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Saturday, 5 July 2008

Sugar, sugar and some fat

Isn't it interesting how you start a post and then little by little, new pieces come to fit into the whole? It happens so often with my blog-posts.
Anyway, onto the science. 4 articles, similar subject.
1) Why and how the sled dogs manage to keep running for miles without feeling fatigue and without decreasing their metabolism. And while burning calories like crazy. Which in normal conditions lead to energy depletion in the cells and fatigue. Mind you, the research is funded by whom? The army. Guess why. In any case, recently i'm finding out about different instincts that change the metabolism for optimal performance. Like the diving reflex we already discussed. Not to mention how in adrenalin rush, we can do stunts we'd never do otherwise.
2) A high-fat diet decreasing the number of seizures of epilepsy sick. Proved it's working. And I mean like HIGH-fat, like in drinking cream! Weird, huh?
3) A new way to watch sugars in cells
4) New insights on the number of fat cells. Very very smart way to watch over fat cells (or any cells). I loved it. Well, the research says fat cells stay constant trough our adulthood, but shrink or replenish to full size. What is interesting is that the brain obviously has some way to keep certain weight in varying conditions.

Researchers Seek to Demystify the Metabolic Magic of Sled Dogs

Published: May 6, 2008

When humans engage in highly strenuous exercise day after day, they start to metabolize the body’s reserves, depleting glycogen and fat stores. When cells run out of energy, a result is fatigue, and exercise grinds to a halt until those sources are replenished.

Dogs are different, in particular the sled dogs that run the annual Iditarod Trail Sled Dog Race in Alaska. This is a grueling 1,100-mile race, and studies show that the dogs somehow change their metabolism during the race.

Dr. Michael S. Davis, an associate professor of veterinary physiology at Oklahoma State University and an animal exercise researcher, said: “Before the race, the dogs’ metabolic makeup is similar to humans. Then suddenly they throw a switch — we don’t know what it is yet — that reverses all of that. In a 24-hour period, they go back to the same type of metabolic baseline you see in resting subjects. But it’s while they are running 100 miles a day.”

Dr. Davis, who studied the sled dogs, found they did not chew up their reserves and avoided the worst aspects of fatigue. He is pursuing the research for the Defense Advanced Research Projects Agency(!!!), which gave him a $1.4 million grant in 2003 to study the physiology of fatigue resistance of sled dogs.

“They have a hidden strategy that they can turn on,” Dr.Davis said. “We are confident that humans have the capacity for that strategy. We have to figure out how dogs are turning it on to turn it on in humans.”

Researchers have not demonstrated that ability in other species, but Dr. Davis said migratory mammals or birds could have it. Nor is it similar to the mammalian diving reflex that lets aquatic mammals like seals, otters and dolphins stay under water for long periods of time by slowing metabolic rates.

“The level of metabolism is staying the same,” Dr. Davis said. “It’s not slowing down their calorie burn rate.”

In fact, sled dogs in long-distance racing typically burn 240 calories a pound per day for one to two weeks nonstop. The average Tour de France cyclist burns 100 calories a pound of weight daily, researchers say.

How the dogs maintain such a high level of caloric burn for an extended period without tapping into their reserves of fat and glycogen (and thus grinding to a halt like the rest of us) is what makes them “magical,” Davis says.

If Dr. Davis and the Texas A&M researchers identify the biomarker, or “switch,” that could help the military understand and develop ways to control and prevent the physiological effects of fatigue in strenuous cases like combat.” source

Evidence a High-Fat Diet Works to Treat Epilepsy


Published: May 6, 2008

A formerly controversial high-fat diet has proved highly effective in reducing seizures in children whose epilepsy does not respond to medication, British researchers are reporting.

As the first randomized trial of the diet, the new study lends legitimacy to a treatment that has been used since the 1920s but has until recently been dismissed by many doctors as a marginal alternative therapy.

“This is the first time that we’ve really got Class 1 evidence that this diet works for treatment of epilepsy,” said Dr. J. Helen Cross, professor of pediatric neurology at University College London and Great Ormond Street Hospital. She is a principal investigator on the study, which will appear in the June issue of The Lancet Neurology.

Though its exact mechanism is uncertain, the diet appears to work by throwing the body into ketosis, forcing it to burn fat rather than sugar for energy. Breakfast on the diet might consist of bacon, eggs with cheese, and a cup of heavy cream diluted with water; some children drink oil to obtain the fats that they need. Every gram of food is weighed, and carbohydrates are almost entirely restricted. Breaking the diet with so much as a few cookies can cause seizures to flare up.

For the British trial, the researchers enrolled 145 children ages 2 to 16 who had never tried the diet, who were having at least seven seizures a week and who had failed to respond to at least two anticonvulsant drugs.

One group began the ketogenic diet immediately. The control group waited three months before starting it. In the first group, 38 percent of the children had seizure rates reduced by half, compared with 6 percent in the control group. Five children in the diet group had reductions exceeding 90 percent.

Perceptions of the diet have changed sharply in the last decade. In 1993, a Hollywood producer, Jim Abrahams, took his 1-year-old son, Charlie, to Dr. John M. Freeman at the Pediatric Epilepsy Center at Johns Hopkins, which was one of the few centers championing the diet. Within three days of starting the diet, Charlie’s incapacitating seizures, which had resisted multiple medications and surgery, stopped entirely.

With his wife, Nancy, Mr. Abrahams founded the Charlie Foundation to Help Cure Pediatric Epilepsy to promote education about the diet. He produced an instructional video for parents and a made-for-television movie, “First Do No Harm,” starring Meryl Streep as a mother who seeks out the diet for her child.

As a result of the Johns Hopkins work, research on the diet blossomed and it became a standard treatment at hospitals and epilepsy centers in the United States and abroad.

Although the diet has to be medically supervised, Dr. Shinnar said, it is a mistake to believe that it requires extensive hospital resources and a staff’s constant attention. “ source

Scientists Finally See Sugar Chains in Action


Published: May 6, 2008

Glycans don’t get a lot of publicity compared with DNA and RNA, but they play important roles in the life of the cell. These sugar chains, also known as oligosaccharides, are often found on cell surfaces, where they are involved in cell-to-cell interactions, both healthy (like embryonic growth) and unhealthy (like viral infection).

While scientists know a lot about glycans (a whole subfield, glycobiology, has taken off in the past several decades), understanding has been hampered by an inability to see these molecules in action in living cells.

That is changing, thanks to work by Carolyn R. Bertozzi and colleagues at the University of California, Berkeley. They report in Science that they have successfully imaged glycans on cell surfaces in living zebrafish embryos.

The researchers used some complicated chemistry, introducing sugars modified with azide functional groups that are incorporated into glycans as they are synthesized. The azides enable the glycans to react with fluorophores, molecules that fluoresce when exposed to light of specific wavelengths. Using light microscopy, the researchers were then able to detect increases in glycan synthesis in the jaw, pectoral fins and other parts of the developing embryo.

They also came up with a neat trick to follow glycan production over time, taking advantage of the fact that fluorophores cannot penetrate into the cell. Existing surface glycans were treated with a fluorophore of a certain color, but this fluorophore could not reach just-synthesized glycans that were not yet at the surface. An hour or two later a different fluorophore was introduced to react with these glycans, now at the surface — so “old” and “new” glycans show up as different colors. source

Study Finds That Fat Cells Die and Are Replaced

Published: May 5, 2008

Every year, whether you are fat or thin, whether you lose weight or gain, 10 percent of your fat cells die. And every year, those cells that die are replaced with new fat cells, researchers in Sweden reported Sunday.

The result is that the total number of fat cells in the body remains the same, year after year throughout adulthood. Losing or gaining weight affects only the amount of fat stored in the cells, not the number of cells.

The finding was published online Sunday in the journal Nature.

Obesity investigators say the study raises tantalizing questions: What determines how many fat cells are in a person’s body? When is that number determined? Is there a way to intervene so people end up with fewer fat cells when they reach adulthood? And could obesity be treated by making fat cells die faster than they are born?

But for now, researchers say, they do not have a clue about how to answer those questions.

“There is a system waiting to be discovered,” said Dr. Jeffrey S. Flier, an obesity researcher and dean of Harvard Medical School.

Dr. Flier and other obesity researchers cautioned, though, that even if scientists knew how the fat cell system worked, it was not clear that it would be safe or effective to treat obesity by intervening. One of the hard lessons of the past couple of decades has been that the body has redundant controls to maintain weight.

“I suspect that the body’s regulation of weight is so complex that if you intervene at this site, something else is going to happen to neutralize this intervention,” Dr. Salans said.

But the discovery is also leading to new ways to address other questions about obesity. For example, what happens to people who are thin until adulthood and then gain a lot of weight? The study focused on people who had been fat since childhood, the usual route for adult obesity. The situation may be different for people who got fat later. They may actually grow new fat cells — the ones they had may have become so stuffed with fat that they could hold no more.

Another question is whether fat cells removed with liposuction grow back.

Both questions are now under investigation by the Swedish researchers.

In a way, Dr. Flier noted, the discovery is a sort of back-to-the-future moment. There was a time a few decades ago, before the current interest in how the brain regulates how much is eaten, when obesity researchers spent all their time studying and discussing fat cells. Investigators discovered that fat people had more fat cells than thin people and that fat cells shrank with weight loss and bulged with weight gain.

Fat cells, the hypothesis said, are laid down early in life and after that, they can change only in size, not in number. When people lose weight and their fat cells shrink, that creates a signal to fill the cells again, making people regain.

But the discussions stalled. It was not clear what to do about those discoveries or what they meant to efforts to help people lose weight. And no one had a method to ask whether fat cells were being created and destroyed during life. Few even thought to ask that question.

That changed only recently when the new paper’s first author, Kirsty L. Spalding, a neurobiologist at the Karolinska Institute in Sweden, developed a way to ask whether new cells grow in the cortical and cerebellum regions of the human brain. She found no new cells there since birth. One day, she was giving a talk on her brain study when a scientist in the audience, Erik Arner, suggested she use the method to look at fat cells. (Dr. Arner is the second author of Dr. Spalding’s paper.) The method for dating human cells takes advantage of an effect caused by above-ground nuclear bomb testing that took place from 1955 to 1963.

When the bombs were tested, their radioactivity created a spike in the amount of a carbon isotope, C14, in the atmosphere. The C14 made its way into plants and animals that ate the plants. When people ate those plants and meat from the animals, the C14 was incorporated into their human DNA. After the nuclear test ban, C14 levels started to drop. The result is that every cell has a C14 level that reflects the level in the atmosphere at the time the cell was born.

First the researchers confirmed that the number of fat cells remained constant in adults. Obese people who had weight loss surgery had as many fat cells two years after the surgery as before it, even though they were much thinner.

Then the investigators asked whether fat cells were being born and dying. To do that, they examined fat cells taken from 35 people, fat and lean, who had had liposuction or abdominal wall reconstruction. The amount of C14 in the cells would reveal how old the cells were. Since the number of fat cells remained constant, the number being born had to equal the number dying. And a mathematical model would reveal the dynamics of the cell turnover.

“We found the cells were really quite young,” Dr. Spalding said. “That tells us new cells are being born.”

She added: “The million-dollar question now is, What regulates this process? And where can we intervene?” source

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