Burning more fat by proteins

Apart from exercise of the contractile functions, muscle play a huge role in producing heat via thermogenesis. Thermogenesis is a process in which heat produced that does not include the contraction of muscles. This is important to know because there is a protein present in muscles that can increase the rate of heat production. Researchers at Sanford Burnham Prebys Medical DiscoveryInstitute have found that the protein called sarcolipin (SLP)—found in muscles—is a key way for fat-burning processes. The process in which it proceeds is SLP will bind to calcium ion transported that is called SERCA which forces the muscle to spend more energy so that the calcium will be moved. Sarcolipin binding with SERCA promotes uncoupling of SERCA CA2+ transport from ATP hydrolysis. This increases heat production.

To proceed with this hypothesis, researchers proceeded an experiment on mice that contained high levels of sarcolipin versus those that did not produce any sarcolipin. By feeding both animals high-fat diet, it showed that those with SLP did not develop fat in their muscles, nor type 2 diabetes. On the other hand, the animals that did not have any sarcolipin in their system struggled to burn the fat. 

This study deserves to be further researched since it is closer on identifying specific obesity-promoting proteins. By this research we could help those that have difficulty with their metabolism and their metabolic pathways. It could also aid those who have trouble exercising or have trouble with their weight.

Inherited Neurological Disorder Understood More Clearly

Researchers discovered a certain gene associated with dystonia, a neurological disorder which causes repetitive muscle contractions which can be painful for a patient. The muscles affected can vary from either a single muscle or to the entire body. There is no cure, but it is a pretty well managed disorder. The gene found codes for hippocalcin, which has recently been put under a spot light to figure out what it does specifically for dystonia. It was found to mess with certain calcium pathways for neural activities and made the channel overactive, and thus caused problems.
By doing this research, it is now not too impossible to find a cure for dystonia and help many lives. Article
 More about Dystonia

Potential Treatment for Myotonic Muscular Dystrophy

One of the discoverers of the gene responsible for myotonic muscular dystrophy, Dr. Mani S. Mahadevan, recently discovered a potential treatment for the disease.  The drug that Dr. Mahadevan identified may be able to slow down the progression of muscle damage and muscle dysfunction associated with muscular dystrophy.  The drug is also currently being evaluated for its ability to treat conditions such as rheumatoid arthritis.

            Dr. Mahadevan and his research team used the drug that was identified to conduct laboratory tests on mice with myotonic dystrophy.  After being treated with the drug, the mice showed evidence of improved muscle function and improved grip strength.  Their muscles also became healthier and many of them lived longer.

            The Food and Drug Administration has not approved the drug so it is not yet available for patient use.  Before the Food and Drug Administration approves the drug for patient use, clinical trials must be performed on people with the disease to determine if it is effective in humans.

            I found this study very intriguing.  I think the results of the study show promise for the drug's potential success in the treatment of people with myotonic muscular dystrophy.  I think the findings of the study and the promise for future clinical trials for the use of the drug on humans will provide a lot of hope for people affected by myotonic muscular dystrophy and their families.

Tracking down cause of eye mobility disorder

Could you imagine having a permanent downward gaze and having to tilt your head up in order to see directly in front of you? A condition known as eye mobility disorder causes a person to not be able to lift up their eyes or eyelids in order to see straight. Scientists at the University of Iowa have been performing experiments on mice that would mimic what would happen in humans, in order to help eliminate this disease. About ten years ago, Elizabeth Engle, one of the authors of this paper, identified the mutated genes that cause eye mobility disorder, and she then developed a mouse with the same genes. However, it was still unknown why this type of disorder occurred. Other researchers started to look into this disease and found a swelling in one of the nerves that goes to the eye muscles, which only occurred in mutant mice. Therefore, with further experiments involving normal and mutated mice, the scientists were able to identify the mutated protein and its function.

                I found this article to be very interesting, because it is the start to finding a cure for this disease. As the article states, future research on this topic will hopefully help families with a genetic predisposition for this disease to be able to have normal children without the mutation.

Article: http://www.sciencedaily.com/releases/2014/04/140416162636.htm

Related Article: http://www.ncbi.nlm.nih.gov/pubmed/8771514

Muscle Aging is NOT Improved by Exercise

Medical News Today reports that the professor of Systems Biology in the School of Sport, Exercise, and Health Sciences at Loughborough University recently issued a press statement that overturned a concept that was long held true by the scientific and medical community.

Professor Timmons and her colleagues have observed that physical exercise has very little to no control over how well the muscles age in the human body.  It has been found that genetic pathways have been identified as the largest deciding factor as to how well your muscles actually age.  These processes are completely distinct from the processes that are regulated by physical activity.  In other words, no matter how much you exercise, genetics wins again...  Physical activity has NOT been observed to alter age-related biological changes.

A test trial on endurance took place over a 20 week time period with a group of volunteers.  It was discovered that through a specific pathway known as mTOR, only those select few who can genetically suppress this pathway are able to gain more lean muscle tissue mass with exercise.  For the majority of the people who could not genetically suppress the mTOR pathway, no amount of exercise could stop or slow their muscle aging.

The anatomy of a Fruit Fly

Recently the Max Planck Institute of Biochemistry in Martinsried (near Germany) preformed a series of tests to try and understand the amazing flight of a common fruit fly. With the fruit flies big bodies and tiny wings they are still able to propel themselves and flap their wings at a frequency of 200 hertz. This large frequency is possible because of a particular gene called splat. Splat aids in the generation of ultra fast super muscles and is responsible for the amazing flight of a fruit fly. Without this particular gene the fruit flies would be flightless.

These results of how splat interacts with the fruit flies genome can help scientists and researchers gain more insight on how the splat gene may interact with in the human body. Since splat is built by the human body cardiac muscle.

This is a summary of an article found on sciencedaily.com

Muscling Toward a Longer Life: Genetic Aging Pathway Identified in Flies

Researchers at Emory University School of Medicine have identified a genetic pathway that regulates aging in Drosophila melanogaster.  In this article, Vrailas-Mortimer and others reported on the surprising effects a pair of genes called p38 MAP kinase had on the aging process and sensitivity to oxidative stress in fruit flies; the scientists were originally expecting the pair of genes to be linked to learning and memory in D. melanogaster.  In their findings, the researchers discovered that if both genes were defective, the fruit fly could be expected to die early: they also suffered from motor impairment, an increased sensitivity to heat, and exposure to oxidative stress.  In addition to this, Vrailas-Mortimer and her team noted the drastic effect an overproduction of p38 MAP kinase had on fruit fly lifespan: those with an increase in p38 MAP kinase lived approximately fifty percent longer than regular flies.  The team was also able to identify two other genes that improved lifespan, MnSOD and MEF2.  In contrast to the genetic pathway that regulates aging in other organisms such as C. elegans and mice, p38, MnSOD, and MEF2 were found to have a pathway that is specific to muscles; p38, MnSOD, and MEF2 are found in mitochondria.  Vrailas-Mortimer and her team plan on examining the effects of dietary antioxidants and caloric restrictions on fruit flies deficient in p38.  I think the research Vrailas-Mortimer and her team are conducting is very important because it can reveal critical information needed to understand and treat muscle degeneration in humans.