was drauf hat sich den folgenden artikel mal durchlesen könnte und mir dann sagen ob die aussagen hand und fuss haben...
ich persönlich halt leinöl auch für sehr gut,aber bei mir ist es reiner erfahrungswert....
mfg,klaus
My name is Eric, and I’m a skinny little endurance athlete. Specifically, I’m a skinny little asthmatic cyclist. Before you click off this article, fearing that you might somehow "catch" what I have and become a skinny little endurance athlete too, let me tell you this. I know how you can safely increase your metabolic rate and increase your capacity to burn fat simply by changing your diet.
I thought that might catch your attention.
Before I pass this wisdom on to you, let me first tell you the story of how I started down my current research path.
A few years ago, I moved to London, Ontario to finish up my Ph.D. Only problem is, London is an absolutely horrible place to be an asthmatic cyclist. The roads are poorly maintained and none of them have shoulders. To make matters worse, I have to share these roads with some of the most inconsiderate human beings to ever drive a car. Riding a bike here is literally an independent risk factor for all causes of mortality. Then there’s the science experiment they call air here in southern Ontario. The air quality is so bad in the summer that I have no chance of controlling my asthma when I ride — no matter how heavily medicated I am. As a result of this, my training volume dropped off significantly. And even worse, when I did drag my lazy butt off the couch, my asthma kept me from training hard.
After a year of living in my own personal hell, I became fat and slow — literally. For the first time in my life I was in the double digits for body-fat percentage. Like every good American, I just assumed that the measurements were wrong and started on a steady regimen of denial and refusal. I continued to enter my gelatinous butt in the occasional race, but the funny thing is when you stop training seriously and get fat, you usually get your butt kicked by guys who have no right to be taking a swing at your butt. During one of my many beatings, I had an asthma attack that I couldn't get under control no matter what I tried. I dropped out of the race and spent a fun-filled night in the emergency room. That was the final straw.
Determined to find a way of dealing with my asthma, I started doing a lot of reading on exactly what happens when you have an asthma attack. I found out that there’s a family of chemicals called eicosanoids that are produced in response to the stimuli that causes the attack. These eicosanoids are produced from fats found in your cell membranes. The eicosanoids that are formed have different chemical properties depending on what type of fat is incorporated into them. To make a long story slightly shorter, omega-6 fatty acids are very pro-inflammatory (asthma and allergies are mainly a disease of inflammation), whereas omega 3 fatty acids (those found in fish oils) are not. Well, I quickly switched my diet. I tried to completely eliminate omega-6 fatty acids and eat as much omega-3 fatty acids as I could.
So what does all this have to do with increasing your ability to burn fat? Without trying, or even noticing, I got very lean again. My training didn't change that much, and if anything I was taking in more calories with all the oil supplements I was using. But I lost the ten plus pounds I had put on. Initially I didn't think too much about it, but then it started to dawn on me that something pretty significant had occurred. Around this time I accidentally stumbled across some studies that had shown that rodents fed a diet rich in omega 3 fatty acids were significantly leaner than rodents that had received the same amount of calories rich in another type of fat. And there it was. The explanation for my return trip to the land of the lean.
How the different types of fat add up
So how can omega-3 fatty acids make you lean? Well, let’s first take a time out for a definition.
As I’m sure you’re all aware, fatty acids are usually lumped into one of three categories — saturated, monounsaturated, or polyunsaturated. These categories are based on the number of double bonds found along the carbon chain. Saturated fatty acids have all their carbons "saturated" with a hydrogen molecule and therefore have no double bonds in their structure. Monounsaturates, as the name would imply, have one double bond somewhere in the carbon chain.
Now if you’ve been following along, you probably already guessed that polyunsaturates have two or more double bonds somewhere along their carbon chain. So where do omega-3 fatty acids fit into this picture? Well, omega-3 fatty acids are a special type of polyunsaturated fatty acid. All omega-3 fatty acids have a common landmark that differentiates them from the other types of polyunsaturated fatty acids. Specifically they have their first double bond exactly 3 carbons from the methyl group.
There are several different omega-3 fatty acids. The mother of all the omega-3 fatty acids is called alpha-linolenic acid (LNA). This fatty acid can be metabolized (elongated and desaturated) in the body to form several other omega-3 fatty acids. The two most talked about omega 3s that are made from LNA are eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). Many people believe that EPA and DHA are more biologically active in the body than LNA, so that’s why some people, like John Berardi, are always harping on you about them.
However, there’s considerable debate about how much LNA can actually be converted to EPA and DHA in the body. This is why most studies have chosen to supplement with EPA or DHA rather than LNA.
LNA is an essential fatty acid. This means that our bodies can't make LNA. As I mentioned above, we can potentially modify the LNA within our body to form other types of omega 3 fatty acids as needed. This has caused most nutritional scientists to label EPA and DHA as non-essential fatty acids. I think this is misleading because at the very least, without lots of LNA, there’s no EPA or DHA.
In a worse case scenario, there may be insufficient conversion of LNA into EPA or DHA within our bodies, which could lead to a functional deficiency of these "non-essential" fatty acids. One thing we do know for sure is that the total amount of omega-3 fatty acids that are found in our body is a result of how much we’re getting in our diet. It used to be that our diet was rich in omega-3 fatty acids, but in modern times they are all but extinct in our diets. Many researchers are now suggesting that this could be a factor that helps explain society’s ever-increasing waistline.
Okay, I sat through your definition. Now what’s this got to do with the fat on my waist?
So now that we’re done with our definitions, it’s time to ask the question: "How exactly can eating omega-3 fatty acids increase your ability to burn fat?" Well, the exact answer to that question isn't completely known at this point, but studies have identified a couple of different mechanisms.
One potential mechanism is that omega 3 fatty acids may allow the body to burn fat in situations where fat oxidation (or fat burning) is normally turned off, or substantially reduced. There’s a reciprocal relationship between carbohydrate and fat oxidation.
When carbohydrate burning goes up, fat burning goes down and vice versa.
This is clearly evident following the ingestion of a high-glycemic carbohydrate. Shortly after eating a sugary snack, carbohydrate oxidation goes through the roof, and fat oxidation becomes almost non-existent. This happens because the glucose, and the insulin that goes along with it, increases the formation of a molecule called malonyl CoA in your cells. Malonyl CoA is actually the first building block in the synthesis of a new fat molecule. It’s formed when CO2 is irreversibly added to a cellular molecule called acetyl CoA. An enzyme called acetyl-CoA carboxylase catalyzes this reaction.
As my old bioenergetics teacher always used to say, "The body abhors waste." Therefore, if we’re increasing the synthesis of fats, we’re going to want to shut down our ability to burn fats. (Makes sense since the synthesis of fat followed by immediate fat breakdown, seems wasteful.)
Malonyl CoA accomplishes this efficient cessation of fat oxidation by inhibiting carnitine acyltransferase I (CAT I), which is the rate limiting enzyme in fat oxidation(21). Therefore, since CAT I dictates how much fat you’ll burn and malonyl CoA shuts it down, having lots of malonyl A hanging around the cell means you don’t burn fat. In addition, the build up of malonyl CoA leads to more fat synthesis.
So what does this have to do with omega-3 fatty acids increasing your fat burning ability? Well first off, it’s been shown in rats that a diet rich in omega 3 fatty acids will inhibit acetyl-CoA carboxylase(24), thus making it very hard to make malonyl CoA (and fat). In addition to decreasing the formation of malonyl CoA, the omega 3 fatty acids also decrease the sensitivity of CAT 1 to malonyl CoA(13;16). Therefore, you have a situation where not only is less fat building malonyl CoA being formed in response to a high carbohydrate meal, but the malonyl CoA that is formed has a less pronounced inhibitory effect on fat oxidation.
It’s also been shown that malonyl CoA (during exercise, the stimulus for its formation is different than the insulin scenario outlined above) is at least partly responsible for "shutting off" fat metabolism and switching us over to carbohydrate metabolism during high-intensity exercise(20). This may mean that dietary omega-3 fatty acids may allow us to burn an increased amount of fat during a workout, just as they can during rest.
More benefits of Omega 3’s
Although it isn't universally accepted, several studies have suggested that a diet rich in omega-3 fatty acids may increase insulin sensitivity (2;5;14;22). If you’re a regular T-mag reader, you’ll know that this means that, among other things, there will be a decrease in the amount of insulin released for a given glucose load. If this is indeed the case, then this could lead to less insulin released and more malonyl CoA formed when we reach for the bag of gummy worms.
Possibly even more exciting, one study in rodents has shown that the fat cells (adipocytes) of rodents fed lots of 3s actually become insulin resistant in terms of glucose uptake into the cell(8). This is big news, since much of the fat stored in our adipocytes is made from glucose.
This means that omega 3s may lead to insulin sensitivity where we want to be sensitive (muscle and liver) and insulin resistance in fat cells.
Unfortunately, this study didn't show any change in insulin's ability to inhibit the breakdown of fat (lipolysis) within the adipocytes following a diet high in omega 3 fatty acids, but at least we aren't making any new fat.
The second way that a diet rich in omega 3 fatty acids may allow us to burn more fat is that they’ll beef up the metabolic machinery responsible for burning fat. Several studies have shown that a diet rich in omega 3 fatty acids will increase the production and activity of several key mitochondrial enzymes involved in fat oxidation(3;10;12;13;16;23;24). (The mitochondria is a cellular organ responsible for fat burning and we have already discussed one of it’s main fat burning enzymes — CAT 1.) Interestingly, many of these mitochondrial changes (and therefore, fat-burning changes) seen with omega 3 supplementation mimic the changes that we see when someone undergoes an aerobic training program.
In addition to giving us super fat burning mitochondria, omega 3 fatty acids have the ability to dramatically influence the activity of some other cells which are capable of burning fat. One of these cells is something called a peroxisome. Peroxisomes function in a manner very similar to mitochondria, but there’s one very important difference in how they handle the oxidation of fats. Specifically, peroxisomal lipid oxidation produces 30-40% more heat and 30% less ATP than does mitochondrial lipid oxidation(17).
Now, in both the mitochondria and the peroxisome, the first step of breaking down fat for energy (beta oxidation) involves the removal of electrons from a lipid molecule. In the mitochondria these electrons ultimately end up in the electron transport chain — thus yielding ATP molecules (yep, this is how ATP is made). However, the electrons freed up in the first step of beta oxidation within the peroxisomes are passed directly to an O2 molecule, thus forming hydrogen peroxide (H2O2), which is immediately broken down into water and oxygen.
Since these electrons never make it to the electron transport chain, less ATP are formed compared to beta oxidation in the mitochondria. Dietary omega 3 fatty acids are very potent activators of peroxisomal lipid oxidation. They do this by increasing the activity and production of the key enzymes involved in peroxisomal beta oxidation(1;12;23). Therefore, omega 3’s increase fat burning that doesn’t ultimately produce a lot of ATP.
It should be pointed out here that most of the studies have looked at liver rather than skeletal muscle peroxisomes. Although the liver is a very metabolically active organ, its small size limits its impact on total daily energy expenditure. It’s still unknown exactly how much fat is oxidized in muscle peroxisomes, but one study has shown an increase in skeletal muscle peroxisome enzyme expression following a high omega 3 fatty acids diet(1), which could have profound impact on daily energy expenditures.
Yet another family of cells that are affected by dietary omega 3 fatty acids are called uncoupling proteins (UCPs). Uncoupling proteins are mitochondrial membrane proteins that allow an alternative route for protons to reenter the mitochondrial matrix. This decreases the electrochemical gradient and uncouples fuel oxidation and ATP production. In plain English, what this means is that uncoupling proteins allow us to oxidize fats, but instead of producing ATP we produce heat. (Editor’s note: for you bodybuilding types, this is one thing that the dangerous toxin DNP does — among other things that aren’t so pleasant).
For years it was thought that uncoupling proteins were only found in something called brown adipose tissue. Brown adipose tissue plays a very important role in maintaining body temperature. When things start to get a little too chilly, the uncoupling proteins kick in and lots of heat is produced (non-shivering thermogenesis). The only problem is, adult humans really don't have any brown adipose tissue to speak of.
A couple of years ago however, some science types discovered two more uncoupling proteins (creatively named UCP-2 and UCP-3). The good news is that they’re almost identical to the UCP-1 found in brown adipose tissue and we humans seem to have lots of them. UCP-2s are found in many tissues in the body, but UCP-3s seems to be located mainly in skeletal muscle.
Even though we’re in the infancy of research on UCPs, we do know that the expression of the UCPs has been shown to correlate with total body metabolic rate(11;18;19). Although there are very large gaps in our current knowledge of uncoupling proteins, it’s clear that a diet rich in omega 3 fatty acids will increase the amount of uncoupling proteins in our body(1;9). What remains unclear at this point is how much of an impact on total daily energy expenditure this represents.
It’s Time Leptin Leapt In
There’s one final dark horse mechanism that I feel I should at least touch on, and that’s the possible impact of omega-3 fatty acids on leptin production. Leptin is a hormone that is produced by adipocytes that essentially tries to tell the body that we have enough energy to last us for a while. The body responds to leptin by decreasing hunger and increasing metabolic rates(15). It’s generally accepted that in healthy individuals, leptin levels are positively correlated to body-fat levels (as body fat goes up, leptin levels go up).
However, rodents that are fed a diet rich in omega 3 fatty acids have circulating leptin levels that are substantially higher than what would be anticipated based on body fat(4). There isn't too much research looking at how omega-3 fatty acids interact with or affect leptin yet, but I believe this could be a very important mechanism and that we’ll see many more studies reporting on this in the near future.
Scientific Studies
In looking back over this article, hopefully I have convinced you that there are indeed some very good reasons to believe that a diet rich in omega 3 fatty acids can increase fat oxidation and metabolic rates. However, most of the studies that I have mentioned so far have been rodent studies. Also, several of them have only looked at isolated cells and not whole body living animals. Unfortunately, we can't always transfer results across species, or extrapolate results from a test tube to a living system. There is however, one fairly well controlled study done in humans that shows that all the theory may indeed be reality.
In this study, six subjects were fed a control diet for 3 weeks. During these 3 weeks they showed up at the lab and ate as much as they wanted of whatever they wanted. The researchers simply recorded everything they ate, and in what amounts. After a short washout period the subjects were once again fed at the lab for another 3 weeks. This time around they received the exact same meals as they ate during the control period with one very important exception. Every day of this 3-week period, 6 grams a day of saturated and omega 6 fatty acids in their food was replaced with 6 grams of omega 3 fatty acids (fish oil).
In the first paper that came out of this study, the researchers looked at how the fish-oil diet would impact fat oxidation following carbohydrate ingestion in 5 of those subjects(7). They found that the subjects were able to oxidize 35% more fat following carbohydrate ingestion after the three weeks on fish oil. This study didn't look at the cellular mechanisms that allowed the increased fat burning in the face of all that glucose, so we don't know exactly what happened.
They did however measure insulin levels, and they found that after three weeks on the fish oil the subjects produced significantly less insulin in response to the carbohydrates they ingested. As mentioned above, this should mean less malonyl CoA formation, which will mean more fat will be burned.
In the second paper that came out of this study, the authors examined how the 3 weeks of fish oil impacted body composition and resting metabolism(6). They found that the subjects lost on average a little less than a pound of fat as determined by dual-energy X-ray absorptiometry (DEXA) during the omega 3 fatty acids diet. There was also a slight increase in lean mass during the omega 3 fatty acids diet, but it wasn't statistically significant. Respiratory exchange ratio (a ratio of the amount of CO2 produced to the amount of O2 consumed) showed that the subjects were burning significantly more fat after the omega 3 fatty acids diet.
There was also an increase in the resting metabolic rates of the subjects after the omega 3 fatty acids diet, but this was no longer statistically significant when the slight increase in lean mass that I mentioned was taken into account. Unfortunately, these two papers are the only published studies using humans that has looked at how omega 3 fatty acids can affect our ability to burn fat and ultimately change body composition. Given the practical implications of this information, you can bet that many more are on their way.
Paydirt
The question I usually get from everyone about 10 seconds after I start to explain my research is, "So what should I eat to lose this fat?" Unfortunately, at this stage of the game, I can't say absolutely what is the best way of maximizing the fat burning potential of omega 3 fatty acids, but I can offer up some educated suggestions.
The first step, and most likely the most beneficial one, is to replace a substantial amount of the fat that is already in your diet with omega-3 fatty acids. Specifically, try and replace the saturated and omega-6 fatty acids in your diet with 3s. This is going to take out the negative fats and add the good ones without increasing the total daily fat, or caloric intake. The general public is slowly starting to become aware of the health benefits of omega 3 fatty acids, and it’s driving the food industry to start offering up many common foods that have been slightly modified to increase their omega-3 fatty acids content.
For the most part, these foods can be found in bigger supermarkets, in the health food section, and are clearly marked that they contain omega-3 fatty acids. Also look for foods that use canola oil instead of vegetable/corn/sunflower or safflower oils. Canola oil has a reasonable amount of 3s, and substantially less 6s than the aforementioned oils do.
Unfortunately, given the current state of affairs for the western diet, it’s probably unrealistic to think that people are going to be getting enough 3s simply through a normal diet. Therefore, I think it is wise that people supplement with some omega-3 oils on top of trying to eat a diet that is low in saturated and omega 6 fatty acids.
Unfortunately, the ideal amount of 3s to supplement with is completely unknown at this time. The rodent studies use a pretty big dose of 3s, and they usually eliminate most of the saturated and omega-6 fatty acids from the diet. This makes extrapolating these doses to free eating humans very challenging. In myself, I saw very good results with a tablespoon of flaxseed oil a day, plus about 10 grams of salmon oil per day (capsules plus the fat found in the salmon I eat on most days).
I chose these levels to bring my daily ratio of 6s/3's down into the 4/1 to 1/1 range which is recommended for optimal health (remember I was trying to cure asthma, not lose fat). Whether this is the ideal, too little, or too much still needs to be determined. But keep in mind that the study mentioned above replaced 6 grams a day of the bad fat with 6 grams a day of the good stuff and the subjects lost about a pound of pure ugly fat. In this day and age of miracle products claiming that you can lose 20 pounds in a week while you sleep, losing a pound of fat every 3 weeks may seem pretty insignificant. However, do the math and look at how that could affect your body composition over the course of a year and I think you'll agree that it is a pretty big deal.
Of course getting lots of 3s in your diet will also significantly decrease your risk of developing heart disease, many types of cancers, type-2 diabetes and a host of other scary diseases, but who cares, ‘cause you'll be looking good in your swimsuit.
Eric E Noreen, MS, is currently finishing his PhD in the area of Exercise and Nutritional Biochemistry at the University of Western Ontario. He has been the nutritional advisor for several of the athletic teams at the University of Western Ontario, along with lecturing at training camps for some of the Canadian National teams. By his own admission, he is also one sexy bastard.
Reference List:
1. Baillie, R. A., Takada, R., Nakamura, M., and Clarke, S. D. Coordinate induction of peroxisomal acyl-CoA oxidase and UCP-3 by dietary fish oil: a mechanism for decreased body fat deposition. Prostaglandins Leukot Essent Fatty Acids 60(5-6), 351-6. 199
3. Berge, R. K., Madsen, L., Vaagenes, H., Tronstad, K. J., Gottlicher, M., and Rustan, A. C. In contrast with docosahexaenoic acid, eicosapentaenoic acid and hypolipidaemic derivatives decrease hepatic synthesis and secretion of triacylglycerol by decreased diacylglycerol acyltransferase activity and stimulation of fatty acid oxidation. Biochem J 343 Pt 1, 191-7. 1999.
4. Cha, M. C. and Jones, P. J. Dietary fat type and energy restriction interactively influence plasma leptin concentration in rats. J Lipid Res 39(8), 1655-60. 1998.
5. Chicco, A., D'Alessandro, M. E., Karabatas, L., Gutman, R., and Lombardo, Y. B. Effect of moderate levels of dietary fish oil on insulin secretion and sensitivity, and pancreas insulin content in normal rats. Ann Nutr Metab 40(2), 61-70. 1996.
6. Couet, C., Delarue, P., Autoine, J. M., and Lamisse, F. Effect of dietary fish oil on body mass and basal fat oxidation in healthy adults. Int J Obes 21, 637-643. 1997.
7. Delarue, J., Couet, C., Cohen, R., Brechot, J. F., Antoine, J. M., and Lamisse, F. Effects of fish oil on metabolic responses to oral fructose and glucose loads in healthy humans. Am J Physiol 270(2 Pt 1), E353-62. 1996.
8. Fickova, M., Hubert, P., Cremel, G., and Leray, C. Dietary (n-3) and (n-6) polyunsaturated fatty acids rapidly modify fatty acid composition and insulin effects in rat adipocytes. J Nutr 128(3), 512-9. 1998.
9. Hun, C. S., Hasegawa, K., Kawabata, T., Kato, M., Shimokawa, T., and Kagawa, Y. Increased uncoupling protein2 mRNA in white adipose tissue, and decrease in leptin, visceral fat, blood glucose, and cholesterol in KK-Ay mice fed with eicosapentaenoic and docosahexaenoic acids in addition to linolenic acid. Biochem Biophys Res Commun 259(1), 85-90. 1999.
10. Ide, T., Kobayashi, H., Ashakumary, L., Rouyer, I. A., Takahashi, Y., Aoyama, T., Hashimoto, T., and Mizugaki, M. Comparative effects of perilla and fish oils on the activity and gene expression of fatty acid oxidation enzymes in rat liver. Biochim Biophys Acta 1485(1), 23-35. 2000.
11. Jekabsons, M. B., Gregoire, F. M., Schonfeld-Warden, N. A., Warden, C. H., and Horwitz, B. A. T(3) stimulates resting metabolism and UCP-2 and UCP-3 mRNA but not nonphosphorylating mitochondrial respiration in mice. Am J Physiol 277(2 Pt 1), E380-9. 1999.
12. Kumamoto, T. and Ide, T. Comparative effects of alpha- and gamma-linolenic acids on rat liver fatty acid oxidation. Lipids 33(7), 647-54. 1998.
13. Madsen, L., Rustan, A. C., Vaagenes, H., Berge, K., Dyroy, E., and Berge, R. K. Eicosapentaenoic and docosahexaenoic acid affect mitochondrial and peroxisomal fatty acid oxidation in relation to substrate preference. Lipids 34(9), 951-63. 1999.
14. Mori, T. A., Bao, D. Q., Burke, V., Puddey, I. B., Watts, G. F., and Beilin, L. J. Dietary fish as a major component of a weight-loss diet: effect on serum lipids, glucose, and insulin metabolism in overweight hypertensive subjects. Am J Clin Nutr 70(5), 817-25. 1999.
15. Pelleymounter, M. A., Cullen, M. J., Baker, M. B., Hecht, R., Winters, D., Boone, T., and Collins, F. Effects of the obese gene product on body weight regulation in ob/ob mice. Science 269(5223), 540-3. 1995.
16. Power, G. W. and Newsholme, E. A. Dietary fatty acids influence the activity and metabolic control of mitochondrial carnitine palmitoyltransferase I in rat heart and skeletal muscle. J Nutr 127(11), 2142-50. 1997.
17. Reddy, J. K. and Mannaerts, G. P. Peroxisomal lipid metabolism. Annu Rev Nutr 14, 343-70. 1994.
18. Schrauwen, P., Troost, F. J., Xia, J., Ravussin, E., and Saris, W. H. Skeletal muscle UCP2 and UCP3 expression in trained and untrained male subjects. Int J Obes Relat Metab Disord 23(9), 966-72. 1999.
19. Schrauwen, P., Xia, J., Bogardus, C., Pratley, R. E., and Ravussin, E. Skeletal muscle uncoupling protein 3 expression is a determinant of energy expenditure in Pima Indians. Diabetes 48(1), 146-9. 1999.
20. Sidossis, L. S., Gastaldelli, A., Klein, S., and Wolfe, R. R. Regulation of plasma fatty acid oxidation during low- and high-intensity exercise. Am J Physiol 272(6 Pt 1), E1065-70. 1997.
21. Sidossis, L. S., Stuart, C. A., Shulman, G. I., Lopaschuk, G. D., and Wolfe, R. R. Glucose plus insulin regulate fat oxidation by controlling the rate of fatty acid entry into the mitochondria. J Clin Invest 98(10), 2244-50. 1996.
22. Storlien, L. H., Jenkins, A. B., Chisholm, D. J., Pascoe, W. S., Khouri, S., and Kraegen, E. W. Influence of dietary fat composition on development of insulin resistance in rats. Relationship to muscle triglyceride and omega-3 fatty acids in muscle phospholipid. Diabetes 40(2), 280-9. 1991.
23. Vamecq, J., Vallee, L., de la Porte, P. L., Fontaine, M., de Craemer, D., van den Branden, C., Lafont, H., Grataroli, R., and Nalbone, G. Effect of various n-3/n-6 fatty acid ratio contents of high fat diets on rat liver and heart peroxisomal and mitochondrial beta-oxidation. Biochim Biophys Acta 1170(2), 151-6. 1993.
24. Willumsen, N., Skorve, J., Hexeberg, S., Rustan, A. C., and Berge, R. K. The hypotriglyceridemic effect of eicosapentaenoic acid in rats is reflected in increased mitochondrial fatty acid oxidation followed by diminished lipogenesis. Lipids 28(8), 683 90. 1993.
ich persönlich halt leinöl auch für sehr gut,aber bei mir ist es reiner erfahrungswert....
mfg,klaus
My name is Eric, and I’m a skinny little endurance athlete. Specifically, I’m a skinny little asthmatic cyclist. Before you click off this article, fearing that you might somehow "catch" what I have and become a skinny little endurance athlete too, let me tell you this. I know how you can safely increase your metabolic rate and increase your capacity to burn fat simply by changing your diet.
I thought that might catch your attention.
Before I pass this wisdom on to you, let me first tell you the story of how I started down my current research path.
A few years ago, I moved to London, Ontario to finish up my Ph.D. Only problem is, London is an absolutely horrible place to be an asthmatic cyclist. The roads are poorly maintained and none of them have shoulders. To make matters worse, I have to share these roads with some of the most inconsiderate human beings to ever drive a car. Riding a bike here is literally an independent risk factor for all causes of mortality. Then there’s the science experiment they call air here in southern Ontario. The air quality is so bad in the summer that I have no chance of controlling my asthma when I ride — no matter how heavily medicated I am. As a result of this, my training volume dropped off significantly. And even worse, when I did drag my lazy butt off the couch, my asthma kept me from training hard.
After a year of living in my own personal hell, I became fat and slow — literally. For the first time in my life I was in the double digits for body-fat percentage. Like every good American, I just assumed that the measurements were wrong and started on a steady regimen of denial and refusal. I continued to enter my gelatinous butt in the occasional race, but the funny thing is when you stop training seriously and get fat, you usually get your butt kicked by guys who have no right to be taking a swing at your butt. During one of my many beatings, I had an asthma attack that I couldn't get under control no matter what I tried. I dropped out of the race and spent a fun-filled night in the emergency room. That was the final straw.
Determined to find a way of dealing with my asthma, I started doing a lot of reading on exactly what happens when you have an asthma attack. I found out that there’s a family of chemicals called eicosanoids that are produced in response to the stimuli that causes the attack. These eicosanoids are produced from fats found in your cell membranes. The eicosanoids that are formed have different chemical properties depending on what type of fat is incorporated into them. To make a long story slightly shorter, omega-6 fatty acids are very pro-inflammatory (asthma and allergies are mainly a disease of inflammation), whereas omega 3 fatty acids (those found in fish oils) are not. Well, I quickly switched my diet. I tried to completely eliminate omega-6 fatty acids and eat as much omega-3 fatty acids as I could.
So what does all this have to do with increasing your ability to burn fat? Without trying, or even noticing, I got very lean again. My training didn't change that much, and if anything I was taking in more calories with all the oil supplements I was using. But I lost the ten plus pounds I had put on. Initially I didn't think too much about it, but then it started to dawn on me that something pretty significant had occurred. Around this time I accidentally stumbled across some studies that had shown that rodents fed a diet rich in omega 3 fatty acids were significantly leaner than rodents that had received the same amount of calories rich in another type of fat. And there it was. The explanation for my return trip to the land of the lean.
How the different types of fat add up
So how can omega-3 fatty acids make you lean? Well, let’s first take a time out for a definition.
As I’m sure you’re all aware, fatty acids are usually lumped into one of three categories — saturated, monounsaturated, or polyunsaturated. These categories are based on the number of double bonds found along the carbon chain. Saturated fatty acids have all their carbons "saturated" with a hydrogen molecule and therefore have no double bonds in their structure. Monounsaturates, as the name would imply, have one double bond somewhere in the carbon chain.
Now if you’ve been following along, you probably already guessed that polyunsaturates have two or more double bonds somewhere along their carbon chain. So where do omega-3 fatty acids fit into this picture? Well, omega-3 fatty acids are a special type of polyunsaturated fatty acid. All omega-3 fatty acids have a common landmark that differentiates them from the other types of polyunsaturated fatty acids. Specifically they have their first double bond exactly 3 carbons from the methyl group.
There are several different omega-3 fatty acids. The mother of all the omega-3 fatty acids is called alpha-linolenic acid (LNA). This fatty acid can be metabolized (elongated and desaturated) in the body to form several other omega-3 fatty acids. The two most talked about omega 3s that are made from LNA are eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). Many people believe that EPA and DHA are more biologically active in the body than LNA, so that’s why some people, like John Berardi, are always harping on you about them.
However, there’s considerable debate about how much LNA can actually be converted to EPA and DHA in the body. This is why most studies have chosen to supplement with EPA or DHA rather than LNA.
LNA is an essential fatty acid. This means that our bodies can't make LNA. As I mentioned above, we can potentially modify the LNA within our body to form other types of omega 3 fatty acids as needed. This has caused most nutritional scientists to label EPA and DHA as non-essential fatty acids. I think this is misleading because at the very least, without lots of LNA, there’s no EPA or DHA.
In a worse case scenario, there may be insufficient conversion of LNA into EPA or DHA within our bodies, which could lead to a functional deficiency of these "non-essential" fatty acids. One thing we do know for sure is that the total amount of omega-3 fatty acids that are found in our body is a result of how much we’re getting in our diet. It used to be that our diet was rich in omega-3 fatty acids, but in modern times they are all but extinct in our diets. Many researchers are now suggesting that this could be a factor that helps explain society’s ever-increasing waistline.
Okay, I sat through your definition. Now what’s this got to do with the fat on my waist?
So now that we’re done with our definitions, it’s time to ask the question: "How exactly can eating omega-3 fatty acids increase your ability to burn fat?" Well, the exact answer to that question isn't completely known at this point, but studies have identified a couple of different mechanisms.
One potential mechanism is that omega 3 fatty acids may allow the body to burn fat in situations where fat oxidation (or fat burning) is normally turned off, or substantially reduced. There’s a reciprocal relationship between carbohydrate and fat oxidation.
When carbohydrate burning goes up, fat burning goes down and vice versa.
This is clearly evident following the ingestion of a high-glycemic carbohydrate. Shortly after eating a sugary snack, carbohydrate oxidation goes through the roof, and fat oxidation becomes almost non-existent. This happens because the glucose, and the insulin that goes along with it, increases the formation of a molecule called malonyl CoA in your cells. Malonyl CoA is actually the first building block in the synthesis of a new fat molecule. It’s formed when CO2 is irreversibly added to a cellular molecule called acetyl CoA. An enzyme called acetyl-CoA carboxylase catalyzes this reaction.
As my old bioenergetics teacher always used to say, "The body abhors waste." Therefore, if we’re increasing the synthesis of fats, we’re going to want to shut down our ability to burn fats. (Makes sense since the synthesis of fat followed by immediate fat breakdown, seems wasteful.)
Malonyl CoA accomplishes this efficient cessation of fat oxidation by inhibiting carnitine acyltransferase I (CAT I), which is the rate limiting enzyme in fat oxidation(21). Therefore, since CAT I dictates how much fat you’ll burn and malonyl CoA shuts it down, having lots of malonyl A hanging around the cell means you don’t burn fat. In addition, the build up of malonyl CoA leads to more fat synthesis.
So what does this have to do with omega-3 fatty acids increasing your fat burning ability? Well first off, it’s been shown in rats that a diet rich in omega 3 fatty acids will inhibit acetyl-CoA carboxylase(24), thus making it very hard to make malonyl CoA (and fat). In addition to decreasing the formation of malonyl CoA, the omega 3 fatty acids also decrease the sensitivity of CAT 1 to malonyl CoA(13;16). Therefore, you have a situation where not only is less fat building malonyl CoA being formed in response to a high carbohydrate meal, but the malonyl CoA that is formed has a less pronounced inhibitory effect on fat oxidation.
It’s also been shown that malonyl CoA (during exercise, the stimulus for its formation is different than the insulin scenario outlined above) is at least partly responsible for "shutting off" fat metabolism and switching us over to carbohydrate metabolism during high-intensity exercise(20). This may mean that dietary omega-3 fatty acids may allow us to burn an increased amount of fat during a workout, just as they can during rest.
More benefits of Omega 3’s
Although it isn't universally accepted, several studies have suggested that a diet rich in omega-3 fatty acids may increase insulin sensitivity (2;5;14;22). If you’re a regular T-mag reader, you’ll know that this means that, among other things, there will be a decrease in the amount of insulin released for a given glucose load. If this is indeed the case, then this could lead to less insulin released and more malonyl CoA formed when we reach for the bag of gummy worms.
Possibly even more exciting, one study in rodents has shown that the fat cells (adipocytes) of rodents fed lots of 3s actually become insulin resistant in terms of glucose uptake into the cell(8). This is big news, since much of the fat stored in our adipocytes is made from glucose.
This means that omega 3s may lead to insulin sensitivity where we want to be sensitive (muscle and liver) and insulin resistance in fat cells.
Unfortunately, this study didn't show any change in insulin's ability to inhibit the breakdown of fat (lipolysis) within the adipocytes following a diet high in omega 3 fatty acids, but at least we aren't making any new fat.
The second way that a diet rich in omega 3 fatty acids may allow us to burn more fat is that they’ll beef up the metabolic machinery responsible for burning fat. Several studies have shown that a diet rich in omega 3 fatty acids will increase the production and activity of several key mitochondrial enzymes involved in fat oxidation(3;10;12;13;16;23;24). (The mitochondria is a cellular organ responsible for fat burning and we have already discussed one of it’s main fat burning enzymes — CAT 1.) Interestingly, many of these mitochondrial changes (and therefore, fat-burning changes) seen with omega 3 supplementation mimic the changes that we see when someone undergoes an aerobic training program.
In addition to giving us super fat burning mitochondria, omega 3 fatty acids have the ability to dramatically influence the activity of some other cells which are capable of burning fat. One of these cells is something called a peroxisome. Peroxisomes function in a manner very similar to mitochondria, but there’s one very important difference in how they handle the oxidation of fats. Specifically, peroxisomal lipid oxidation produces 30-40% more heat and 30% less ATP than does mitochondrial lipid oxidation(17).
Now, in both the mitochondria and the peroxisome, the first step of breaking down fat for energy (beta oxidation) involves the removal of electrons from a lipid molecule. In the mitochondria these electrons ultimately end up in the electron transport chain — thus yielding ATP molecules (yep, this is how ATP is made). However, the electrons freed up in the first step of beta oxidation within the peroxisomes are passed directly to an O2 molecule, thus forming hydrogen peroxide (H2O2), which is immediately broken down into water and oxygen.
Since these electrons never make it to the electron transport chain, less ATP are formed compared to beta oxidation in the mitochondria. Dietary omega 3 fatty acids are very potent activators of peroxisomal lipid oxidation. They do this by increasing the activity and production of the key enzymes involved in peroxisomal beta oxidation(1;12;23). Therefore, omega 3’s increase fat burning that doesn’t ultimately produce a lot of ATP.
It should be pointed out here that most of the studies have looked at liver rather than skeletal muscle peroxisomes. Although the liver is a very metabolically active organ, its small size limits its impact on total daily energy expenditure. It’s still unknown exactly how much fat is oxidized in muscle peroxisomes, but one study has shown an increase in skeletal muscle peroxisome enzyme expression following a high omega 3 fatty acids diet(1), which could have profound impact on daily energy expenditures.
Yet another family of cells that are affected by dietary omega 3 fatty acids are called uncoupling proteins (UCPs). Uncoupling proteins are mitochondrial membrane proteins that allow an alternative route for protons to reenter the mitochondrial matrix. This decreases the electrochemical gradient and uncouples fuel oxidation and ATP production. In plain English, what this means is that uncoupling proteins allow us to oxidize fats, but instead of producing ATP we produce heat. (Editor’s note: for you bodybuilding types, this is one thing that the dangerous toxin DNP does — among other things that aren’t so pleasant).
For years it was thought that uncoupling proteins were only found in something called brown adipose tissue. Brown adipose tissue plays a very important role in maintaining body temperature. When things start to get a little too chilly, the uncoupling proteins kick in and lots of heat is produced (non-shivering thermogenesis). The only problem is, adult humans really don't have any brown adipose tissue to speak of.
A couple of years ago however, some science types discovered two more uncoupling proteins (creatively named UCP-2 and UCP-3). The good news is that they’re almost identical to the UCP-1 found in brown adipose tissue and we humans seem to have lots of them. UCP-2s are found in many tissues in the body, but UCP-3s seems to be located mainly in skeletal muscle.
Even though we’re in the infancy of research on UCPs, we do know that the expression of the UCPs has been shown to correlate with total body metabolic rate(11;18;19). Although there are very large gaps in our current knowledge of uncoupling proteins, it’s clear that a diet rich in omega 3 fatty acids will increase the amount of uncoupling proteins in our body(1;9). What remains unclear at this point is how much of an impact on total daily energy expenditure this represents.
It’s Time Leptin Leapt In
There’s one final dark horse mechanism that I feel I should at least touch on, and that’s the possible impact of omega-3 fatty acids on leptin production. Leptin is a hormone that is produced by adipocytes that essentially tries to tell the body that we have enough energy to last us for a while. The body responds to leptin by decreasing hunger and increasing metabolic rates(15). It’s generally accepted that in healthy individuals, leptin levels are positively correlated to body-fat levels (as body fat goes up, leptin levels go up).
However, rodents that are fed a diet rich in omega 3 fatty acids have circulating leptin levels that are substantially higher than what would be anticipated based on body fat(4). There isn't too much research looking at how omega-3 fatty acids interact with or affect leptin yet, but I believe this could be a very important mechanism and that we’ll see many more studies reporting on this in the near future.
Scientific Studies
In looking back over this article, hopefully I have convinced you that there are indeed some very good reasons to believe that a diet rich in omega 3 fatty acids can increase fat oxidation and metabolic rates. However, most of the studies that I have mentioned so far have been rodent studies. Also, several of them have only looked at isolated cells and not whole body living animals. Unfortunately, we can't always transfer results across species, or extrapolate results from a test tube to a living system. There is however, one fairly well controlled study done in humans that shows that all the theory may indeed be reality.
In this study, six subjects were fed a control diet for 3 weeks. During these 3 weeks they showed up at the lab and ate as much as they wanted of whatever they wanted. The researchers simply recorded everything they ate, and in what amounts. After a short washout period the subjects were once again fed at the lab for another 3 weeks. This time around they received the exact same meals as they ate during the control period with one very important exception. Every day of this 3-week period, 6 grams a day of saturated and omega 6 fatty acids in their food was replaced with 6 grams of omega 3 fatty acids (fish oil).
In the first paper that came out of this study, the researchers looked at how the fish-oil diet would impact fat oxidation following carbohydrate ingestion in 5 of those subjects(7). They found that the subjects were able to oxidize 35% more fat following carbohydrate ingestion after the three weeks on fish oil. This study didn't look at the cellular mechanisms that allowed the increased fat burning in the face of all that glucose, so we don't know exactly what happened.
They did however measure insulin levels, and they found that after three weeks on the fish oil the subjects produced significantly less insulin in response to the carbohydrates they ingested. As mentioned above, this should mean less malonyl CoA formation, which will mean more fat will be burned.
In the second paper that came out of this study, the authors examined how the 3 weeks of fish oil impacted body composition and resting metabolism(6). They found that the subjects lost on average a little less than a pound of fat as determined by dual-energy X-ray absorptiometry (DEXA) during the omega 3 fatty acids diet. There was also a slight increase in lean mass during the omega 3 fatty acids diet, but it wasn't statistically significant. Respiratory exchange ratio (a ratio of the amount of CO2 produced to the amount of O2 consumed) showed that the subjects were burning significantly more fat after the omega 3 fatty acids diet.
There was also an increase in the resting metabolic rates of the subjects after the omega 3 fatty acids diet, but this was no longer statistically significant when the slight increase in lean mass that I mentioned was taken into account. Unfortunately, these two papers are the only published studies using humans that has looked at how omega 3 fatty acids can affect our ability to burn fat and ultimately change body composition. Given the practical implications of this information, you can bet that many more are on their way.
Paydirt
The question I usually get from everyone about 10 seconds after I start to explain my research is, "So what should I eat to lose this fat?" Unfortunately, at this stage of the game, I can't say absolutely what is the best way of maximizing the fat burning potential of omega 3 fatty acids, but I can offer up some educated suggestions.
The first step, and most likely the most beneficial one, is to replace a substantial amount of the fat that is already in your diet with omega-3 fatty acids. Specifically, try and replace the saturated and omega-6 fatty acids in your diet with 3s. This is going to take out the negative fats and add the good ones without increasing the total daily fat, or caloric intake. The general public is slowly starting to become aware of the health benefits of omega 3 fatty acids, and it’s driving the food industry to start offering up many common foods that have been slightly modified to increase their omega-3 fatty acids content.
For the most part, these foods can be found in bigger supermarkets, in the health food section, and are clearly marked that they contain omega-3 fatty acids. Also look for foods that use canola oil instead of vegetable/corn/sunflower or safflower oils. Canola oil has a reasonable amount of 3s, and substantially less 6s than the aforementioned oils do.
Unfortunately, given the current state of affairs for the western diet, it’s probably unrealistic to think that people are going to be getting enough 3s simply through a normal diet. Therefore, I think it is wise that people supplement with some omega-3 oils on top of trying to eat a diet that is low in saturated and omega 6 fatty acids.
Unfortunately, the ideal amount of 3s to supplement with is completely unknown at this time. The rodent studies use a pretty big dose of 3s, and they usually eliminate most of the saturated and omega-6 fatty acids from the diet. This makes extrapolating these doses to free eating humans very challenging. In myself, I saw very good results with a tablespoon of flaxseed oil a day, plus about 10 grams of salmon oil per day (capsules plus the fat found in the salmon I eat on most days).
I chose these levels to bring my daily ratio of 6s/3's down into the 4/1 to 1/1 range which is recommended for optimal health (remember I was trying to cure asthma, not lose fat). Whether this is the ideal, too little, or too much still needs to be determined. But keep in mind that the study mentioned above replaced 6 grams a day of the bad fat with 6 grams a day of the good stuff and the subjects lost about a pound of pure ugly fat. In this day and age of miracle products claiming that you can lose 20 pounds in a week while you sleep, losing a pound of fat every 3 weeks may seem pretty insignificant. However, do the math and look at how that could affect your body composition over the course of a year and I think you'll agree that it is a pretty big deal.
Of course getting lots of 3s in your diet will also significantly decrease your risk of developing heart disease, many types of cancers, type-2 diabetes and a host of other scary diseases, but who cares, ‘cause you'll be looking good in your swimsuit.
Eric E Noreen, MS, is currently finishing his PhD in the area of Exercise and Nutritional Biochemistry at the University of Western Ontario. He has been the nutritional advisor for several of the athletic teams at the University of Western Ontario, along with lecturing at training camps for some of the Canadian National teams. By his own admission, he is also one sexy bastard.
Reference List:
1. Baillie, R. A., Takada, R., Nakamura, M., and Clarke, S. D. Coordinate induction of peroxisomal acyl-CoA oxidase and UCP-3 by dietary fish oil: a mechanism for decreased body fat deposition. Prostaglandins Leukot Essent Fatty Acids 60(5-6), 351-6. 199
3. Berge, R. K., Madsen, L., Vaagenes, H., Tronstad, K. J., Gottlicher, M., and Rustan, A. C. In contrast with docosahexaenoic acid, eicosapentaenoic acid and hypolipidaemic derivatives decrease hepatic synthesis and secretion of triacylglycerol by decreased diacylglycerol acyltransferase activity and stimulation of fatty acid oxidation. Biochem J 343 Pt 1, 191-7. 1999.
4. Cha, M. C. and Jones, P. J. Dietary fat type and energy restriction interactively influence plasma leptin concentration in rats. J Lipid Res 39(8), 1655-60. 1998.
5. Chicco, A., D'Alessandro, M. E., Karabatas, L., Gutman, R., and Lombardo, Y. B. Effect of moderate levels of dietary fish oil on insulin secretion and sensitivity, and pancreas insulin content in normal rats. Ann Nutr Metab 40(2), 61-70. 1996.
6. Couet, C., Delarue, P., Autoine, J. M., and Lamisse, F. Effect of dietary fish oil on body mass and basal fat oxidation in healthy adults. Int J Obes 21, 637-643. 1997.
7. Delarue, J., Couet, C., Cohen, R., Brechot, J. F., Antoine, J. M., and Lamisse, F. Effects of fish oil on metabolic responses to oral fructose and glucose loads in healthy humans. Am J Physiol 270(2 Pt 1), E353-62. 1996.
8. Fickova, M., Hubert, P., Cremel, G., and Leray, C. Dietary (n-3) and (n-6) polyunsaturated fatty acids rapidly modify fatty acid composition and insulin effects in rat adipocytes. J Nutr 128(3), 512-9. 1998.
9. Hun, C. S., Hasegawa, K., Kawabata, T., Kato, M., Shimokawa, T., and Kagawa, Y. Increased uncoupling protein2 mRNA in white adipose tissue, and decrease in leptin, visceral fat, blood glucose, and cholesterol in KK-Ay mice fed with eicosapentaenoic and docosahexaenoic acids in addition to linolenic acid. Biochem Biophys Res Commun 259(1), 85-90. 1999.
10. Ide, T., Kobayashi, H., Ashakumary, L., Rouyer, I. A., Takahashi, Y., Aoyama, T., Hashimoto, T., and Mizugaki, M. Comparative effects of perilla and fish oils on the activity and gene expression of fatty acid oxidation enzymes in rat liver. Biochim Biophys Acta 1485(1), 23-35. 2000.
11. Jekabsons, M. B., Gregoire, F. M., Schonfeld-Warden, N. A., Warden, C. H., and Horwitz, B. A. T(3) stimulates resting metabolism and UCP-2 and UCP-3 mRNA but not nonphosphorylating mitochondrial respiration in mice. Am J Physiol 277(2 Pt 1), E380-9. 1999.
12. Kumamoto, T. and Ide, T. Comparative effects of alpha- and gamma-linolenic acids on rat liver fatty acid oxidation. Lipids 33(7), 647-54. 1998.
13. Madsen, L., Rustan, A. C., Vaagenes, H., Berge, K., Dyroy, E., and Berge, R. K. Eicosapentaenoic and docosahexaenoic acid affect mitochondrial and peroxisomal fatty acid oxidation in relation to substrate preference. Lipids 34(9), 951-63. 1999.
14. Mori, T. A., Bao, D. Q., Burke, V., Puddey, I. B., Watts, G. F., and Beilin, L. J. Dietary fish as a major component of a weight-loss diet: effect on serum lipids, glucose, and insulin metabolism in overweight hypertensive subjects. Am J Clin Nutr 70(5), 817-25. 1999.
15. Pelleymounter, M. A., Cullen, M. J., Baker, M. B., Hecht, R., Winters, D., Boone, T., and Collins, F. Effects of the obese gene product on body weight regulation in ob/ob mice. Science 269(5223), 540-3. 1995.
16. Power, G. W. and Newsholme, E. A. Dietary fatty acids influence the activity and metabolic control of mitochondrial carnitine palmitoyltransferase I in rat heart and skeletal muscle. J Nutr 127(11), 2142-50. 1997.
17. Reddy, J. K. and Mannaerts, G. P. Peroxisomal lipid metabolism. Annu Rev Nutr 14, 343-70. 1994.
18. Schrauwen, P., Troost, F. J., Xia, J., Ravussin, E., and Saris, W. H. Skeletal muscle UCP2 and UCP3 expression in trained and untrained male subjects. Int J Obes Relat Metab Disord 23(9), 966-72. 1999.
19. Schrauwen, P., Xia, J., Bogardus, C., Pratley, R. E., and Ravussin, E. Skeletal muscle uncoupling protein 3 expression is a determinant of energy expenditure in Pima Indians. Diabetes 48(1), 146-9. 1999.
20. Sidossis, L. S., Gastaldelli, A., Klein, S., and Wolfe, R. R. Regulation of plasma fatty acid oxidation during low- and high-intensity exercise. Am J Physiol 272(6 Pt 1), E1065-70. 1997.
21. Sidossis, L. S., Stuart, C. A., Shulman, G. I., Lopaschuk, G. D., and Wolfe, R. R. Glucose plus insulin regulate fat oxidation by controlling the rate of fatty acid entry into the mitochondria. J Clin Invest 98(10), 2244-50. 1996.
22. Storlien, L. H., Jenkins, A. B., Chisholm, D. J., Pascoe, W. S., Khouri, S., and Kraegen, E. W. Influence of dietary fat composition on development of insulin resistance in rats. Relationship to muscle triglyceride and omega-3 fatty acids in muscle phospholipid. Diabetes 40(2), 280-9. 1991.
23. Vamecq, J., Vallee, L., de la Porte, P. L., Fontaine, M., de Craemer, D., van den Branden, C., Lafont, H., Grataroli, R., and Nalbone, G. Effect of various n-3/n-6 fatty acid ratio contents of high fat diets on rat liver and heart peroxisomal and mitochondrial beta-oxidation. Biochim Biophys Acta 1170(2), 151-6. 1993.
24. Willumsen, N., Skorve, J., Hexeberg, S., Rustan, A. C., and Berge, R. K. The hypotriglyceridemic effect of eicosapentaenoic acid in rats is reflected in increased mitochondrial fatty acid oxidation followed by diminished lipogenesis. Lipids 28(8), 683 90. 1993.
