Glutamine could help people with obesity reduce fat mass and inflammation

Glutamine could help people with obesity reduce fat mass and inflammation

Glutamine could help people with obesity reduce fat mass and inflammation

Lower glutamine-levels were also associated with larger fat cell size and higher body fat percentage independently of body-mass index (BMI), according to the study.

#glutamine #leanmass #inflammation

”Glutamine links obesity to inflammation in human white adipose tissue,” Paul Petrus, Simon Lecoutre, Lucile Dollet, Clotilde Wiel, André Sulen, Hui Gao, Beatriz Tavira, Jurga Laurencikiene, Olav Rooyackers, Antonio Checa, Iyadh Douagi, Craig E. Wheelock, Peter Arner, Mark McCarthy, Martin O. Bergo, Laurienne Edgar, Robin P. Choudhury, Myriam Aouadi, Anna Krookand Mikael Rydén, Cell Metabolism, online December 19, 2019.

Resveratrol helps preserve muscle in space

Resveratrol helps preserve muscle in space

Resveratrol helps preserve muscle in space

“Resveratrol treatment promotes muscle growth in diabetic or unloaded animals, by increasing insulin sensitivity and glucose uptake in the muscle fibers. This is relevant for astronauts, who are known to develop reduced insulin sensitivity during spaceflight.”

Marie Mortreux, Daniela Riveros, Mary L. Bouxsein, Seward B. Rutkove. A Moderate Daily Dose of Resveratrol Mitigates Muscle Deconditioning in a Martian Gravity Analog. Frontiers in Physiology, 2019; 10 DOI: 10.3389/fphys.2019.00899

#resveratrol #microgravity #mars

Bedtime protein for bigger gains? Here’s the scoop

Bedtime protein for bigger gains? Here’s the scoop

Downing a casein shake just before sleep increases muscle mass and strength gains from resistance training, without ‘making you fat’ — but is the effect any different to your regular post-workout protein supplement.

Tim Snijders, Jorn Trommelen, Imre W. K. Kouw, Andrew M. Holwerda, Lex B. Verdijk, Luc J. C. van Loon. The Impact of Pre-sleep Protein Ingestion on the Skeletal Muscle Adaptive Response to Exercise in Humans: An Update. Frontiers in Nutrition, 2019; 6 DOI: 10.3389/fnut.2019.00017

#nighttimeprotein #casein #muscle

Research Paves Way for Development of Cyborg Moth ‘Biobots’

Matt Shipman | News Services | 919.515.6386

Dr. Alper Bozkurt | 919.515.7349

Release Date: 08.20.14

North Carolina State University researchers have developed methods for electronically manipulating the flight muscles of moths and for monitoring the electrical signals moths use to control those muscles. The work opens the door to the development of remotely-controlled moths, or “biobots,” for use in emergency response.

“In the big picture, we want to know whether we can control the movement of moths for use in applications such as search and rescue operations,” says Dr. Alper Bozkurt, an assistant professor of electrical and computer engineering at NC State and co-author of a paper on the work. “The idea would be to attach sensors to moths in order to create a flexible, aerial sensor network that can identify survivors or public health hazards in the wake of a disaster.”

Continue reading “Research Paves Way for Development of Cyborg Moth ‘Biobots’”

The big male nose

New study explains why men’s noses are bigger than women’s
Richard C. Lewis | 2013.11.18 | 11:26 AM
nasal comparison
Male noses grow disproportionately larger than female noses beginning at puberty, a University of Iowa study has found. The reason: Males need to breathe in more oxygen to feed muscle mass than females. Image courtesy of the College of Dentistry.

Human noses come in all shapes and sizes. But one feature seems to hold true: Men’s noses are bigger than women’s.

Continue reading “The big male nose”

Lift weights to lower blood sugar? White muscle helps keep blood glucose levels under control

Contact: Laura J. Williams 734-615-4862 University of Michigan

ANN ARBOR—Researchers in the Life Sciences Institute at the University of Michigan have challenged a long-held belief that whitening of skeletal muscle in diabetes is harmful.

In fact, the white muscle that increases with resistance training, age and diabetes helps keep blood sugar in check, the researchers showed.

In addition, the insights from the molecular pathways involved in this phenomenon and identified in the study may point the way to potential drug targets for obesity and metabolic disease.

“We wanted to figure out the relationship between muscle types and body metabolism, how the muscles were made, and also what kind of influence they have on diseases like type 2 diabetes,” said Jiandie Lin, Life Sciences Institute faculty member and associate professor at the U-M Medical School.

Lin’s findings are scheduled to be published online April 7 in Nature Medicine.

Much like poultry has light and dark meat, mammals have a range of muscles: red, white and those in between. Red muscle, which gets its color in part from mitochondria, prevails in people who engage in endurance training, such as marathon runners. White muscle dominates in the bodies of weightlifters and sprinters—people who require short, intense bursts of energy.

“Most people are in the middle and have a mix of red and white,” Lin said.

When you exercise, nerves signal your muscles to contract, and the muscle needs energy. In response to a signal to lift a heavy weight, white muscles use glycogen to generate adenosine triphosphate (ATP)—energy the cells can use to complete the task. While this process, called glycolysis, can produce a lot of power for a short time, the glycogen fuel soon depletes.

However, if the brain tells the muscle to run a slow and steady long-distance race, the mitochondria in red muscles primarily use fat oxidation instead of glycogen breakdown to generate ATP. The supply of energy lasts much longer but doesn’t provide the burst of strength that comes from glycolysis.

People with diabetes see whitening of the mix of muscle.

“For a long time, the red-to-white shift was thought to make muscle less responsive to insulin, a hormone that lowers blood sugar,” Lin said. “But this idea is far from proven. You lose red muscle when you age or develop diabetes, but is that really the culprit?”

To find out, the team set out to find a protein that drives the formation of white muscle. They sifted through microarray data sets from public databases and identified a list of candidate proteins that were prevalent in white muscle but not in red.

Further studies led the team to focus on a protein called BAF60c, a sort of “zip code” mechanism that tells the cells when and how to express certain genes. The Lin team made a transgenic mouse model to increase BAF60c only in the skeletal muscle. One of the first things they noticed was that mice with more BAF60c had muscles that looked paler.

“That was a good hint that we were going in the white-muscle direction,” said lead author Zhuo-xian Meng, a research fellow in Lin’s lab.

They used electron microscopy to see the abundance of mitochondria within the muscle, and confirmed that muscle from BAF60c transgenic mice had less mitochondria than the normal controls.

“We saw predicted changes in molecular markers, but the ultimate test would be seeing how the mouse could run,” Lin said.

If the BAF60c mice could run powerfully for short distances but tired quickly, the scientists would be able to confirm that the BAF60c pathway was a key part of the creation of white muscle.

Using mouse treadmills, they compared the endurance of BAF60c mice to a control group of normal mice, and found that the BAF60c transgenic mice could only run about 60 percent of the time that the control group could before tiring.

“White muscle uses glycogen, and the transgenic mice depleted their muscles’ supplies of glycogen very quickly,” Lin said.

After some follow-up experiments to figure out exactly which molecules were controlled by BAF60c, Lin and his team were confident that they had identified major players responsible for promoting white muscle formation. Now that they knew how to make more white muscle in animals, they wanted to determine whether white muscle was a deleterious or an adaptive characteristic of diabetes.

The team induced obesity in mice by feeding them the “Super Size Me” diet, Lin said. On a high-fat diet, a mouse will double its body weight in two to three months. They found that obese mice with BAF60c transgene were much better at controlling blood glucose.

“The results are a bit of a surprise to many people,” Lin said. “It really points to the complexity in thinking about muscle metabolism and diabetes.”

In humans, resistance training promotes the growth of white muscle and helps in lowering blood glucose. If future studies in humans determine that the BAF60c pathway is indeed the way in which cells form white muscle and in turn optimize metabolic function, the finding could lead to researching the pathway as a drug target.

“We know that this molecular pathway also works in human cells. The real challenge is to find a way to target these factors,” Lin said.


Lin is a research faculty member of the Life Sciences Institute, where his laboratory is located and all his research is conducted. He is also an associate professor in the Department of Cell and Developmental Biology at the U-M Medical School.

In addition to Lin and Meng, other authors on the paper were Siming Li and Lin Wang from the U-M Life Sciences Institute; Hwi Jin Ko, Yongjin Lee, Dae Young Jung and Jason K. Kim from the Program in Molecular Medicine at the University of Massachusetts Medical School; and Mitsuharu Okutsu and Zhen Yan from the University of Virginia departments of Medicine and Pharmacology and Center for Skeletal Muscle Research at Robert M. Berne Cardiovascular Research Center. Support for the research was provided by the Michigan Diabetes Research and Training Center, Nutrition Obesity Research Center, National Institutes of Health and the American Heart Association.

Why your brain tires when exercising : Excess Serotonin shuts down the brain causing fatigue


A marathon runner approaches the finishing line, but suddenly the sweaty athlete collapses to the ground. Everyone probably assumes that this is because he has expended all energy in his muscles. What few people know is that it might also be a braking mechanism in the brain which swings into effect and makes us too tired to continue. What may be occurring is what is referred to as ‘central fatigue’.

“Our discovery is helping to shed light on the paradox which has long been the subject of discussion by researchers. We have always known that the neurotransmitter serotonin is released when you exercise, and indeed, it helps us to keep going. However, the answer to what role the substance plays in relation to the fact that we also feel so exhausted we have to stop has been eluding us for years. We can now see it is actually a surplus of serotonin that triggers a braking mechanism in the brain. In other words, serotonin functions as an accelerator but also as a brake when the strain becomes excessive,” says Associate Professor Jean-François Perrier from the Department of Neuroscience and Pharmacology, who has spearheaded the new research.

Help in the battle against doping

Jean-François Perrier hopes that mapping the mechanism that prompts central fatigue will be useful in several ways. Central fatigue is a phenomenon which has been known for about 80 years; it is a sort of tiredness which, instead of affecting the muscles, hits the brain and nervous system. By conducting scientific experiments, it is possible to observe and measure that the brain sends insufficient signals to the muscles to keep going, which in turn means that we are unable to keep performing. This makes the mechanism behind central fatigue an interesting area in the battle against doping, and it is for this reason that Anti Doping Danmark has also helped fund the group’s research.

“In combating the use of doping, it is crucial to identify which methods athletes can use to prevent central fatigue and thereby continue to perform beyond what is naturally possible. And the best way of doing so is to understand the underlying mechanism,” says Jean-François Perrier.

Developing better drugs

The brain communicates with our muscles using so-called motoneurons (see fact box). In several diseases, motoneurons are hyperactive. This is true, for example, of people suffering from spasticity and cerebral palsy, who are unable to control their movements. Jean-François Perrier therefore hopes that, in the long term, this new knowledge can also be used to help develop drugs against these symptoms and to find out more about the effects of antidepressants.

“This new discovery brings us a step closer to finding ways of controlling serotonin. In other words, whether it will have an activating effect or trigger central fatigue. It is all about selectively activating the receptors which serotonin attaches to,” explains Jean-François Perrier.

“For selective serotonin re-uptake inhibitor (SSRI) drugs which are used as antidepressants, we can possibly help explain why those who take the drugs often feel more tired and also become slightly clumsier than other people. What we now know can help us develop better drugs,” concludes Jean-François Perrier.


The new results have just been published in the renowned scientific journal PNAS. Read the article ‘Serotonin spillover onto the axon initial segment of motoneurons induces central fatigue by inhibiting action potential initiation’. DOI: 10.1073 PNAS article #: 201216150.


Associate Professor Jean-François Perrier Department of Neuroscience and Pharmacology University of Copenhagen Telephone: +45 23 81 27 46 E-mail: Skype: jfoboulot

Jean-François Perrier will be travelling until March 11. If you cannot reach him by phone, send him an email and he will call you back.


Communications Officer

Louise Graa Christensen Faculty of Health and Medical Sciences University of Copenhagen Mobile: +45 24 34 03 22 E-mail:


About the research

In addition to Jean-François Perrier, the research team responsible for mapping the braking mechanism includes Florence Cotel and two researchers from the University of Oxford (Stephanie Cragg and Richard Exley). In order to be able to study the motoneurons, the researchers have studied large American turtles. This is because the adult turtle’s spinal marrow, where the motoneurons are found, is accessible to experimentation but also resemble conditions in humans. It is in precisely this respect that that results obtained from  cross-sections of the spinal marrow in turtles, help researchers to understand central fatigue in the nervous system of humans.

Masterful motoneurons

In the human brain there are about 100 billion nerve cells, or neurons. Each neuron consists of a cell body with dendrites and a nerve fiber called the axon, and they communicate with one another via synapses. Nerve cells use nerve impulses to send signals with the axon from the cell body to the nerve ends, which form synapses with the dendrites of the receiving cell.

A special kind of neuron, the motoneurons, are extremely important as they are responsible for ensuring contact between the brain and the muscles. Every time a motoneuron sends impulses to the muscles, it leads to the contraction of the muscle fibres contacted and thus a movement. In order to control the body’s movements, the brain has to be able to control the impulse activity in groups of motoneurons so they are activated in the right sequence and to the right degree. It is here that serotonin plays a role as one of the neurotransmitters which are released from the synapses during the brain’s ingenious control of the motoneurons and thereby our patterns of movement.

Serotonin and central fatigue

Serotonin is well known for being involved in many different human functions: Appetite, sleep, sex and motor control. Serotonin is released as soon as you start moving, and the more you move, the more serotonin is released. In other words, serotonin functions as an accelerator for movement and makes the motoneurons more active. However, when large amounts of serotonin are released, it causes a glut at the synapses through which the neurons communicate. This means that the serotonin starts binding with the receptors lying outside the synapses. Some of these receptors sit at the initial part of the axon, i.e. where nerve impulses are formed. And when the serotonin activates these receptors, the nerve impulse is obstructed, the result being that the muscle contraction is weakened and fatigue occurs

Low muscle strength in adolescence linked to increased risk of early death

Contact: Stephanie Burns
BMJ-British Medical Journal

Effect similar to classic risk factors such as weight and blood pressure

Research: Muscular strength in male adolescents and premature death: cohort study of one million participants

Low muscle strength in adolescence is strongly associated with a greater risk of early death from several major causes, suggests a large study published on today.

The effect is similar to well established risk factors for early death like being overweight or having high blood pressure, leading the authors to call for young people, particularly those with very low strength, to engage in regular physical activity to boost their muscular fitness.

High body mass index (BMI) and high blood pressure at a young age are known risk factors for premature death, but whether muscular strength in childhood or adolescence can predict mortality is unclear.

So a team of researchers, led by Professor Finn Rasmussen at the Karolinska Institutet in Sweden, tracked more than one million Swedish male adolescents aged 16 to 19 years over a period of 24 years.

Participants underwent three reliable muscular strength tests at the start of the study (knee extension strength, handgrip strength and elbow flexion strength). BMI and blood pressure were also measured. Premature death was defined as death before age 55 years.

During the follow-up period, 26,145 participants (2.3% of the group) died. Suicide was the most common cause of death (22.3%) compared with cardiovascular diseases (7.8%) or cancer (14.9%).

High muscular strength was associated with a 20-35% lower risk of early death from any cause and also from cardiovascular diseases, independently of BMI or blood pressure. No association was seen with cancer deaths.

Stronger adolescents also had a 20-30% lower risk of early death from suicide and were up to 65% less likely to have any psychiatric diagnosis, such as schizophrenia and mood disorders. These results suggest that physically weaker individuals might be more mentally vulnerable, say the authors.

In contrast, male adolescents with the lowest level of muscular strength showed the greatest all-cause mortality and also the greatest mortality in cardiovascular disease and suicide before age 55 years.

Death rates from any cause (per 100,000 person years) ranged between 122.3 and 86.9 for weakest and strongest adolescents respectively. Rates for cardiovascular diseases were 9.5 and 5.6 and for suicide were 24.6 and 16.9.

The authors say that low muscular strength in adolescents “is an emerging risk factor for major causes of death in young adulthood, such as suicide and cardiovascular diseases.” The effect sizes of these associations “are similar to classic risk factors such as body mass index and blood pressure,” they add.

They suggest that muscular strength tests, in particular handgrip strength, could be assessed with good reliability in almost any place, including clinical settings, schools and workplaces.

They also support the need for regular physical activity in childhood and adolescence, saying: “People at increased risk of long term mortality, because of lower muscular strength, should be encouraged to engage in exercise programmes and other forms of physical activity.”

Botulinum toxin ( Botox ) A creates muscle weakness and atrophy following long term use

Contact: Don McSwiney 403-220-7652 University of Calgary

New insights about Botulinum toxin A

A new study by researchers at the Faculty of Kinesiology, University of Calgary, is raising questions about the therapeutic use of botulinum toxin A.

The study found that animals injected with Clostridium Botulinum type A neurotoxin complex (BOTOX, Allergan, Inc., Toronto, Ontario, Canada) experienced muscle weakness in muscles throughout the body, even though they were far removed from the injection site. The study also found that repeated injection induced muscle atrophy and loss of contractile tissue in the limb that was not injected with the Toxin.

“We were surprised by the degree of muscle loss and atrophy in the limb that was not injected with the Botulinum toxin,” says Rafael Fortuna the lead author of the paper will soon be published in The Journal of Biomechanics, “I think it’s fair to say that the paper raises some important questions about the long-term therapeutic use of Botox, especially with children and adolescents.”

The study used dosages that approximated therapeutic doses used to treat conditions like cerebral palsy where muscle contraction can’t be controlled resulting in muscle dystonia and spasticity. The study follows previous research in Dr. Walter Herzog’s lab, which found that Botulinum toxin A, easily crosses the muscle membrane barrier, resulting in muscles weakness in the surrounding (non-injected) muscles.

This study shows, for the first time, that over time Botulinum toxin A use also results in muscle weakness, atrophy and loss of contractile tissue in non-injected muscles far-removed from the injection site.”It may be that the benefits of using Botox for these kinds of therapeutic, medical uses, outweighs these potential long-term consequences,” says Dr. Herzog, “however I think this study raises some important issues that need to be followed to ensure the best possible outcomes for patients, in the long term.”

Botulinum Toxin A is also used as a cosmetic treatment, where the drug paralyzes small muscles in the face to reduce the appearance of wrinkles.

Herzog notes that while this study was looking at larger doses, the results should be valid for any application of the drug

Lipstick chemical alert: Ingredient in hundreds of household products ’causes heart problems’ -Triclosan

By Tamara Cohen

PUBLISHED:19:56 EST, 13  August 2012| UPDATED:07:52 EST, 14 August 2012

chemical commonly used in lipsticks, face  washes and toothpaste may cause heart and muscle problems, according to  scientists.

They found triclosan, which is in hundreds of  household products, can hinder the process by which  muscles, including the  heart, receive signals from the brain.

In tests on mice, they noted a ‘dramatic’ 25  per cent reduction in heart function within 20 minutes of exposure, and warned  there is ‘strong evidence’ it could affect human health.

However regulators and other experts insist  triclosan levels in products are safe, and that the doses injected into the mice  were higher than those to which humans would ever be exposed.

Although previous studies have found that  triclosan may have links to thyroid and fertility problems, this is the first  time its effects have been tested on muscles.

Scientists had thought that the chemical – which was devised to prevent bacterial infections in  hospitals – was  metabolised quickly by the body without harmful effects.

However, the researchers at the University of  California say it may remain active and be transported to organs, causing  damage.

Professor Isaac Pessah, who led the study,  published in the Proceedings of the National Academy of Sciences, said: ‘These  findings provide strong evidence that it is  of concern to both human and  environmental health.

‘For someone who is healthy a 10 per cent  drop in heart function may not have an effect, but if you have heart disease it  could make a big difference.’ His team injected a group of mice with triclosan.  They saw a ‘significantly reduced’ function in the heart’s left ventricle within  20 minutes.

Another test looked at the mice’s skeletal  muscles by getting them to grip wire mesh. Those injected in the past hour had  an 18 per cent fall in their grip strength – although it was restored within a  day

Read more:

Antibacterial soap may hinder muscle function: study

A chemical found in soap, toothpaste, clothes and toys may cause muscle   problems and should be used with caution, experts have said.

By , Medical Editor 7:20AM BST 14 Aug 2012

Researchers found an antibacterial agent, called triclosan, hampers muscle   function in animals and fish and may have implications for human health.

After testing the substance on mice and fish they found muscle strength was   reduced, including heart function and fish were unable to swim as well.

The findings were published online in the Proceedings of the National   Academy of Sciences.

Isaac Pessah, professor and chair of the Department of Molecular Biosciences   in the UC Davis School of Veterinary Medicine and principal investigator of   the study, said: “Triclosan is found in virtually everyone’s home and   is pervasive in the environment.

“These findings provide strong evidence that the chemical is of concern   to both human and environmental health.”

In experiments the researchers exposed animals and fish to levels of triclosan   equivalent to that which people may receive daily.

The team also found that triclosan impairs heart and skeletal muscle   contractility in living animals.

Anaesthetised mice had up to a 25 per cent reduction in heart function   measures within 20 minutes of exposure to the chemical.

Nipavan Chiamvimonvat, professor of cardiovascular medicine at UC Davis and a   study co-author, said: “The effects of triclosan on cardiac function   were really dramatic.

“Although triclosan is not regulated as a drug, this compound acts like   a potent cardiac depressant in our models.”

Bruce Hammock, a study co-author and professor in the University of California   Davis’ Department of Entomology, said: “We were surprised by the large   degree to which muscle activity was impaired in very different organisms and   in both cardiac and skeletal muscle.

“You can imagine in animals that depend so totally on muscle activity   that even a 10 per cent reduction in ability can make a real difference in   their survival.

“Triclosan can be useful in some instances, however it has become a   ubiquitous ‘value added’ marketing factor that actually could be more   harmful than helpful. At the very least, our findings call for a dramatic   reduction in its use.”

Further studies are needed to establish the effect triclosan has on human   muscles, the researchers said.