore, carnitine is not an essential amino acid because it is synthesized in the body. Carnitine contains nitrogen and oxygen, which gives it charges - allowing it to react with water. That is why it is needed to cross the membrane.
Once across the inner membrane, carnitine comes off and CoA attaches back, catalyzed by the enzyme carnitine palmitoyltransferase I (CPTI) to the fatty acyl, making it back into fatty acyl CoA. At this point, it is ready to undergo Beta-oxidation inside the mitochondrial matrix.
Beta-oxidation is a spiral-like pathway that continues to cleave the fatty acyl by two-carbon acetyl CoA units, beginning at the carboxyl end of the molecule, until only a 4 carbon fatty acyl CoA remains, which is broken into 2 acetyl CoA's.
Beta-oxidation consists of four different types of reactions.
1. the first reaction, catalyzed by acyl CoA dehydrogenase, results in a double bond with the trans configuration when hydrogen is transferred from between the alpha and beta carbons to FAD to make FAH(2H).
2. the second reaction, catalyzed by enoyl CoA hydratase, adds an OH group to the Beta carbon, and an H to the alpha carbon.
3. The third reaction, catalyzed by beta-hydroxyacyl CoA dehydrogenase, the OH group on the beta carbon is oxidized and forms a ketone. 2 hydrogen get transferred to NAD+, forming NADH+H+. This results in the beta-carbon becoming the carbonyl carbon.
4. The last step is catalyzed by Beta-ketothiolase, and in this step the bond between the alpha and beta carbons is broken, releasing acetyl CoA, and resulting in a new fatty acyl CoA that is 2 carbons shorter.
The new fatty acyl CoA will go through several more cycles of Beta-oxidation, losing 2 more carbons each time, until only a 4 carbon unit is left-which is broken to two molecules of acetyl CoA. These acetyl CoA's can then enter the TCA, or Kreb's, cycle.
This results in a very large amount of energy being produced, because each Acetyl CoA that enters the Kreb's cycle makes 10 ATP.
So, if a 16 carbon fatty acyl like palmytic acid goes through oxidation, it goes through 7 total cycles (number of cycles=number of carbon/2 - 1). This makes 8 acetyl CoA (number of acetyl CoA=number of carbon/2). So, 8 acetyl CoA's go through Kreb's and make 10 ATP each - that's 80 ATP so far.
Also, each cycle of Beta-oxidation produces 1 NADH2 and 1 FADH2. In this case, 7 cycles yields 7 of each. These also enter the Kreb's cycle. Each NADH2 can make 2.5 ATP - so there's another 17.5 ATP. FADH2 can each make 1.5 ATP - an additional 10.5.
All together, the complete oxidation of a 16 carbon fatty acid can make 108 ATP - but we have to subtract 2 of these, because 2 are used to initially make it into a fatty acyl CoA. A small price to pay - we still get a net gain of 106 ATP.
In comparison, the complete oxidation of one glucose molecule only generates 32 ATP. So, fat is a very important source of energy in our diet. It may cost us a lot of calories (9 calories per gram, compared to carbohydrates and protein, which are 4 calories per gram) but it gives a lot back!
Beta-oxidation is the process that fat undergoes which produces large amounts of energy. This process occurs within the mitochondrial matrix of the cells. Between meals, during fasting, or during prolonged exercise, fatty acids are released from the adipose tissue in response to a drop in insulin and an increase in glucagon. The main type of fats released are the long-chain fatty acids palmitate (C-16), oleate (C-18), and stearate (C-18:1), since these encompass the highest proportion of fats consumed in the diet and also synthesized in the body.
When these fatty acids enter the blood, they cannot travel far without assistance because they are extremely hydrophobic. Therefore, they bind to albumin, which is the major protein in the blood. Once they reach the cells, they still need a lot of help to get inside. They are able to enter the cell by binding to a fatty acid binding protein located at the plasma membrane, which facilitates their transport through. Once in the cytosol, the fatty acid becomes activated by reacting with ATP and coenzyme A (CoA), making it into a fatty acyl CoA.
At this point, fatty acyl CoA may take several paths:
1. It can go on into the mitochondrial matrix to undergo Beta-oxidation or ketogenesis and create energy.
2. It can go to storage in the form of triglyceride
3. It can become part of phospholipids or sphingolipids
If fatty acyl CoA goes toward energy formation, it can pass through into the outer mitochondrial membrane alone. However, it still needs help to cross the inner membrane, again due to being hydrophobic. It goes through the inner mitochondrial membrane by binding with carnitine and becoming fatty acyl carnitine. Carnitine is made from the essential amino acids lysine and methionine. Therefore, carnitine is not an essential amino acid because it is synthesized in the body. Carnitine contains nitrogen and oxygen, which gives it charges - allowing it to react with water. That is why it is needed to cross the membrane.
Once across the inner membrane, carnitine comes off and CoA attaches back, catalyzed by the enzyme carnitine palmitoyltransferase I (CPTI) to the fatty acyl, making it back into fatty acyl CoA. At this point, it is ready to undergo Beta-oxidation inside the mitochondrial matrix.
Beta-oxidation is a spiral-like pathway that continues to cleave the fatty acyl by two-carbon acetyl CoA units, beginning at the carboxyl end of the molecule, until only a 4 carbon fatty acyl CoA remains, which is broken into 2 acetyl CoA's.
Beta-oxidation consists of four different types of reactions.
1. the first reaction, catalyzed by acyl CoA dehydrogenase, results in a double bond with the trans configuration when hydrogen is transferred from between the alpha and beta carbons to FAD to make FAH(2H).
2. the second reaction, catalyzed by enoyl CoA hydratase, adds an OH group to the Beta carbon, and an H to the alpha carbon.
3. The third reaction, catalyzed by beta-hydroxyacyl CoA dehydrogenase, the OH group on the beta carbon is oxidized and forms a ketone. 2 hydrogen get transferred to NAD+, forming NADH+H+. This results in the beta-carbon becoming the carbonyl carbon.
4. The last step is catalyzed by Beta-ketothiolase, and in this step the bond between the alpha and beta carbons is broken, releasing acetyl CoA, and resulting in a new fatty acyl CoA that is 2 carbons shorter.
The new fatty acyl CoA will go through several more cycles of Beta-oxidation, losing 2 more carbons each time, until only a 4 carbon unit is left-which is broken to two molecules of acetyl CoA. These acetyl CoA's can then enter the TCA, or Kreb's, cycle.
This results in a very large amount of energy being produced, because each Acetyl CoA that enters the Kreb's cycle makes 10 ATP.
So, if a 16 carbon fatty acyl like palmytic acid goes through oxidation, it goes through 7 total cycles (number of cycles=number of carbon/2 - 1). This makes 8 acetyl CoA (number of acetyl CoA=number of carbon/2). So, 8 acetyl CoA's go through Kreb's and make 10 ATP each - that's 80 ATP so far.
Also, each cycle of Beta-oxidation produces 1 NADH2 and 1 FADH2. In this case, 7 cycles yields 7 of each. These also enter the Kreb's cycle. Each NADH2 can make 2.5 ATP - so there's another 17.5 ATP. FADH2 can each make 1.5 ATP - an additional 10.5.
All together, the complete oxidation of a 16 carbon fatty acid can make 108 ATP - but we have to subtract 2 of these, because 2 are used to initially make it into a fatty acyl CoA. A small price to pay - we still get a net gain of 106 ATP.
In comparison, the complete oxidation of one glucose molecule only generates 32 ATP. So, fat is a very important source of energy in our diet. It may cost us a lot of calories (9 calories per gram, compared to carbohydrates and protein, which are 4 calories per gram) but it gives a lot back!
Saturday, October 23, 2010
Limited Resource Audiences
A person's resources may include many things besides money. There are also emotional (the stamina to keep going when things are hard/avoid engaging in destructive behaviors), mental (ability to deal with daily life), spiritual (faith, sense of community), and physical (mobility that allows one to be self sufficient and take care of themselves and their family) resources.
Those who are limited in some or all of these resources may be difficult to reach with normal educational techniques. For example, long term planning is not something that is commonly used by this group. This is because they are used to survival tactics which force them to do whatever is needed at the moment. Therefore, it is more effective to focus on the now and use short term goal setting, and avoid talking about the implications which could occur the long term future. Only "need to know" information should be given, rather than "nice to know".
When working with this population it is important to recognize the fact that there may be a sense of failure related to education. Many may not have completed school and will see anything "school like" as a challenge that is too big for them to handle. Therefore "classes" should be kept very casual and held in familiar surroundings (community centers, or other places participants frequent). They should be fun and include games/activities to keep participants interested. Activities should be achievable in order to preserve participants self esteem.
Those who are limited in some or all of these resources may be difficult to reach with normal educational techniques. For example, long term planning is not something that is commonly used by this group. This is because they are used to survival tactics which force them to do whatever is needed at the moment. Therefore, it is more effective to focus on the now and use short term goal setting, and avoid talking about the implications which could occur the long term future. Only "need to know" information should be given, rather than "nice to know".
When working with this population it is important to recognize the fact that there may be a sense of failure related to education. Many may not have completed school and will see anything "school like" as a challenge that is too big for them to handle. Therefore "classes" should be kept very casual and held in familiar surroundings (community centers, or other places participants frequent). They should be fun and include games/activities to keep participants interested. Activities should be achievable in order to preserve participants self esteem.
Digestion and absorption of dietary lipids, OR More than you ever wanted to know about what happens to food after you swallow it
The fat in our diet consists mainly of triglycerides (95%), with the other 5% being phospholipids, cholesterol and cholesterol esters, and fat soluble vitamins. Digestion of fat begins minimally in the mouth with the enzyme lingual lipase, and in the stomach with gastric lipase. These lipases mainly break down milk fats, which have short and medium chain fatty acids. Most of the fat in our diet is long chain.
This fat enters the small intestine intact, where the gut hormone CCK is released and stimulates the release of bile, pancreatic lipase, and colipase. The hormone secretin stimulates the release of bicarbonate, which helps keep a less acidic atmosphere so that enzymes can become active.
Bile is made from cholesterol in the liver and stored in the gallbladder. It is released in response to CCK and acts in the small intestine. It acts as an emulsifier and breaks the fat into smaller particles, which increases the surface area so that pancreatic lipase can attack it more easily. Once bile has finished its job it continues on to the ileum of the small intestine where 90% of it is reabsorbed, returning to the liver (enterhepatic cycle). The rest goes to the colon and is excreted. The entire pool of bile is recycled twice per fat containing meal. Soluble fibers from our diet and some cholesterol lowering drugs bind to bile so that more of it is excreted. This can help lower blood cholesterol.
Pancreatic lipase breaks the bonds connecting the fatty acids on carbon #1 and #3 of the triglycerides. This results in free fatty acids, 2-monoacylglycerol, and some glycerol.
Cholesterol esters are broken down to cholesterol by the enzyme cholesterol enterase. Phospholipids are broken down to lysophospholipids by the enzyme phospholipase.
Short and medium chain fatty acids are water miscible, so they can be absorbed directly from the intestinal cell to the portal vein, which brings them to the liver. In order to absorb long chain fatty acids, they must be packaged into a delivery device called a micelle. Micelles are tiny droplets emulsified by bile salts which contain all of the remaining dietary components (long chain fatty acids, 2-monoglycerides, glycerol, fat soluble vitamins, cholesterol, and lysophospholipids) along with bile. Micelles bring these lumps of particles to the microville of the small intestine, where everything except the bile gets absorbed into the cell.
But the fun doesn't stop here! Inside the intestinal cell, the dietary particles are rebuilt, once again, into triglycerides. The fatty acids are activated to fatty acyl coenzyme A (FACoA). FACoA reacts with 2-monoacylglycerol to form a diacylglycerol, and then with another to reform a triglyceride.
The triglycerides are very hydrophobic and cannot be transported alone, so they get packed with apoproteins (mainly B-48), phospholipids, cholesterol and vitamins to form what is known as a chylomicron. Chylomicrons are a type of lipoprotein. They are mainly made of triglyceride because they are representative of the fat in our diet. They have a single layer of phospholipid on the outside with the hydrophillic end facing out, which keeps water from entering. The hydrophobic components are hidden on the inside. The apoproteins sit on the outside of the structure. Chylomicrons are too large to go directly into the blood, so they enter the lymphatic system. They circulate to the thoracic duct and enter the bloodstream from there. As a chylomicron matures it receives more apoproteins upon its surface from HDL. ApoE and ApoCII are only found on these mature chylomicrons, and both serve important purposes. The enzyme lipoprotein lipase is activated based upon the presence of ApoCII. Lipoprotein lipase is found in the capillaries of the adipose and muscle cells, and interacts with the chylomicron and digests some of the triglycerides into fatty acids and glycerol. The fatty acids are taken up for storage into adipose and/or muscle cells, and the glycerol goes to the liver. What is left over is called a chylomicron remnant, and is returned to the liver. The presence of ApoE on the chylomicron remnant allows it to be recognized by the liver cells so that it can enter them by endocytosis and get digested by lysosomes and its contents reused.
The triglyceride components get reused, along with newly synthesized triglycerides, by creating VLDL in the liver. VLDL gets released into the bloodstream, where some of the triglycerides get taken up by adipose cells. The VLDL then becomes IDL (intermediate density lipoprotein) or LDL.
This fat enters the small intestine intact, where the gut hormone CCK is released and stimulates the release of bile, pancreatic lipase, and colipase. The hormone secretin stimulates the release of bicarbonate, which helps keep a less acidic atmosphere so that enzymes can become active.
Bile is made from cholesterol in the liver and stored in the gallbladder. It is released in response to CCK and acts in the small intestine. It acts as an emulsifier and breaks the fat into smaller particles, which increases the surface area so that pancreatic lipase can attack it more easily. Once bile has finished its job it continues on to the ileum of the small intestine where 90% of it is reabsorbed, returning to the liver (enterhepatic cycle). The rest goes to the colon and is excreted. The entire pool of bile is recycled twice per fat containing meal. Soluble fibers from our diet and some cholesterol lowering drugs bind to bile so that more of it is excreted. This can help lower blood cholesterol.
Pancreatic lipase breaks the bonds connecting the fatty acids on carbon #1 and #3 of the triglycerides. This results in free fatty acids, 2-monoacylglycerol, and some glycerol.
Cholesterol esters are broken down to cholesterol by the enzyme cholesterol enterase. Phospholipids are broken down to lysophospholipids by the enzyme phospholipase.
Short and medium chain fatty acids are water miscible, so they can be absorbed directly from the intestinal cell to the portal vein, which brings them to the liver. In order to absorb long chain fatty acids, they must be packaged into a delivery device called a micelle. Micelles are tiny droplets emulsified by bile salts which contain all of the remaining dietary components (long chain fatty acids, 2-monoglycerides, glycerol, fat soluble vitamins, cholesterol, and lysophospholipids) along with bile. Micelles bring these lumps of particles to the microville of the small intestine, where everything except the bile gets absorbed into the cell.
But the fun doesn't stop here! Inside the intestinal cell, the dietary particles are rebuilt, once again, into triglycerides. The fatty acids are activated to fatty acyl coenzyme A (FACoA). FACoA reacts with 2-monoacylglycerol to form a diacylglycerol, and then with another to reform a triglyceride.
The triglycerides are very hydrophobic and cannot be transported alone, so they get packed with apoproteins (mainly B-48), phospholipids, cholesterol and vitamins to form what is known as a chylomicron. Chylomicrons are a type of lipoprotein. They are mainly made of triglyceride because they are representative of the fat in our diet. They have a single layer of phospholipid on the outside with the hydrophillic end facing out, which keeps water from entering. The hydrophobic components are hidden on the inside. The apoproteins sit on the outside of the structure. Chylomicrons are too large to go directly into the blood, so they enter the lymphatic system. They circulate to the thoracic duct and enter the bloodstream from there. As a chylomicron matures it receives more apoproteins upon its surface from HDL. ApoE and ApoCII are only found on these mature chylomicrons, and both serve important purposes. The enzyme lipoprotein lipase is activated based upon the presence of ApoCII. Lipoprotein lipase is found in the capillaries of the adipose and muscle cells, and interacts with the chylomicron and digests some of the triglycerides into fatty acids and glycerol. The fatty acids are taken up for storage into adipose and/or muscle cells, and the glycerol goes to the liver. What is left over is called a chylomicron remnant, and is returned to the liver. The presence of ApoE on the chylomicron remnant allows it to be recognized by the liver cells so that it can enter them by endocytosis and get digested by lysosomes and its contents reused.
The triglyceride components get reused, along with newly synthesized triglycerides, by creating VLDL in the liver. VLDL gets released into the bloodstream, where some of the triglycerides get taken up by adipose cells. The VLDL then becomes IDL (intermediate density lipoprotein) or LDL.
Friday, October 22, 2010
Fat is where it's at
This week's topic is lipids, AKA fat. Lipids are water insoluble, or immiscible. They are, however, soluble in some organic solvents such as acetone and benzene. Lipids are a very concentrated source of energy, and therefore may contribute to obesity, which contributes to the mortality rate in the US. Types of lipids include fatty acids, triglycerides, phospholipids, cholesterol, eicosanoids, lipoproteins, and the fat soluble vitamins A, D, E, and K.
The fat cells in our body (also known as adipocytes or adipose tissue) serve to store fat. The form that fat is stored in is triacyglycerol, or triglyceride.
Fatty acids are not found alone in nature or in the body. They are part of the structure of triacylglycerols. The structure of fatty acids is a chain of CH with carboxyl group (COOH) at one end of the chain. A saturated fatty acid has no double bonds. Unsaturated fatty acids have at least one double bond. Monounsaturated has one double bond, and polyunsaturated has two or more double bonds.
The number of carbons in fatty acids is usually an even number in nature. The most abundant have 16, 18, or 20 carbons.
To name the fatty acid, you start at the carboxyl group end and number the carbons. Then you count the number of double bonds and note it like this - example 18:1 is a fatty acid with an 18 carbon chain and one double bond. In this case, the double bond occurs between carbon # 9 and # 10, so you note this by adding a delta 9 after the name. This one is 18:1 (delta)9, or oleic acid. A fatty acid named 18:2 (delta) 9,12 has 18 carbons and two double bonds, occurring at carbon #9 and #12. There is always a difference of 3 carbons between the double bonds.
Monounsaturated and polyunsaturated fats come from plant sources and include canola oil and olive oil (mono) and vegetable, sunflower, and safflower oil (poly).
Tropical oils include palm and coconut. Although they come from plant sources, they are highly saturated and should be limited. This is confusing to some people because typically saturated fats are more solid at room temperature. Tropical oils appear more liquid at room temperature due to their content of shorter chains of fatty acids.
Most saturated fats are from animal sources: butter, beef fat, and lard.
The essential fatty acids are omega 6 (linoleic acid) and omega 3 (linolenic acid). They are essential because they cannot be synthesized in the body and must be obtained from the diet.
The omega fatty acids are named differently than others. Instead of starting the numbering at the carboxyl end, you start at the methyl end. So the first double bond on an omega 3 fatty acid is at the 3rd carbon from the methyl end.
Omega 3 fatty acids have been shown to decrease the incidence of cardiovascular disease (CVD) by decreasing blood cholesterol levels and lowering blood clotting. They are also thought to be good for brain development and functioning, vision, the immune system, and memory. Linolenic acid is just one type of omega 3 fatty acid, and comes from plant sources. Other types, such as eicosapentaenoic acid (EPA) and docohexaenoic acid (DHA) come from fish oils. EPA and DHA are both highly unsaturated. EPA contains 5 double bonds, and DHA contains 6. Omega 3 fatty acids produce the important biomolecules prostoglandins, leukotrienes, and thromboxanes.
Hydrogenation is a process that turns polyunsaturated fats into saturated fats by adding hydrogen at the double bonds. This process generates trans fatty acids when vegetable oils are partially hydrogenated - i.e. not all of the double bonds are filled with hydrogen. When this happens the double bond is twisted from the cis (hydrogens are on the same side of the double bond) to trans (hydrogens are on opposite sides of the double bond). If the fat gets fully hydrogenated, this makes a saturated fatty acid, not a trans fat.
Trans fats are a huge health concern because they increase the risk of heart disease. They increase bad cholesterol and prevent good fats from functioning, promoting heart disease and circulatory disorders. They also depress the immune system, interfere with pregnancy (can cause low birth weights and poorer quality of breast milk), increase insulin resistance which can worsen diabetes and hypertension, and disturb liver function.
Other reactions that fat can undergo include emulsification, oxidation, and anti-oxidation.
Emulsification is the breaking of large fat molecules into smaller particles, such as the homogenization of milk. Bile and lecithin are able to undergo this process.
Oxidation results in the spoilage/rancidity of fats. This occurs when the double bond forms a peroxide and results in a bad taste and smell.
The fat soluble vitamin E can act as an antioxidant, and prevent spoilage. That is why it is added to products that contain fat. Vegetable oil naturally has some vitamin E in it, but more is often added to prolong shelf life.
Triglycerides are what we typically think of when we think of fat. It is the most abundant form both in our body and in nature (up to 95% of all fat). It is a neutral fat, meaning it is not polar and does not react with water.
The structure of a triglyceride is a glycerol with 3 fatty acids (acyl groups) attached, or estrified.
A diglyceride would have two attached fatty acids, and a monoglyceride would have 1.
Glycerol is the backbone of these structures. It contains 3 carbons with a hydroxyl group. The fatty acids get attached to the carbons in this backbone. In a monoglyceride, the fatty acid is attached to carbon #1. On a diglyceride, the fatty acid groups are attached to carbon #1 and #3.
Phospholipids are another important type of lipid. They are known as structural lipids because they are the main lipid found in the plasma membrane of cells. Human cells are all different, but the common feature is the plasma membrane. It keeps the structure of the cell intact which allows all of its contents to stay inside.
Human/animal cells also contain the glycocalyx, a carbohydrate rich area that includes glycoprotein and glycolipids.
Proteins in the cell may be integral (penetrating the cell membrane) or peripheral (stay on the surface of the membrane).
Cholesterol is also found in the plasma membrane. It has a 4 ring structure, and like phospholipid has a polar OH group which is hydrophyllic, and a tail group (including the ring structure) that is hydrophobic and hides inside the membrane. Cholesterol is synthesized in the body and is used to make cholic acid, which is part of bile. Because it is both hydrophobic and hydrophillic it can act as an emulsifier. Cholesterol is also used to make hormones like estradiol, a female sex hormone.
There are 4 types of transport mechanisms for moving molecules through the plasma membrane of cells: diffusion (simple or facilitated), active transport, and endocytosis.
Diffusion allows molecules to move from areas of high concentration to areas of low concentration, without requiring energy because it is a passive process. Simple diffusion simply moves the molecules/ions between lipids or other parts of the membrane. Sometimes pores are formed, which are known as gated channels for them to move through.
Facilitative diffusion requires a carrier protein which attaches to the molecule and undergoes a transformational change, allowing the molecule to move through.
Active transport also requires a carrier molecule, as well as energy. It allows movement from areas of low concentration to high concentration. An example is Sodium/potassium/ATPase in which energy is released when sodium binds to the carrier protein, releasing ADP and phosphate. Phosphate then attaches and undergoes a conformational change, dumping sodium into the extracellular fluid. Potassium then attaches at the binding site, releasing the phosphate group and undergoing another conformational change which in turn brings in the molecule and released potassium inside the cell.
Endocytosis occurs when the molecules approach the membrane, and it folds in to move them inside the cell.
Saturation phenomenon is the idea that the maximum velocity has been reached when all of the binding sites of transporter proteins are occupied.
Phospholipids are polar lipids, meaning that they contain molecules that react with water, such as nitrogen and oxygen. The basic structure is a glycerol backbone with 2 fatty acid chains plus a phosphate group. There will be another group attached to the phosphate group, known as the head group, which allows for classification of that specific phospholipid.
Phospholipids are distinct in that they contain a polar head and a hydrophobic tail in the same molecule. Because of this they are called ampipathic molecules. The head is hydrophillic (likes to react with water) and the tail is hydrophobic, or immiscible (does not like to react with water). This allows them to form a structural bilayer in the cell membrane. The hydrophyllic ends face outward while the hydrophobic ends remain inward. Lecithin is the major phospholipid found in the membrane. It can be synthesized in the body, but is also found in foods such as liver, egg yolk, and soybeans. Lecithin is an effective emulsifier.
Phospholipids are also found in lipoproteins, which are the transport vehicles for lipid in the blood. Lipids need help being transported because they are water immiscible. Therefore, they are hidden inside the lipoproteins. The hydrophyllic part of the phospholipid faces outward from the surface of the lipoprotein to allow it to freely move through the blood.
There are several types of lipoproteins: chylomicrons, which are made in the intestine; VLDL, which is made in the intestine and liver; LDL, which is made from VLDL in the blood; and HDL, which is made in the intestine and liver. The density depends upon the amount of protein and fat. A chylomicron has the highest amount of fat and the lowest protein, so it is the lowest density. HDL is the highest density due to its high protein content relative to fat.
The fat cells in our body (also known as adipocytes or adipose tissue) serve to store fat. The form that fat is stored in is triacyglycerol, or triglyceride.
Fatty acids are not found alone in nature or in the body. They are part of the structure of triacylglycerols. The structure of fatty acids is a chain of CH with carboxyl group (COOH) at one end of the chain. A saturated fatty acid has no double bonds. Unsaturated fatty acids have at least one double bond. Monounsaturated has one double bond, and polyunsaturated has two or more double bonds.
The number of carbons in fatty acids is usually an even number in nature. The most abundant have 16, 18, or 20 carbons.
To name the fatty acid, you start at the carboxyl group end and number the carbons. Then you count the number of double bonds and note it like this - example 18:1 is a fatty acid with an 18 carbon chain and one double bond. In this case, the double bond occurs between carbon # 9 and # 10, so you note this by adding a delta 9 after the name. This one is 18:1 (delta)9, or oleic acid. A fatty acid named 18:2 (delta) 9,12 has 18 carbons and two double bonds, occurring at carbon #9 and #12. There is always a difference of 3 carbons between the double bonds.
Monounsaturated and polyunsaturated fats come from plant sources and include canola oil and olive oil (mono) and vegetable, sunflower, and safflower oil (poly).
Tropical oils include palm and coconut. Although they come from plant sources, they are highly saturated and should be limited. This is confusing to some people because typically saturated fats are more solid at room temperature. Tropical oils appear more liquid at room temperature due to their content of shorter chains of fatty acids.
Most saturated fats are from animal sources: butter, beef fat, and lard.
The essential fatty acids are omega 6 (linoleic acid) and omega 3 (linolenic acid). They are essential because they cannot be synthesized in the body and must be obtained from the diet.
The omega fatty acids are named differently than others. Instead of starting the numbering at the carboxyl end, you start at the methyl end. So the first double bond on an omega 3 fatty acid is at the 3rd carbon from the methyl end.
Omega 3 fatty acids have been shown to decrease the incidence of cardiovascular disease (CVD) by decreasing blood cholesterol levels and lowering blood clotting. They are also thought to be good for brain development and functioning, vision, the immune system, and memory. Linolenic acid is just one type of omega 3 fatty acid, and comes from plant sources. Other types, such as eicosapentaenoic acid (EPA) and docohexaenoic acid (DHA) come from fish oils. EPA and DHA are both highly unsaturated. EPA contains 5 double bonds, and DHA contains 6. Omega 3 fatty acids produce the important biomolecules prostoglandins, leukotrienes, and thromboxanes.
Hydrogenation is a process that turns polyunsaturated fats into saturated fats by adding hydrogen at the double bonds. This process generates trans fatty acids when vegetable oils are partially hydrogenated - i.e. not all of the double bonds are filled with hydrogen. When this happens the double bond is twisted from the cis (hydrogens are on the same side of the double bond) to trans (hydrogens are on opposite sides of the double bond). If the fat gets fully hydrogenated, this makes a saturated fatty acid, not a trans fat.
Trans fats are a huge health concern because they increase the risk of heart disease. They increase bad cholesterol and prevent good fats from functioning, promoting heart disease and circulatory disorders. They also depress the immune system, interfere with pregnancy (can cause low birth weights and poorer quality of breast milk), increase insulin resistance which can worsen diabetes and hypertension, and disturb liver function.
Other reactions that fat can undergo include emulsification, oxidation, and anti-oxidation.
Emulsification is the breaking of large fat molecules into smaller particles, such as the homogenization of milk. Bile and lecithin are able to undergo this process.
Oxidation results in the spoilage/rancidity of fats. This occurs when the double bond forms a peroxide and results in a bad taste and smell.
The fat soluble vitamin E can act as an antioxidant, and prevent spoilage. That is why it is added to products that contain fat. Vegetable oil naturally has some vitamin E in it, but more is often added to prolong shelf life.
Triglycerides are what we typically think of when we think of fat. It is the most abundant form both in our body and in nature (up to 95% of all fat). It is a neutral fat, meaning it is not polar and does not react with water.
The structure of a triglyceride is a glycerol with 3 fatty acids (acyl groups) attached, or estrified.
A diglyceride would have two attached fatty acids, and a monoglyceride would have 1.
Glycerol is the backbone of these structures. It contains 3 carbons with a hydroxyl group. The fatty acids get attached to the carbons in this backbone. In a monoglyceride, the fatty acid is attached to carbon #1. On a diglyceride, the fatty acid groups are attached to carbon #1 and #3.
Phospholipids are another important type of lipid. They are known as structural lipids because they are the main lipid found in the plasma membrane of cells. Human cells are all different, but the common feature is the plasma membrane. It keeps the structure of the cell intact which allows all of its contents to stay inside.
Human/animal cells also contain the glycocalyx, a carbohydrate rich area that includes glycoprotein and glycolipids.
Proteins in the cell may be integral (penetrating the cell membrane) or peripheral (stay on the surface of the membrane).
Cholesterol is also found in the plasma membrane. It has a 4 ring structure, and like phospholipid has a polar OH group which is hydrophyllic, and a tail group (including the ring structure) that is hydrophobic and hides inside the membrane. Cholesterol is synthesized in the body and is used to make cholic acid, which is part of bile. Because it is both hydrophobic and hydrophillic it can act as an emulsifier. Cholesterol is also used to make hormones like estradiol, a female sex hormone.
There are 4 types of transport mechanisms for moving molecules through the plasma membrane of cells: diffusion (simple or facilitated), active transport, and endocytosis.
Diffusion allows molecules to move from areas of high concentration to areas of low concentration, without requiring energy because it is a passive process. Simple diffusion simply moves the molecules/ions between lipids or other parts of the membrane. Sometimes pores are formed, which are known as gated channels for them to move through.
Facilitative diffusion requires a carrier protein which attaches to the molecule and undergoes a transformational change, allowing the molecule to move through.
Active transport also requires a carrier molecule, as well as energy. It allows movement from areas of low concentration to high concentration. An example is Sodium/potassium/ATPase in which energy is released when sodium binds to the carrier protein, releasing ADP and phosphate. Phosphate then attaches and undergoes a conformational change, dumping sodium into the extracellular fluid. Potassium then attaches at the binding site, releasing the phosphate group and undergoing another conformational change which in turn brings in the molecule and released potassium inside the cell.
Endocytosis occurs when the molecules approach the membrane, and it folds in to move them inside the cell.
Saturation phenomenon is the idea that the maximum velocity has been reached when all of the binding sites of transporter proteins are occupied.
Phospholipids are polar lipids, meaning that they contain molecules that react with water, such as nitrogen and oxygen. The basic structure is a glycerol backbone with 2 fatty acid chains plus a phosphate group. There will be another group attached to the phosphate group, known as the head group, which allows for classification of that specific phospholipid.
Phospholipids are distinct in that they contain a polar head and a hydrophobic tail in the same molecule. Because of this they are called ampipathic molecules. The head is hydrophillic (likes to react with water) and the tail is hydrophobic, or immiscible (does not like to react with water). This allows them to form a structural bilayer in the cell membrane. The hydrophyllic ends face outward while the hydrophobic ends remain inward. Lecithin is the major phospholipid found in the membrane. It can be synthesized in the body, but is also found in foods such as liver, egg yolk, and soybeans. Lecithin is an effective emulsifier.
Phospholipids are also found in lipoproteins, which are the transport vehicles for lipid in the blood. Lipids need help being transported because they are water immiscible. Therefore, they are hidden inside the lipoproteins. The hydrophyllic part of the phospholipid faces outward from the surface of the lipoprotein to allow it to freely move through the blood.
There are several types of lipoproteins: chylomicrons, which are made in the intestine; VLDL, which is made in the intestine and liver; LDL, which is made from VLDL in the blood; and HDL, which is made in the intestine and liver. The density depends upon the amount of protein and fat. A chylomicron has the highest amount of fat and the lowest protein, so it is the lowest density. HDL is the highest density due to its high protein content relative to fat.
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