'Obesity gene' does not hinder weight loss

This article is about how the discovered "obesity gene" might not be all it is cracked up to be. Through several trials of researchers trying to figure out the genetic aspects of obesity, they tested the gene FTO. This gene has a high association with obesity along with a few other genes. The results turned out that this gene has no correlation with weight gain/lost as it pertains to their experiment. I believe this information is important to know. When it comes to genetics, it goes without saying that genes can affect a person's body type. On the other hand, that doesn't mean we should pin the hopes of weight and body management on genes, rather than traditional methods that are proven to work.


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Science of Metabolism

Psoriasis and Obesity May Share Genetic Source

Both Psoriasis and Metabolic disorders have been linked to genetic and environmental exposure, with bad life styles such as smoking, alcohol, stress and decreased physical activities these two go hand in hand for immunoinflammatory pathways. Researchers from the University of Copenhagen in Denmark conducted a study by using twins after filling out a questioner the results concluded that psoriasis affected 4.2% of the participants, 630 of them were men and 771 women, 1.4% had diabetes. Average BMI overall was 24.5 and 6.3% had a BMI of 30-34 which is classified as obese. People with psoriasis had a greater risk of high BMI and obesity than those without psoriasis. In conclusion, researchers stated psoriasis and obesity could partly stem from the same genetic cause, but not one condition does not necessarily lead to the other.

Those individuals who are ignored with psoriasis tend to chose a more sedentary life style which eventually leads to obesity and a higher risk of diabetes. Since there are many, many factors that can correlate these two, further research must be conducted.

I personally enjoyed learning about this topic since I am a pre-med major and psoriasis and obesity are diseases that I will eventually come across with my patients one day. It is interesting to know that these two possibly can correlate with each other. It makes me think as what else can be a correlation due to genes.

Click here for original source: http://www.medicalnewstoday.com/articles/309592.php

Fat? Thin? Molecular switch may turn obesity on or off

Identical twins are usually alike in everything but; can diverge in one important characteristic, their weight. A new study uncovers a molecular mechanism for obesity that might explain why in twins, one can be extremely over weight even while the other is thin.

Heredity influences whether we become obese , gene researchers have found this link but yet doesn't explain the many differences in weight among people. Identical twins with non-identical weights are a prime example.

Researchers are now taking a closer look at this phenomena to see what accounts for this variation. Could it be changes in the intestinal micro-biome (Collection of bacteria living in the gut) or is it epigenetic changes (Alternations in gene activity)? These changes occur when molecules latch on to DNA proteins, turning sets of genes "on" or "off". Triggered by the factors in the environment, epigenetic modifications can be passed down from one generation to the next.

Physiologist J. Andrew Pospisilik of the Max Planck Institute of Immunobiology and Epigenetic's in Germany noticed an odd pattern of weight gain in mutant mice. After DNA testing the mice only had one copy of a gene called Trim28, the researcher found that most of them were obese. Trim28 is an epigenetic modifier which implicates it is a major gene in the bodies weight management. The exact functions remain unclear, but Pospisilik and colleagues hypothesize that Trim28 helps form an epigenetic switch that can flip on obesity by suppressing these genes.

Could this be the same mechanism to cause obesity in humans?

 The thing is mice only have one copy vs humans who have two. To compare, the team took fat samples form obese children in hospitals as it turns out Trim28 activity was abnormally low in those kids. The researchers then analyzed data on 13 pairs of identical twins in which one twin was obese.

Trim28 was diminished in the fat of the obese twin,  could this be the key to obesity ? This opens up the possibility of DNA screening at birth to see in fact if that new born will be obese.

This study gives a new potential mechanism of obesity and is a step closer to prevent or even reverse the condition of obesity.

Genetics and Obesity:

Obesity has been a very common point for the United States for decades. The United States obesity rate is far too high, and a large amount of that is contributed to genetics. There are several diseases regarding obesity, a few examples are Prader–Willi syndrome, Albright hereditary osteodystrophy,  and ulnar-mammary syndrome, all three are autosomal dominant disorders. There are many loci in which each disorder is present.While there is widespread acceptance that hereditary factors might predispose to human obesity, it is frequently assumed that such factors would influence metabolic rate or the selective partitioning of excess calories into fat. However, it is notable that, thus far, all monogenic defects causing human obesity actually disrupt hypothalamic pathways and have a profound effect on satiety and food intake. Along with the genetic  predisposition to obesity, many individuals also have environmental predispose to obesity, which only compounds the patients problem making them eat more and more. 

Obesity Linked to Genetics

Two papers published in the journal Nature on February 11, discuss new research, which found that genes play a significant role in obesity, and could help explain why some people are more likely to gain weight and develop obesity-linked conditions than others.  After the researchers analyzed genetic samples from more that 300,000 people, they were able to identify more that 140 locations across their sets of DNA that play a role in obesity.  In addition to these findings, they also located new biological pathways that play important role in obesity.  One of the papers focused on genes that affect where fat is stored in the body, which affects health risk.  This is important because if the gene that influences where fat is deposited, it could help the understanding of the biology that leads to various health conditions such as diabetes and heart disease.  The other paper examined the link between genes and body mass index based on height and weight.  A second study published in a different journal called Cell, also identified a genetic mutation that could be linked to obesity in humans.  This study found that patients with this mutation were at risk for health problems, and were more likely to become obese at a younger age.  With these findings researchers hope to eventually defeat obesity, and the major health problems associated with it.  They also hope to someday develop target therapies to treat the mutations that predispose humans to obesity.  More research will be done to figure out exactly how these genes function and how they make people more susceptible to obesity.

Original Article: http://health.usnews.com/health-news/articles/2015/02/11/studies-find-more-genetic-links-to-obesity

Additional Article: http://www.foxnews.com/health/2013/10/25/researchers-discover-new-gene-linked-to-obesity/

How Obesity Alters Genetic Structure

According to a recent study by researchers at Hopkins University there is a direct correlation between genes and the ability to develop type 2 diabetes.  As it is well known another cause of developing diabetes is obesity, but researchers have discovered that obesity may cause a change in the chemical structure of DNA which in turn affects the bodies ability to release insulin.  This change in gene structure from obesity is what triggers the onset of diabetes in many people, and is known as the epigenome. Researchers examined the DNA of obese mice before and after gastric bypass surgery to determine wether genetic alteration will remain the same or go back to normal once the fat has been removed. According to the experiment the genes of the mice remained the same after surgery and still showed the same change in DNA structure. This study helped to show the exact correlation between obesity and diabetes and how it is the change in gene structure that brings the onset of this disease on people.

Reading this article opened my eyes on the many side affects of obesity and how important it is to maintain a healthy lifestyle. My grandmother was recently diagnosed with type II diabetes and doctors have said it was due to her poor diet. I can now determine the exact cause of this and hopefully be able to prevent other members of my family from developing diabetes. 

The Genetic Link to Obesity

        With obesity rates at an all time high, researchers from the International Genetic Investigation of Anthropometric Traits (GIANT) have analyzed the DNA of over 300,000 individuals in the hopes to discover how genes affect obesity. There are several risk factors that can contribute to obesity. People with a higher waist to hip ratio, are more likely to have fat around their stomach. This can make them susceptible to more cardiovascular problems or diseases such as diabetes. By determining how genes can affect the location of fat deposits, researchers hope to better understand diseases that arise due to obesity. The genes that are thought to play a role in the location of fat deposit was previously understood as important in the creation of adipose tissue. Researchers have found 97 different regions within the human genome that can influence a person's obesity rates. However this is only the beginning. The next step for researchers will to see how these genes increase a person's chances to gain weight. 

I found this article to be interesting because many times we are focused on treatment rather than prevention. Over the summer I shadowed several doctors and they were all treating patients based on what they were presenting at the moment. Don't get me wrong, we need to help sick people when they are sick, but think of all the money we would save by catching an illness before it presented itself. Obesity is a growing problem in America. With research like this we can help patients that are at risk for obesity and help them to make lifestyle changes early in their life. 

Article Link: http://www.medicalnewstoday.com/releases/289343.php

Secondary Link: http://www.mayoclinic.org/diseases-conditions/obesity/basics/definition/con-20014834

New "Obesity Gene" Found

Researchers from the University of Chicago have said that they have found a gene that is associated to obesity. They have said that they think that the gene IRX3 controls body mass and regulates body composition. Although the research showed an association between the gene and obesity, it did not prove a cause-and-effect link. The IRX3 gene was first found though the analysis if 150 samples of DNA from people of European descent. To verify the role of IRX3 in obesity, the researchers created mice without the gene and found that they weighed about 30 percent less than normal mice. Most of the weight difference were due to the lack of body fat of these altered mice. These new rats were completely resistant to high-fat diet-induced obesity. The only problem with this research is that animal studies cannot often be replicated in humans. Previous studies have said that mutations of the gene FTO has a significant role in determining the risk of obesity in people. But this new study shows that this obesity mutation in FTO interacts with the IRX3 gene and alone the FTO mutation has only a minor effect on obesity risk.
          It is interesting that certain genes increases the risk in obesity in people. But the final deciding factor whether someone will be obese or not is that person. It is up to the individual to determine whether they will either exercise and eat healthy, or be lazy and eat McDonald's every day.

"Obesity gene" shows positive results in mice; also found in humans

Obesity is a clear and debilitating epidemic in our society today, not only nationally, but globally as well. Researchers throughout the world have been unrelentingly searching for the easiest, fastest, and safest way to combat this problem in humans. Recently, researchers at the University of Colorado School of Medicine believe they have found the "obesity gene", Perilipin (Plin2), that when deleted, it prevents mice from becoming obese regardless of their dietary macronutrient intake.

“When fed a diet that induces obesity these mice don’t get fat. It may be possible to duplicate this in humans using existing technology that targets this specific gene,” Prof McManaman said.

This discovery is exceedingly significant in human obesity since we possess the same exact gene, Plin2, just as mice do. If this process can be replicated in humans, that is deleting the gene Plin2, then there shows great promise to fight the mostly eternal problem of obesity that plagues the globe today. The results of the research were published in the Journal of Lipid Research.