BioQuakes

AP Biology class blog for discussing current research in Biology

Tag: diabetes

Is COVID-19 Linked to Diabetes?

COVID-19 Virus diabetesToday’s children are being born into a world much different than what we once knew. The new reality of our world involves grappling with the effects of COVID-19. However, it seems that some children are experiencing greater effects than we could have imagined. As it was recently discovered, after a child is infected with COVID, he or she may have a heightened risk of developing Type 1 Diabetes. This adds another complicated layer to the pandemic that we thought we had mostly seen the end of. This article will detail the facts of the research while also providing insight from my AP Biology studies.

Over the past three years, we have become all too familiar with SARS-CoV-2, known as the virus that causes COVID-19. We have seen its effects in many different ways in our own lives and the lives of those around us. Now, as research improves, new discoveries have been made about COVID’s link to Diabetes in children. This article from NewScientist by Chen Ly highlights these studies. The article mentions that inside the pancreas are these structures called islets of Langerhans. These islets are groups of pancreatic cells that are responsible for producing insulin and glucagon, the two hormones that are crucial for the regulation of our blood sugar. The body can develop an autoimmune response to these islet beta cells and then fight against them with autoantibodies. If enough autoantibodies are created, they can trigger the onset of type 1 diabetes after killing too many islets in the pancreas. In a research study conducted by Annette-Gabriele Ziegler at The Technical University of Munich in Germany, it was concluded that children who had COVID antibodies were twice as likely to develop islet antibodies than those who have not been infected. This information provides insight on the relationship between COVID antibodies and diabetes. If children’s bodies can create these autoantibodies that kill the islets, the insulin production in young children can be weakened by COVID infection.

As stated in this article from the University of Minnesota, diagnoses of Type 1 Diabetes increased as a result of documented COVID infections. The incidence rate of T1D was 29.9 from January 2020 to December 2021. This was a jump up from the 19.5 incidence rate recorded in 2018 and 2019. This jump suggests that COVID infection is correlated to an observed increase in T1D. In an article by the CDC, it was reported that people under the age of 18 were more likely to receive a diabetes diagnosis after 30 days from COVID infection. This highlights the importance of COVID prevention strategies in order to additionally prevent other chronic diseases. In addition, this PubMed states that during the pandemic, we observed an increase in cases of hyperglycemia, diabetic ketoacidosis, and new diabetes. Th alludes to the possibility that COVID may trigger or unmask T1D.

Recently in our AP Biology class, we have been learning about the immune system and cell communication. This can be related to the research mentioned above in that we have covered the topic of blood sugar regulation and studied the pathway of insulin and glucagon throughout our bodies. Insulin regulates our blood sugar by helping to store the excess glucose in the liver when there is too much of it in the bloodstream. Glucagon does the inverse of this by taking the stored glucose from the liver and bringing it to the bloodstream when blood sugar levels are low. Both of these hormones seek to maintain homeostasis. In addition, we have focused on how our bodies react to viruses, and the different kinds of cellular responses that are necessary to fight infections. This is related to my research for this article because it dives deeper into the concepts of immune responses and blood sugar regulation. Getting to read about these topics in relation to the COVID-19 pandemic has further enhanced my understanding of them. 

I chose to write about this topic because of the impact that both COVID-19 and Diabetes has had on my family, which helps me to connect with these topics and heightens my curiosity. I welcome any comments regarding these topics and how they may have affected you or someone you know. What are your thoughts on these findings?

Do Eating Times Lesson Your Chances of Developing Type 2 Diabetes?

On April 6th, 2023 an experiment  to test how we can reduce the chances of developing type 2 diabetes was conducted by the University of Adelaide and published on Science direct.  This experiment  compared  two different eating habits, one was an intermittent fasting diet and the second was a lessened-calorie diet. The purpose was to see which diet was more effective in limiting the chances of type 2 diabetes in people who are more likely to develop it.

 

Type 2 diabetes occurs when a body’s cells doest effectively use and make insulin. Type 2 diabetes also effects people’s blood glucose levels. In biology class, we have learned the importance of insulin. Insulin is an essential hormone in our bodies. It helps our bodies turn food into energy and controls our blood sugar levels. Without insulin, our blood glucose levels can become dangerously high. About 60 percent of type 2 diabetes cases could be helped with changes to diet and lifestyle.

Insulin glucose metabolism

It was discovered that people who followed the intermittent fasting diet, eating between 8am and 12pm for three days had a higher tolerance to glucose after 6 months and had lower chances of developing type 2 diabetes than those on a low calorie diet. It was also revealed that participants who were intermittent fasting had more sensitivity to insulin and had decreased blood lipids compared to those on a low calorie diet. As we learned in biology class high insulin sensitivity allows the cells of the body to use blood glucose more effectively, reducing blood sugar.

 

The conclusion of this study implies that meal timing and fasting have many health benefits to reduce the chance of type 2 diabetes and other health issues. This is very intriguing to me because I have heard many mixed opinions from friends and family if eating times do have any type of effect on our health!



How CRISPR Can Help Individuals Overcome Obesity

Fat, which is made up of cells that have been distended with greasy or oily materials, or triglycerides, is required for the body to function, but it may also be hazardous if consumed in excess. Fat cells are distinct from other cells such that they lack surface receptors and constitute only a small percentage of the cells in fat tissue. While restricting diets can assist those who are obese lose weight, the results are typically solely temporary. If only there were a way to target fat cells specifically… Well, there just might be!

Breast tissue showing fat necrosis 4X

A group of doctors discuss a potential prospective breakthrough utilizing CRISPR-Cas9, a technology that has proven particularly elusive in the study of adipose tissue, in a recent publication published in the Journal of Biological Chemistry. Their study was tested on mice, in order to see how it worked and what it targeted. The gene-editing technology CRISPR-Cas9 changes genes by precisely cutting DNA and then allowing natural DNA repair mechanisms to take charge. This technology has changed the ability of deleting or inserting certain genes of interest into an organism. Cas9, an enzyme that can break DNA strands as well as a piece of RNA that directs the Cas9 enzyme to a specific location in the genome for modification, is encased in a non-harmful virus and supplied to the cells being studied. The equipment has also been used to study the heart, liver, neurons, and skin cells, to name a few. However, brown fat adipose cells have never been studied.

Brown fat cell

Using CRISPR-Cas9 components, the physicians were eventually able to target brown fat adipose cells. In mature mice, they were able to knock off the UCP1 gene, which specifies brown adipose tissue and allows it to generate heat. They discovered that knockout mice were able to adjust to the absence of the gene and maintain their body temperature under freezing settings, indicating the existence of additional mechanisms involved in temperature regulation. Overall, the CRISPR interference system assisted mice in losing about twenty percent of their body weight, proving that CRISPR can accurately target fat cells.

3LFM FAT Mass and Obesity Associated (Fto) Protein

Genetics can have a significant impact on the quantity of fat cells you are born with. However, the proportion of tendency to becoming overweight differs by individual. For example, in some people, genes account for just 25 percent of the tendency, but in others, the genetic effect might be as high as 70 percent to 80 percent. Obesity is most commonly associated with the FTO gene. This FTO gene is not found in everyone. For example, around 20 percent of white people have a variation of the gene that increases their risk of obesity. The FTO gene is located on chromosome 16, which is one of the 23 pairs of chromosomes in humans. While this chromosome pair represents under 3 percent of the total DNA in cells, if FTO is present, it can affect whether if one is obese or not, depending on the alleles of the gene. CRISPR has the potential to target this gene as well as other genes that affect body weight, such as brown fat adipose cells.

Diagram of Chromosome 16

Your health is essential for the rest of your life! A healthy lifestyle can aid in the prevention of chronic diseases and long-term ailments. The alleles on the FTO gene can have an impact on your health and are linked to type 2 diabetes, obesity, and other health concerns.

How Diabetes Is Emerging In Patients With COVID-19

COVID-19 has a plethora of underlying effects. However, researchers may have just identified the most dangerous long-term impact.

3D medical animation still of Type One Diabetes

While researchers have been studying COVID-19 for the past two years, pharmacy technician Nola Sullivan of Kellogg, Idaho, has uncovered the virus’s extending underlying conditions. Sullivan faced an additional struggle as a result of being infected with COVID-19 last year, despite the virus’s long-term effects, which included a loss of taste and smell, nausea, and diarrhea. Many COVID-19 patients too are grappling with an additional struggle: the onset of diabetes. In a research involving nearly 3,800 patients infected with the virus, cardiologist James Lo and colleagues discovered that just under half of the patients acquired elevated blood sugar levels that were not previously present. How is it conceivable for COVID-19 patients to develop diabetes? Many researchers have been tackling this exact issue for a long time.

WHO EN Be SAFE from CORONAVIRUS COVID-19 9Mar2020COVID-19 biểu trưng

When a patient develops diabetes, he or she must learn to control the illness and live an active life due to an insulin shortage. Because diabetes is incurable, the prospect that it is a long-term side effect of COVID-19 is very troubling. Insulin is essential in the human body because it lowers triglycerides by boosting lipoprotein lipase activity, which degrades triglycerides into glycerol and fatty acids. A lack of pancreatic B-cells, which release proper quantities of insulin, has a direct impact on mitochondria and the glycolysis process which is utilized for energy synthesis by all cells in the human body, eventually prompting the pyruvate product to join the Krebs cycle for ongoing energy production. Both processes are required for continual energy generation. Glucose is broken down into pyruvate and energy during glycolysis. The process can take place in the absence of oxygen, making it anaerobic. Insulin promotes glycolysis by raising the rate of glucose transport across the cell membrane and the rate of glycolysis by boosting the activities of hexokinase and 6-phosphofructokinase.

Glycolysis metabolic pathway 3

Nonetheless, people with COVID-19 have experienced sugar surges. The elevated blood sugar levels were new after infection for the majority of the patients, suggesting that many of them had not been diagnosed with diabetes prior to contracting the virus. According to Lo and other experts, the mechanism by which COVID-19 causes diabetes is currently being investigated. Patients with ARDS caused by COVID-19 and a high blood sugar level were in the hospital three times longer than those with normal blood sugar levels. While the exact cause of diabetes is unknown, researchers have discovered evidence that the coronavirus attacks pancreatic B-cells, which produce insulin. This does not yet address the question because patients who received COVID-19 continued to generate significant amounts of C-peptide, indicating that pancreatic cells were still generating insulin. Despite this, their blood sugar levels remained elevated, suggesting that something else was at fault. The virus-infected fat cells must be stimulating other cells in a detrimental way, resulting in diabetes. As a result, Lo and colleagues observed that individuals with COVID-19 had low amounts of adiponectin, a hormone generated by fat cells that helps other cells respond to insulin’s urge to take up sugar. COVID-19 can clearly infect fat cells. The virus may also cause replication in human fat, which provides another indication as to how fat is implicated in the virus and, as a result, diabetes. While obesity has a significant impact on the onset of diabetes as a result of the virus, this is not always the case. The miscommunication of fat cells is to blame. 

How may fat cell miscommunication be controlled, and who is directly affected? This is the next question that has to be addressed in order to develop a deep understanding of the long term effects of the virus.

Yes, Some of Us Have Different Human Ecosystems.

Our human ecosystems inside of us are composed of countless quantities of cells. However, only 10% of those cells are human cells.  Jeroen Raes , a Biologist based in Belgium, made a vital and fascinating discovery about the other 90%. He discovered that there are three different possible ecosystems inside individual humans. Each person has one of these three ecosystems: bacteriode, prevotella or ruminococcus. These ecosystems are composed of hundreds of trillions of harmless bacteria. One could explain our relationship with these bacteria as symbiotic, as we give them a share of food and they return the favor by helping us digest food and convert it to energy. Furthermore, these bacteria help us fight disease, and can even make us happier by triggering our neurons to release more serotonin. Raes’ experiment tested people from the US, Japan, and Denmark. Despite each regions unique diets, Raes claims to have found no correlation between diets and their individual ecosystems. Furthermore, Raes found no correlation between their age/genetic makeup and individual ecosystems.

People who have the bacteriode system “have a bias” toward bacteria that get most of their energy from proteins and carbohydrates. Bacteriode ecosystems also have more bacteria that make greater quantities of vitamins C, B2, B5, and H. On the contrary, both prevotella and ruminococcus ecosystems mostly digest proteins that are sugar coated. Both of these ecosystems also have more bacteria that create vitamin B1 and folic acid.

Raes’ findings have yielded very confusing results. Even Raes has conceded that he is unsure as to why only three total human ecosystems exist. Moreover, Raes admits his sample size of only a few hundred people will increase with more time and funding. Raes hopes to further his research on these unique human ecosystems, and potentially find links to obesity, diabetes, Crohn’s disease, and autism.

 

Biggest Ever Epigenetics Project!!

 

Marian_and_Vivian_Brown

Identical Twins

 

This article is about a project that has recently been planned out with respect to

epigenetics. It is the largest project to date and will cost around $30,000,000 to complete. Epigenetics is the study of cellular and psychological trait variations that are not caused by DNA sequence, but rather what within the DNA is triggered and shown. It is a relatively new field and has exploded in recent years. The heads of this project are TwinsUK and BGI, both very credited organizations in the realm of epigenetics. Epigenetics is the newest and recently the most popular field of all genetics and the goal of this project is to use the twins and the resources given to understand why and how epigenetics occurs.

The plan is to review the patterns of 20,000,000 sites in the DNA of each identical twin (they must be identical because their DNA must be the same and not vary) and compare the DNA with the other twins. The aim is to not look at similarities, but to look at differences and figure out how twins get different diseases if their DNA is identical. They will focus on obesity, diabetes, allergies, heart diseases, etc. at first. Until recently, science did not understand why twins could receive different diseases since their DNA is identical to their other twin, but by studying epigenetics and how genes can be triggered to do different things based on surroundings and circumstance, this idea is plausible.

Being able to locate what genes turn on to trigger certain diseases along with how to control this is something that will benefit not only our general knowledge but will also advance health care to levels that it has never seen. Experiments such as this have been done before but only with a handful of twins. The goal in this experiment is to increase the amount of twins tremendously in order to increase the accuracy of their data.

The Executive Director of BGI, Professor Jun Wang stated that the goal of this experiment is to “unlock many secrets about human genetics that we don’t currently understand, and to accelerate research and applications in human healthcare.”

 

#EpigeneticInheritance

Professor Marcus Pembrey of the University College of London transcribes the complexity of epigenetics into an understandable definition, simply put as “a change in our genetic activity without changing our genetic code.” The study of “epigenetic/transgenerational inheritance” has been a field of increasing popularity within the last decade, as studies and further research are beginning to show evidence of lifestyle stresses carrying over in the genome of each generation. Now, this is not to say that our grandparents way of living changed our DNA coding but rather potentially altered the way certain genetic information is or is not expressed.

 

To further explore the possibility of epigenetic inheritance, a laboratory in Boston conducted an experiment on three generations of mice.  A pregnant mouse was ill-fed in the late stages of pregnancy and as expected the offspring were born relatively small and later in life developed diabetes. However, the F2 generation experienced a high risk of acquiring diabetes, despite being well nourished. Another study on mice showed similar results; after a father was artificially taught to fear a particular smell, the offspring of that mouse also demonstrated a fear to the same smell.

 

Although the excitement over the groundbreaking research of epigenetics seems promising, researchers are still working to compile a stronger foundation of evidence to prove that this phenomena actually occurs in mammals. Professor Azim Surani of the University of Cambridge fully supports the idea of epigenetic inheritance in plants and worms, but has yet to commit to the same notion in mammals, as their biological processes differ greatly.

 

Links Between Human and Mice Obesity

A new study of the genomes and epigenomes of mice and humans is beginning to link the two, especially in regards to obesity.

As Andrew Feinberg, MD states, “It’s well known that most common diseases like diabetes result from a combination of genetic and environmental risk factors. What we haven’t been able to do is figure out how, exactly, the two are connected,”. Therefore, Feinberg began to study epigenetic tags to further understand gene usage.

His project with his team was to study the epigenetics of identical mice that were fed either normal or high-calorie diets. He found that the difference between normal and obese mice was the presence of chemical tags, or methyl groups, that prevent the production of proteins. This is significant because as we have learned, these types of modifications of DNA can be copied and inherited, which is then passed on into the next generation. This revealed that the normal and obese mice did not have the same location sites of their tags, giving them that alteration in their DNA. This is often seen in the alterations of the Agouti gene in mice.

Pictured here is effect of epigenetics on the physical appearances of mice (Agouti gene)

This proves that epigenetic changes are related to the environment and food sources that are around us, creating patterns based on one’s diet (which can create risk if a high-calorie intake is continuous).They also found that epigenetic changes affect genes that are already both linked to diabetes as well as those who aren’t, allowing them to further conclude that genes plays more of a role in diabetes than we previously thought.

This allows hope for future to provide epigenetic tests, which can prevent diabetes in those who are on track to have it later in life.

Article  Source: http://www.sciencedaily.com/releases/2015/01/150106130510.htm

 

Drinking Coffee May Have Health Benefits?

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Petr Kratochvil

A new study at the University of Georgia indicates that a chemical compound commonly found in coffee might prevent obesity-related disease. While previous studies show that coffee consumption can lower the risk of cardiovascular disease and Type 2 Diabetes, scientists have recently focused on chlorogenic acid, a compound also known to be in tomatoes, apples, blueberries, and pears.

The test consisted of a group of mice that were fed a high fat diet for 15 weeks while giving them CGA solution injections twice a week. Researchers found that the CGA shots helped the mice maintain normal blood sugar levels, a healthy liver composition, and prevent weight gain. It is important to note, however, that the mice received an extremely high dosage of CGA, much greater than what the average human would obtain by drinking coffee on a regular basis or eating a diet rich in fruits and vegetables.

For the past 20 years obesity has become an issue of increasing incidence in the US. Obesity often leads to two major side effects aside from weight gain: increased insulin resistance and fat buildup in the liver. In the paper published in Pharmaceutical Research, researchers write that the CGA, significantly reduced insulin resistance and accumulation of fat in the livers of mice. They plan to extend the project to develop CGA formulation for humans.

As the Liu Lab writes “CGA is a powerful antioxidant that reduces inflammation,” but they are not to quick to jump to conclusions. Scientists still believe that proper diet and regular exercise are the most effective ways to reduce obesity-related risks. That being said, I definitely think this makes us feel better about drinking coffee every morning.

Original Article:

http://www.sciencedaily.com/releases/2014/11/141114124907.htm

For More Info:

http://www.medicaldaily.com/antioxidant-coffee-might-lower-risk-weight-gain-obesity-related-diseases-310816

Artificial Sugars Causing Health Problems

Examples of Artificial Sugar

Examples of Artificial Sugars

When people consume artificial sugars, they are usually doing so instead of consuming regular sugar.  Scientists have studied the artificial sugar Saccharin in mice and some humans, and have recorded that intaking the sugar leads to obesity and Diabetes. Although the research is relatively recent, scientists recorded that 4 of  7 people with high Saccharine intakes have experienced impaired glucose metabolism, which is a symptom for Type II Diabetes.

Until recently, artificial sugars have been seen as viable alternatives to real sugar. Unlike natural sugar, artificial sugars such as Saccharine have no calories and are in beverages such as Diet Coke. Recently, however, scientists have begun to realize that artificial sugar may not be as harmless as expected, and may even be more damaging than natural sugars.

Scientists studied the intake of artificial sugars with mice. They noticed that over the course of 11 weeks, both skinny and fat mice had abnormally high glucose levels in their blood. Although scientists tested the mice for various types of artificial sugars, they noticed that one kind in particular affected the mice, Saccharin. They then tested mice again, while only feeding them high levels of Saccharin in their diet, and in only 5 weeks were able to see a difference in the glucose levels in the mice.

Next, the scientists studied microbes in mice’s intestines. The scientists noticed that the microbes in mice without Saccharin in their diets and mice with Saccharin in their diets varied greatly.

Although it is not known why Saccharin has such an effect on mice, scientists continued the study on to humans and found similar results. They studied 40 people with high Saccharin intakes and compared them to 236 people who do not intake Saccharin noticed that people who intake Saccharin have more of a tendency to have “impaired glucose metabolism.” Even healthy people who begin to intake Saccharine almost immediately begin to experience different glucose metabolism.

The reason why I chose this article is because the use of Artificial Sugars has always fascinated me. I have always been skeptical about drinking Diet Coke and other zero-calorie drinks because they seemed too good to be true. This article answered those questions for me. How do you feel about Artificial Sugars, such as Saccharin, after reading this?

Scientist Cathryn Nagler stated:”We have to respect the power of the microbiota. We need to step back and see what we are doing.”

Article Link: https://www.sciencenews.org/article/artificial-sweeteners-may-tip-scales-toward-metabolic-problems

Other Related Links:

http://en.wikipedia.org/wiki/Sugar_substitute

http://en.wikipedia.org/wiki/Saccharin

https://www.sciencenews.org/article/artificial-sweeteners-may-tip-scales-toward-metabolic-problems

http://en.wikipedia.org/wiki/Sugar

Artificial Sweeteners: Not So Sweet After All?

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Amy van der Hiel

A recent study conducted at the Weizmann Science Institute suggests that artificial sweeteners may trigger health problems instead of benefiting people. This is important because not only is saccharin in artificial sweeteners, but it is also found in salad dressings, vitamins, and in low/zero calorie items we often eat.

Previously, sweeteners were known to pass through the gut undigested, therefore allowing people with health issues to use the sugar substitute. Recent tests on mice and humans found that saccharin actually interferes and alters microbiota bacteria found in the gut and small intestines, leading to serious conditions such as obesity and diabetes.

Mice were monitored for 11 consecutive weeks when given drinking water doped with saccharin and the results showed they had abnormally high levels of glucose in their bloodstream. When food is digested it is broken down into glucose, the most common carbohydrate, and then enters the bloodstream to either be used as fuel or stored. When glucose metabolism is blocked, the blood glucose level is high. The test was repeated with mice on high-fat diet and the results were the same, showing that the saccharin had the same effect irrespective of the animal’s weight. Four of seven humans that ate a high-saccharin diet were also found to have an impaired glucose metabolism.

Why the microbiota are affected is still unknown as the test is preliminary, but the conclusion has been made that certain saccharin sugar substitutes are not simply passing through the intestines.

Original Article: https://www.sciencenews.org/article/artificial-sweeteners-may-tip-scales-toward-metabolic-problems

Photo Credit: https://www.flickr.com/photos/amyvdh/425555319

More Links:

http://www.biologynews.net/archives/2014/09/17/gut_bacteria_artificial_sweeteners_and_glucose_intolerance.html

http://well.blogs.nytimes.com/2014/09/17/artificial-sweeteners-may-disrupt-bodys-blood-sugar-controls/

http://wis-wander.weizmann.ac.il/gut-bacteria-artificial-sweeteners-and-glucose-intolerance#.VB48n4ARD1h

Diabetes–More Then Meets The Eye

In recent studies, it is said that people diagnosed with type 2 diabetes may also show signs of the beginnings  of Alzheimer’s. As we studied in our last unit, type 2 diabetes develops in a person who has taken in a lot of glucose in their lifetime. So much glucose that after a while–receptors begin to not recognize insulin. Eating too much sugary, high-fat foods, is extremely detrimental to ones health. Common side affects of diabetes include: heart disease, nerve damage, vision loss, kidney damage, and foot damage. According to my article, not only can insulin resistance cause type 2 diabetes, but also can lead to memory loss and cognitive issues. In a study done at Brown University, it was found that not only can you’re liver and fat cells become diabetic but even you’re brain can become diabetic! The hippocampus, as our class is familiar with, deals with learning and memory. When insulin is resisted in the hippocampus, cognitive problems can occur. One of the main causes of Alzheimer’s is the mass build up of the protein beta-amyloid, in the brain. This build up leaves insoluble plaques between dead cells in the brain.

An investigation was conducted to find out if beta-amyloid buildup may be a cause of cognitive decline in type 2 diabetes. 20 rats were given a high-fat diet that led to type 2 diabetes and another group of 20 rats were given a healthy diet. Both groups of rats were trained to expect a shock while in a dark cage. When rats returned to their dark cages, scientists would measure how long it took for the rats to react to the shock. Of course, the rats with type 2 diabetes proved weaker. They stood still in their dark cages twice as long as the healthy rats did.

Diabetes and Alzheimer’s epidemic is only becoming more and more relevant as the years go by. This study is important. Although preventing diabetes may not prevent types of dementia, it will prevent many other serious health problems. Because of recent findings of links between the two diseases, scientists are doing everything possible  to prevent Alzheimer’s in patients with type 2 diabetes.

 

 

 

diabetes

 

http://www.flickr.com/creativecommons/  by: GDS Infographics

 

 

 

 

 

 

Genome Project Helps Connect Ethnicity to Diseases

Though people from all over the globe share over 99% of the same DNA, there are subtle differences that make us all individuals

Scientists at the Washington University School of Medicine in St. Louis have started the “1,000 Genomes Project” in which they will decode the genomes of 1,000 people from all over the world in hopes of finding genetic roots of both rare and common diseases worldwide. On October 31st, the results of DNA variations on people from 14 different ethnic groups were published, but the scientists hope for the project to expand to involve 2,500 people from 26 different world populations. According to Doctor Elaine Mardis, co-director of the Genome Institution at Washington University, “[scientists] estimate that each person carries up to several hundred rare DNA variants that could potentially contribute to disease. Now, scientists can investigate how detrimental particular rare variants are in different ethnic groups.”

 

We are One

Everyone on earth share 99% of the same DNA. That means you, your best friend, your mortal enemy, your boyfriend/girlfriend, next door neighbor, and The President of the United States all share 99% of your DNA. However, there are rare variants that occur with a frequency of less than 1% in a population that are thought to contribute to both rare diseases and common conditions (i.e cancer, diabetes). The rare variants explain why some medications do not effect certain people or cause nasty side effects (i.e insomnia, vomiting, and even death).

 

The goal of the “1,000 Genomes Project” is to identify rare variants across different populations. In the pilot phase of the program, researchers found that most rare variants different from one population to another, and the current study supports this theory.

 

The Study

Researches tested genomes from populations from the Han Chinese in Beijing (and the Southern Han Chinese in China) to Utah Residents with ancestry from Europe to the Toscani people of Italy to the Colombians in Columbia. Participants submitted an anonymous DNA sample and agreed to have their genetic material on an online database. Researchers than sequenced the entire genome of each individual in the study five times. However, decoding the entire genome only detects common DNA changes. In order to find the rare variants, researchers sequences small portions of the genomes about 80 times to look for single letter changes in the DNA called Single Nucleotide Polymorphisms, or SNPs.

 

The Results and Importance

The Study concluded that rare variants vary from one population to another. Researchers found a total of 38 million SNPs, including 99% of the rare variants in the participants’ DNA. In addition, researchers found 1.4 million small sections of insertions or deletions and 14,000 large sections of DNA deletion. The “1,000 Genomes Project” is incredibly important in medical science. It now allows researchers to study diseases, such as cancer, in specific ethnic groups. I personally think this project in incredibly important. As an Ashkenazi Jew from Eastern Europe, my family has a medical history of certain cancers and diseases. With the results of the “1,000 Genome Project,” researches could potentially find out why, and maybe even find a cure for some of these diseases.

S U G A R !

Mmm, sugar, so yummy…

Dr. David Katz, the director at the Yale Prevention Research Center writes of the negative effects of sugar in our lives in his article “Medicine, Museums, and Spoons Full of Sugar.” It’s a fact: kids and adults are eating way too much sugar, and this excess is known to contribute to the obesity epidemic.  Obesity itself causes other complications like diabetes and other diseases.

We’ve always known that having too much sugar is a bad thing, but how does it all add up? Soda like Coke, Sprite and Fanta are regarded by some public health experts as “liquid candy.”  Soda adds tons of calories and sugar to a typical diet.  So there you have it: soda is one of the many guilty culprits in the add up of sugar.

Taken by Yasmin Kibria

That’s only part of the problem–most of the excess sugar actually comes from foods.  “A how much is too much? According to Dr. Andrew Weil, everyone has a different response to sugar.  For some it triggers modd swings, brings on a sugar rush followed by a crash, and for some, there are no noticeable effects.  Sugar tends to drive obesity, high blood pressure, and Type II diabetes in people who are genetically programmed to develop insulin resistance.

How does too much sugar lead to obesity? According to Dr. Robert Lustig, sugar causes more insulin resistance in the liver than does other foods.  The pancreas then has to release more insulin to satisfy the liver’s needs.  High insulin levels obstruct the brain from receiving signals form leptin, a hormone secreted by fat cells.

Dr. iPhones

Just when we thought apple technology was the greatest things ever. Once again the apps on our iphones, ipads, and ipods are changing our lives. Now they are finding ways to connect our physical health to our iphone apps. How? Is this possible?

Researchers are working on technology that when you take a “smart pill” or some sort of microchip that an iphone app will be able to pick up a signal and record the health of our bodies to be sent to the physicians. This reminded me of the movie we are watching in class, GATTACA, where machines are able to anayzlize our well-being and dieaseas.

Another interesting iphone app meets medicine, is insulin shots and being able to figure out how much diabetics should take. Instead of using pumps and taking blood, iphones can be all your all one in package. Phone calls, texting, camera, internet, games, facebook, music… and now get a check up. Whats next?

 

 

Is Type 1 Diabetes Curable?

Right now, on Grey’s Anatomy, one of the plot lines involves Type 1 diabetes and mice. Dr. Miranda Bailey is performing a trial, attempting to create a device with a molecule that can be placed in humans to cure diabetes. She is using mice as the trial guinea pigs. This sounds crazy! However, this same trial is being done in real life!

“Type 1 diabetes is characterized by the body’s inability to manufacture insulin because its own immune system is attacking it.”

Diabetes has doubled in our population in the last ten years. In fact, doctors have found themselves able to predict if someone has or will have Type 1 diabetes ninety percent of the time. The experiment that physicians are now doing on mice started two and a half years a go. Testing different molecules on mice, the doctors have tried to find which molecules will stop the production of Type 1 diabetes. The doctors look for particular structural pockets in the mouse’s body that are lining areas of proteins, and they then place the molecules in those particular pockets. It seems that doctors have tried this experiment on mice with hundreds of molecules in the past, but the one that works is glyphosphine. When the glyphosphine is entered into the mouse’s body, it “enhances insulin presentation”

Mice at the Louisville Zoo, Taken by: Ltshears

and kills the chances of early signs of diabetes in mice becoming Type 1 diabetes. However, if the mouse already has Type 1 diabetes, the treatment is not as effective in getting rid of it, for it has already found a home in the body. In reality, this molecule called glyphosphine is only a preventative molecule, one that can save people who have had diabetes in their family history, or are just unlucky with symptoms of a future diagnosis. This trial has been published in the Journal of Immunology and gives hope to doctors working to fight Type 1 Diabetes.  The clinical trial is to be performed on humans throughout the next five years.

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