Protein may cause obesity by interfering with brown fat

There are two main types of fat in the human body, white fat and brown fat.  The white fat typically stores energy as triglycerides and is typically referred to as the less healthy form of fat, as it's associated with heart disease and diabetes.  Brown fat however is made up of more mitochondria and serves to turn energy into food, especially by thermogenesis.  Brown fat has been shown to reduce obesity, however a certain protein, Id1, diminishes the positive effects of brown fat.  A study was done using mice and it found that mice who overproduced the Id1 protein gained much more weight then mice who didn't.  Id1 specifically regulates the ability of the brown fat carry out thermogenesis, therefore inhibiting the efficiency of the brown fat.  The study with mice also determined that removal of this protein didn't show that it was necessary for normal functioning.  This study is thought to parallel the potential of this protein in humans.
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Study on Mice

Temperature Dependent Bacteria as a Remedy

A new study conducted at the Massachusetts Institute of Technology shows that temperature dependent bacteria may be used in the future. This treatment will be administered to patients by placing bacteria in them. The bacteria will contain medicine that will be pumped into the body based on the temperature of the bacteria. The bacteria will be changed in temperature by use of ultrasound technology. Furthermore, if the individual has a fever this will cause the bacteria to self-destruct and be expelled from the body through defecation. This treatment may be useful in cancer patients because bacteria tend to gravitate toward tumors. This is due to tumors containing less oxygen.

            

This is very interesting and informative. I hope to see more information on this topic in the future. This will be very useful in medicinal technology. Doctors should look more into this technology to treat their patients. 

Genetic Memory

Studies have shown that information can be passed down between generations through genes. This can be easily seen in the animal kingdom. Scientist have trained their first generation of mice to fear the scent of cherry blossoms. The next generation of mice were very sensitive to the scent of cherry blossoms even though they never experience the scent of cherry blossoms in their lives before. This experiment demonstrates that fears can be inherited through genes.

Another example of information being transferred through genes is shown in a surprising way with humans. Leslie Lemke became a musical genius at such a young age that it was impossible for him to learn. He spontaneously developed vast syntax (the rules) of music. There have been other people like Lemke who have developed complex information in other fields such as mathematics and art.

I believe once we identify and evaluate the proteins linked to genetic memory that we could produce some amazing results. Imagine if we could genetically transfer calculus or genetic engineering into our children. It could become common to have the information of an average college student before one reaches middle school. The possibilities would be endless. 

Genetics Behind Anxiety Disorders

Researchers at Massachusetts General Hospital move into researching the specific genetics behind anxiety disorders. The latest research has found that a specific gene is in association with anxiety traits. In individuals with these particular traits, it was found that vital neurotransmitter activity was compromised.

After studies performed with mice, it was found that the RGS2 protein, which is coded for by a specific gene is associated with fearful behavior. This theory was then tested in children twenty one months up to six years through over one hundred different families. The findings were consistent with the same sort of association in mice. The testing was extended to over seven hundred college students. The information from this study further supported the previous findings.
These findings and tests are so important considering what a serious and wide spread problem anxiety disorders are. Being someone who has Generalized Anxiety Disorder, I really look forward to how these discoveries will develop into treatment. I hope that in identifying specifics, scientists and doctors will be able to narrow treatment to target the real genetic issues. I am also always prideful in seeing more and more science discovered in association and causation of mental illnesses because it belittles the taboo association with these serious disorders.

Source: http://psychcentral.com/news/2008/03/04/genetic-disposition-for-anxiety/1997.html

Turning Off A Fat Accumulation Gene To Reduce Obesity

 In this short article, it discusses how investigators from Beth Israel Deaconess Medical Center have found a "switch" (in mice) that can accelerate a person's basal metabolic rate, which could lead to the decrease of obesity and diabetes. The research involves "turning off" a gene that encodes for a protein called nicotinamide N-methyltransferase (NNMT). The gene was turned off using antisense oligonucleotide technology, which can be designed to prevent the synthesis of specific proteins. This allowed the researches to interrupt only the expression of the gene in fat cells and the liver.  This protein has also been linked to some forms of cancer. If this research turns out to be applicable to people, those who have "slow metabolism" could use this discovery as a great equalizer. This seems like a quick and easy fix but there is no telling what the negative short term or long term ramifications could be by turning off this, or any other gene. Before they try this on people I think there needs to be some longitudinal type studies to ensure that turning off a gene does not cause some other catastrophic failure within the body.  

Related Article (original study): http://www.nature.com/nature/journal/v508/n7495/full/nature13198.html

Grasshopper Mice Are Numb to the Pain of the Bark Scorpion Sting

A recent study conducted by Ashlee Rowe, Assistant Professor of Zoology at Michigan State, investigated the effect of the scorpion toxin on the Grasshopper Mice. The deadly sting of this scorpion for a mammal of this size and bigger is well documented; however, the Grasshopper mice appears to be unaffected by the scorpions sting.  Scientists began conducting controlled trials with the mice and the scorpion. This video, "Mouse v Scorpion" illustrates a portion of the experiment.  It can be viewed on YouTube at:

                                   http://youtube/3S4sMBFBZ0M 

 

            After analysis of this trial, scientists needed to test the mice to discover what caused the absence of pain response. They injected their paw with a small dose of venom and nontoxic saline to see the response. The response was that the mice came up with less pain from the venom then saline. When they observed this, they examined pain neurons that have a couple of different sodium channels, called 1.7 and 1.8; the channels, shows that when toxins bind to 1.7 channels, the channels open, sodium flows in and the pain neuron fires.  The research discovered that channel 1.8 in the grasshopper mice has an amino acid to block the pain of scorpion stings that are different from mammals.  The scorpion toxin binds to one of these amino acids to block the activation of channel 1.8 and thus inhibit the pain response. 

 

This research will be the start of the development of new analgesics for humans in the future. Hopefully, it will lead to relief for many people.

http://www.sciencedaily.com/releases/2013/10/131024143422.htm 

http://www.utexas.edu/news/2013/10/24/grasshopper-mice-bark-scorpion/

 

Could You Be Wearing "Fat Jeans" Because of Fat Genes?

According to a recent study conducted by researchers at the University of California Los Angeles, in addition to environmental factors such as diet and exercise, obesity is indeed linked to an individual's genes. For 16 weeks, over 100 genetic strains of mice were treated in laboratories under identical conditions. Each were first given a healthy, well-balanced diet for a duration of 8 weeks followed by a high-sugar, high-fat content diet for the remaining 8 weeks. The results were very interesting; Although handled under the same environmental conditions, there was a prominent variation in weight gain among all of the mice. Some showed little to no change while others increased their body fat by over "600 percent." Therefore, scientists contributed this variation to genetic influences.

If people consume a high-fat diet, the response will be predominantly determined by genetics," Dr. Lusis said. "But whether you choose to eat a high-fat diet in the first place is largely environmental."

Eleven genetic loci associated with obesity and fat storage were identified, several of which were "linked to obesity in humans." It was found that some mice had higher fat burning mechanisms, thus eliminating more calories, while others had greater propensities to be more physically active. Data from this study can greatly contribute to targeting more efficient weight loss treatments and pharmacology in the near future. In addition, researchers hope to also study more specifically "brown fat" which is metabolically responsible for creating heat and burning caloric intake. While it is certain that what one consumes and how one utilizes those calories (through exercise or inactivity) has a significant effect on fat loss and storage, it is also now inferred that obesity can be highly inheritable and pre-existent in one's genome.

[For more on this article, check out the following links: http://www.huffingtonpost.com/2013/01/10/fat-genes-obesity-ucla-study-diet-exercise_n_2450108.html & http://healthland.time.com/2013/01/09/what-mice-can-tell-us-about-obesity-and-genetics/ ]