Sunday, June 28, 2009

Glycogen Stores Energy

Adipose or fat tissue stores most of the body's energy reserves in the form of triglycerides. The body is also able to store a limited amount of energy as carbohydrates, and it does it in the form of glycogen.

Glycogen is a large, complex molecule made up of branched chains of glucose molecules. The illustration above, found at Wikipedia, shows a cross section through the middle of a spherical glycogen molecule. At the center is a glycosyltransferase enzyme. The enzyme takes glucose-6-phosphate (the form of glucose found inside a cell) and strings it together as long, branched chains. In the picture above, each tiny circle represents a glucose molecule. The glycogen molecules are therefore large polymers of glucose which are then packed together and stored in granules in the cytosol of liver and muscle cells.

Glycogen makes up as much as 10% of the weight of the liver and represents about 100 grams of glucose in the adult human. Glycogen in the liver can be broken down first into glucose-6-phosphate and then into glucose. In the form of glucose it can be released back into the circulation. In a previous post we have seen that release of glucose from liver glycogen is the body's chief means of maintaining a normal blood sugar between meals.

Glycogen can also be stored in skeletal muscle, as illustrated in the figure below.

When glucose is present in the blood (and in a living person, it always is), a muscle cell is able to take up the glucose both actively and passively. Once the glucose is inside the muscle cell, the glucose molecule is phosphorylated. This adds a large ionic group which makes it impossible for the glucose to diffuse back out of the muscle cell. The phosphorylated glucose then has two possible fates.

  1. It can proceed directly into glycolysis and be turned into pyruvate. If there is enough oxygen available, the pyruvate will enter the mitochondria and be turned into lots of ATP, the energy currency of the cell. If there is not enough oxygen available, the pyruvate will be turned into lactic acid plus a little ATP. The buildup of lactic acid produces a sensation of pain, and the pain will continue until the lactic acid diffuses back out of the muscle cell, a process which takes about an hour.
  2. Alternatively, the phosphorylated glucose may instead be stored in the muscle in the form of glycogen. Muscle glycogen makes up only 1-2% of the weight of skeletal muscle, but because the body contains so much skeletal muscle, the total quantity of muscle glycogen in an adult is about 200 grams.

What makes muscle glycogen different from liver glycogen is that when muscle glycogen is broken down, it cannot leave the cell. Muscle cells lack the enzyme that removes the large ionic phosphate group from the glucose, and the glucose cannot be returned to the blood. For that reason, the phosphorylated glucose must be used inside the muscle cell. What then?

No problem. The phosphorylated glucose feeds right into the glycolytic pathway inside the muscle cell, where it is turned into pyruvate and lots of ATP or into lactic acid and a little ATP, depending on the amount of oxygen available to it.

When we hear about carb loading for athletic events, it is tempting to think that most of the energy in our muscles comes from carbohydrates. It does not. There is only a little glycogen stored in each muscle cell, and it is easily exhausted. Compare the 200 grams of total muscle glycogen with the pounds of fat available in a healthy individual, and it becomes obvious that muscle cells must use free fatty acids for most of their energy. This is illustrated on the right side of the illustration above. As seen previously (How Are Fats Metabolized?), once the free fatty acids are inside the cell, they are broken down very efficiently to produce much more ATP than could be obtained from an equal number of glucose molecules. However, when an extra burst of energy is needed, muscle cells are able to use the glucose they have stored in glycogen granules to supply a little more ATP than they would normally receive from using fatty acids alone.

Thursday, June 18, 2009

Low-Carb Doesn't Work!

Low-carbers hear it over and over. "I can't get to goal." "Nobody I know has reached goal." "Almost all the low-carb gurus are obese."

There are many reasons for weight loss to slow or stop while low-carbing. Read any of Dr. Atkins' books or follow any of the low-carb websites and you will find lots of possible explanations, including factors like low thyroid function and yeast infections.

Another reason for failure to lose weight and for weight regain on low-carb is seldom mentioned. An example is pictured above--low-carb substitutes for high-carb foods. (The picture is taken from a post about a low-carb sponge cake at Cafe Nilson.) But low-carb substitute foods are still low-carb! Why should they interfere with a low-carb diet?

A 2005 study on binge eating in rats may give some insight. In one experiment, the rats were separated into two groups, food-sated and food-restricted. They were then exposed to several food choices, including normal rat chow and a cereal called "Choc and Crisp" which appears to be a German version of Cocoa Krispies. The food-restricted rats took about three minutes to find the rat chow, and they ate about half a gram of it. By contrast, they found Choc and Crisp in only ten seconds and when they reached it, they ate nearly five grams of it.

As expected, the food-sated rats were not interested in the rat chow. They took about 20 minutes to wander over to it and when they got there, they didn't eat it. However, even though these rats had already eaten until they were full, the food-sated group took one fiftieth of that time (25 seconds) to find the Choc and Crisp, and once they reached it, they ate 3 grams of it, or 60% of the amount the food-restricted rats had consumed.

To confirm these responses, each rat was put on a runway with a food-filled box at the other end. When the goal box contained rat chow, it took the food-sated group about 40 seconds to reach the goal, while the food-deprived ones took about 10 seconds. Not surprising. However, when the goal box contained Choc and Crisp, both groups made the trip in about five seconds, though the food-restricted group was a little faster. One might expect that after the first day, the rats would be less excited about the Choc and Crisp, but the time needed to reach the goal boxes persisted over ten consecutive trial days.

The obvious conclusion is that if you feed pet rats with Cocoa Krispies, they will probably get fat. A less obvious inference might be that if a low-carber is freqently exposed to low-carb versions of very enticing high-carb foods, he or she will probably eat those foods to excess. The rat study indicates that the easy availability of very palatable foods may shut off the body's ability to adjust food intake to match energy expenditure. What happens in a rat does not necessarily happen in a human, but their tendency to eat much more of a very palatable food is definitely something to consider when low-carbers have a hard time reaching or maintaining their goal weight.

Tuesday, June 9, 2009

How Are Fats Metabolized?

In a previous post we saw that the fats we eat are made up of a group of molecules called tri-glycer-ides--three fatty acids covalently bonded to one glycerol backbone. In a subsequent post we learned that triglycerides are absorbed, packaged and transported to the cells of the body through the circulatory system. In muscle cells these triglycerides can be used for energy, and in adipose tissue (fat cells), they can be stored for future use.

What happens when it is time to use the fat we have stored in our bodies? The first thing that must happen is that insulin levels must be low. In the presence of low insulin, the hormones glucagon from the pancreas or epinephrine from the adrenal glands will stimulate the activity of hormone-sensitive lipase (HSL). Hormone-sensitive lipase (plus another enzyme called diacylglycerol lipase) will convert a triglyceride stored in a fat cell back into one glycerol molecule plus three fatty acids.

Once the fatty acids are detached from the glycerol backbone, they are able to dissolve in the cell wall of the adipocyte or fat cell. From there they are able to diffuse passively out of the adipocyte back into the blood, where they attach themselves to serum albumin and are carried throughout the body. The free fatty acids are able to diffuse passively into tissues as well.

Once inside one of the body's cells, the free fatty acid is activated with a "handle" called CoA. (Pronunciation note: CoA rhymes with "No Way." It does NOT rhyme with Boa.) The fatty acid plus its handle is called acyl-CoA. The acyl-CoA heads for a mitochondrion, a small organelle that functions as the powerhouse of most cells. Once inside the mitochondrion, the acyl-CoA is dismantled, two carbon units at a time. Each time a two-carbon unit is released, energy is produced from the breaking of the covalent bonds. Not only that, the two-carbon units themselves enter something called the TCA or tricarboxylic acid cycle where they are broken down further to produce carbon dioxide plus even more energy.

The energy released by all of these chemical reactions eventually results in the formation of many molecules of adenosine-5'-triphosphate or ATP. ATP molecules are the energy currency of the cell. The energy contained in ATP molecules is used for activities such as building the tissues the body needs, fueling the reactions that enable the body to move, and coordinating the activities the body needs to stay alive.

Did you ever wonder why robots need some sort of external or rechargeable power supply but people do not? The robot relies on electricity for its energy source. People, by contrast, rely on ATP for their energy and, amazingly enough, that ATP can be produced from something as simple as the fat they eat for dinner.

Monday, June 1, 2009

The Swedes Are Eating More Butter!

The graph above shows tons of butter (ton/Ă¥r) sold per year in Sweden. From April 2007 to April 2008, sales of butter in Sweden went up by 13%. Therein lies a tale.

Doctor Annika Dahlqvist was a family practitioner at the Njurunda clinic in Sweden when her daughter, a physician in training, took part in a low-carbohydrate dietary study. The results were so impressive that Dr. Dahlqvist tried the low-carb diet for herself. She was pleased that she was able to lose weight, and she also noticed that her problems with gastrointestinal inflammation and fibromyalgia were significantly improved. She began recommending a low-carb, high-fat (LCHF) diet to her patients who suffered from type 2 diabetes and obesity.

The idea of a low-carb, high-fat way of eating was no more welcome in Sweden than it has been in the United States. In December 2005, the chairman of the Swedish National Association of Dieticians made a formal complaint to the Swedish National Board of Health and Welfare, questioning Dr. Dahlqvist’s low-carb dietary advice and suggesting that it might jeopardize the safety of her patients. Dr. Dahlqvist was threatened with the loss of her medical license.

Although Dr. Dahlqvist’s LCHF diet was quite compatible with a traditional Atkins-type diet, she stopped treating patients and instead began working on a blog and giving lectures to spread the word about LCHF.

Flash forward to January 17, 2008.

Professor Christian Berne, one of Sweden’s leading diabetes experts, had carefully investigated the case against Dr. Dahlqvist and presented his findings to the Swedish National Board of Health and Welfare. He said, “...a low-carbohydrate diet can today be said to be in accordance with science and well-tried experience for reducing [obesity] and type 2 diabetes...a number of trials has shown no effects in the shorter run and that no evidence for it being harmful has emerged in systematic literature researches performed so far. [There is] no scientific support yet for treatments in excess of 1 year. A thorough evaluation of long time treatment results is therefore an important demand on the practitioner.”

By objecting to the low-carb, high-fat diet, the chairman of the Swedish National Association of Dieticians had inadvertently given it validation. In fact, because of the governmental investigation into the scientific support for LCHF, the diet was approved as an alternative approach for the treatment of type 2 diabetes and obesity. New Board guidelines are expected to be completed by autumn of 2009.

As for Dr. Dahlqvist, she continues to lecture, to blog, and to gain in popularity in her native land. In 2008, Radio Västernorrland listeners chose her as Personality of the Year. The seventy percent who voted for her said, “...she stood up against the Health and Welfare and Food Administration's current dietary recommendations, campaigning instead for a diet she believes in—low in carbohydrate but high in natural animal fat.”

Even more impressively, Swedish consumers have started to consider whole milk and butter more natural and healthful than reduced-fat products and are now changing their habits to buy more of the former and less of the latter. There are still plenty of dietary traditionalists in Sweden, but for some people at least, butter is now a health food.