Posts Tagged ‘Weight loss’

 

Researchers in Purdue University’s School of Veterinary Medicine have discovered genetic and drug-treatment methods to arrest the type of muscle atrophy often caused by muscle disuse, as well as aging and diseases such as cancer.
The findings might eventually benefit people who have been injured or suffer from diseases that cause them to be bedridden and lose muscle mass, or sometimes limbs, due to atrophy, said Amber Pond, a research scientist in the school’s Department of Basic Medical Sciences.
“The weight loss and muscle wasting that occurs in patients with cancer or other diseases seriously compromises their well-being and is correlated with a poor chance for recovery,” Pond said. “In addition, muscle weakness caused by atrophy during aging can lead to serious falls and bone loss. Exercise is the most beneficial strategy to treat atrophy. However, many individuals are too ill to adequately participate in exercise programs.
“We’ve found a chemical ‘switch’ in the body that allows us to turn atrophy on, and, from that, we also have learned how to turn atrophy off.”
Findings based on the research, funded in large part by the American Heart Association, are detailed in a study available online today (Wednesday, May 24) in The FASEB Journal, published by the Federation of American Societies for Experimental Biology. The study will be in the journal’s print edition in July.
The research team found atrophy of skeletal muscle in mice could be inhibited with both gene therapy and drug treatment using astemizole (as-TEM-uh-zole), an antihistamine. This new insight has potential in many different areas of research, Pond said.
“We have discovered a direct link between atrophy and a protein in the skeletal muscle,” Pond said. “This led us to develop methods that would block the protein’s ability to cause atrophy. Through drug treatment, we were able to block atrophy, allowing muscle to retain 97 percent of its original fiber size in the face of atrophy.”
Astemizole, which was withdrawn from the market in 2000 because of its potential to cause serious cardiovascular problems, wouldn’t be suitable for use in humans, Pond said. The drug can be used in mice because it doesn’t affect their hearts to the same extent.
“Astemizole administration to humans poses too great a risk,” Pond said. “There’s a need for more study to avoid those side effects, but the key is that we found a protein capable of sensing muscle disuse and initiating atrophy.”
In the drug study, researchers used four groups of mice: a control group, a second group that was given astemizole, and two additional groups in which muscle atrophy was introduced. One of these two groups received astemizole while the second did not. Both of these groups were placed in cages constructed to elevate them so that they were unable to place any weight on their back legs.
“Use of the custom cages to produce atrophy was established in the ’80s for simulation of NASA space flight; you can’t mimic these effects on muscle and bone in cell culture,” said Kevin Hannon, associate professor of developmental anatomy and one of the study’s authors. “The mice were able to move around the cage and eat and drink on their own. We monitored their food and water intake and overall health and ensured that they were playing and eating normally.”
This method allowed the scientists to demonstrate the effects of skeletal muscle atrophy and investigate reasons for the link with the Merg1a protein. The Merg1a protein is a channel that normally passes a small electrical current across the cell.
The researchers implanted a gene into the skeletal muscle that resulted in a mutant form of this protein that combines with the normal protein and stops the current. The researchers found that the mutant protein would inhibit atrophy in mice whose ability to use their back legs was limited.
Because gene therapy is not yet a practical treatment option in humans, the researchers decided to go a step further and stop the function of the protein with astemizole, which is a known “Merg1a channel blocker.” The researchers found that the drug produced basically the same results as the gene therapy. In fact, muscle size increased in mice in the group that were given the drug without any other treatment.
“We are now looking at the differences in the structure of the heart and the skeleton to give us clues on how to specifically target muscles without the cardiac side effects,” Pond said.
###
This research also was partially supported by the U.S. Department of Agriculture and Purdue’s basic medical sciences department.
Writer: Maggie Morris, (765) 494-2432, maggiemorris@purdue.edu
Sources: Amber Pond, (765) 494-6185, pond@purdue.edu 
Kevin Hannon, (765) 494-5949, hannonk@purdue.edu
Related Web sites: 
Purdue School of Veterinary Medicine: http://www.vet.purdue.edu/ 

Researchers in Purdue University’s School of Veterinary Medicine have discovered genetic and drug-treatment methods to arrest the type of muscle atrophy often caused by muscle disuse, as well as aging and diseases such as cancer.

The findings might eventually benefit people who have been injured or suffer from diseases that cause them to be bedridden and lose muscle mass, or sometimes limbs, due to atrophy, said Amber Pond, a research scientist in the school’s Department of Basic Medical Sciences.

“The weight loss and muscle wasting that occurs in patients with cancer or other diseases seriously compromises their well-being and is correlated with a poor chance for recovery,” Pond said. “In addition, muscle weakness caused by atrophy during aging can lead to serious falls and bone loss. Exercise is the most beneficial strategy to treat atrophy. However, many individuals are too ill to adequately participate in exercise programs.

“We’ve found a chemical ‘switch’ in the body that allows us to turn atrophy on, and, from that, we also have learned how to turn atrophy off.”

Findings based on the research, funded in large part by the American Heart Association, are detailed in a study available online today (Wednesday, May 24) in The FASEB Journal, published by the Federation of American Societies for Experimental Biology. The study will be in the journal’s print edition in July.

The research team found atrophy of skeletal muscle in mice could be inhibited with both gene therapy and drug treatment using astemizole (as-TEM-uh-zole), an antihistamine. This new insight has potential in many different areas of research, Pond said.

“We have discovered a direct link between atrophy and a protein in the skeletal muscle,” Pond said. “This led us to develop methods that would block the protein’s ability to cause atrophy. Through drug treatment, we were able to block atrophy, allowing muscle to retain 97 percent of its original fiber size in the face of atrophy.”

Astemizole, which was withdrawn from the market in 2000 because of its potential to cause serious cardiovascular problems, wouldn’t be suitable for use in humans, Pond said. The drug can be used in mice because it doesn’t affect their hearts to the same extent.

“Astemizole administration to humans poses too great a risk,” Pond said. “There’s a need for more study to avoid those side effects, but the key is that we found a protein capable of sensing muscle disuse and initiating atrophy.”

In the drug study, researchers used four groups of mice: a control group, a second group that was given astemizole, and two additional groups in which muscle atrophy was introduced. One of these two groups received astemizole while the second did not. Both of these groups were placed in cages constructed to elevate them so that they were unable to place any weight on their back legs.

“Use of the custom cages to produce atrophy was established in the ’80s for simulation of NASA space flight; you can’t mimic these effects on muscle and bone in cell culture,” said Kevin Hannon, associate professor of developmental anatomy and one of the study’s authors. “The mice were able to move around the cage and eat and drink on their own. We monitored their food and water intake and overall health and ensured that they were playing and eating normally.”

This method allowed the scientists to demonstrate the effects of skeletal muscle atrophy and investigate reasons for the link with the Merg1a protein. The Merg1a protein is a channel that normally passes a small electrical current across the cell.

The researchers implanted a gene into the skeletal muscle that resulted in a mutant form of this protein that combines with the normal protein and stops the current. The researchers found that the mutant protein would inhibit atrophy in mice whose ability to use their back legs was limited.

Because gene therapy is not yet a practical treatment option in humans, the researchers decided to go a step further and stop the function of the protein with astemizole, which is a known “Merg1a channel blocker.” The researchers found that the drug produced basically the same results as the gene therapy. In fact, muscle size increased in mice in the group that were given the drug without any other treatment.

“We are now looking at the differences in the structure of the heart and the skeleton to give us clues on how to specifically target muscles without the cardiac side effects,” Pond said.

———————————–
Article adapted by MD Sports from original press release.
———————————–

Contact: Maggie Morris
Purdue University 

This research also was partially supported by the U.S. Department of Agriculture and Purdue’s basic medical sciences department.

Related Web sites: 
Purdue School of Veterinary Medicine: http://www.vet.purdue.edu/ 
FASEB Journal: http://www.fasebj.org/ 

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It’s fewer calories not Carbs or fluid loss responsible for weight loss.

PHILADELPHIA —  A new three-week in-hospital study of 10 volunteers found that during the two-week period on a strictly controlled very-low carbohydrate diet, participants lost an average of 3.6 pounds, voluntarily reduced their calorie intake from 3,111 calories per day to 2,164 calories per day, and did not eat more of the readily available fat and protein to make up for the lost carbohydrate calories.The study, “Effect of a Low-Carbohydrate Diet on Appetite, Blood Glucose Levels, and Insulin Resistance in Obese Patients with Type 2 Diabetes,” compared a very low-carbohydrate diet with a regular diet. It is published in the March 15, 2005, issue of Annals of Internal Medicine and is the subject of a video news release.

During the first study week, participants, who were obese and had mild type 2 diabetes mellitus, ate a regular diet in which they could eat anything and as much as they wanted. They ate about 3,000 calories and 300 grams of carbohydrates per day and remained at entry weight.

In the following two weeks, when restricted to 20 grams of carbohydrates per day, as specified in the Atkins induction diet, and despite readily available protein and fat foods, the participants voluntarily ate about 1,000 fewer calories per day, a calorie intake considered appropriate to their height.

Participants’ blood sugar improved on the low-carb diet, with better insulin sensitivity and lower blood triglycerides and cholesterol levels.

“We proved that people lose weight on the Atkins diet because they eat less (consume fewer calories), not because they get bored with the diet or lose body water or because the carbohydrate calories are treated differently by the body than fat or protein calories,” said Guenther Boden, MD, a Laura H. Carnell Professor of Medicine and chief of the division of endocrinology/diabetes/metabolism at Temple University School of Medicine.

“All the weight loss was in fat,” said Boden, the lead study author. “We weighed and measured every calorie that participants ate and every calorie they spent. We knew what went in and what went out.”

“On the very low-fat diet, participants spontaneously reduced their calories by about 1,000 per day. One gram of fat equals 9 calories, so, doing the math, you can determine how much fat will be lost by cutting 1,000 calories.”

Boden also believes that the carbohydrates actually stimulated the patients’ big appetites during the regular-diet week.

“Participants went from an excessive caloric intake to a normal caloric intake for their height and weight when we reduced their carbohydrates. This indicates to me that it was the carbohydrates that stimulated the excessive appetite,” Boden said.

Throughout the three-week study, researchers weighed all food, monitored exercise, measured participants’ calorie energy intake, expenditure and body water composition, and tested blood sugar, cholesterol, and several hormone levels believed to be involved in appetite regulation.

“You don’t have to cut carbs as drastically as participants did,” said Boden. “If you cut carbs modestly, you cut calories, and you’ll lose weight.”

“The message is: Calories count,” Boden said. “If you want to lose weight, you have to decrease your food intake or increase your physical activity. It helps to know that carbohydrates make it more difficult to reduce food intake. So cutting the carbohydrates, at least to some extent, will help keep down the caloric intake. With fewer carbohydrates, you’re going to eat fewer total calories a day.”

George A. Bray, MD, Chief, Division of Clinical Obesity and Metabolism at the Pennington Biomedical Research Center in Baton Rouge, La., and a well-known researcher in obesity and diabetes, wrote an accompanying editorial, “Is There Something Special about Low-Carbohydrate Diets?”

Bray notes that the study is small but calls it “a nicely done, short-term metabolic ward study.” He says that using “many different diets with different approaches to food restriction for individual patients at different times in their efforts to lose weight may be the most effective way a clinician can use the available diets. … (I) am not yet convinced that one diet has any more value than another — they all have value.”

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Article adapted by MD Sports from original press release.
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Contact: Susan Anderson
American College of Physicians