Obesity and Diabetes – Is Your Gut in Control?

August 28, 2015 by

Aug. 21, 2015

By Medical Discovery News

Your body is like a forest, providing a home to microscopic flora and fauna. In fact, your body is home to up to 100 times more microbes than your own cells, which make up your microbiome. While we provide them residence, these microbes help us out by providing a first line of defense against disease trying to invade our bodies, even breaking down food during digestion and producing vitamins. Now, the microbes that live in the digestive tract are helping us understand diabetes better.

According to the Human Microbiome Project sponsored by the National Institutes of Health, the microbiome plays a huge role in human health. When the microbiome is altered or imbalanced, it can cause conditions like obesity, irritable bowel syndrome, skin disease, urogenital infection, allergy, and can even affect emotion and behavior.

Recently, scientists from Israel discovered another surprising effect of the microbiome while investigating the use of artificial sweeteners in relation to glucose intolerance and diabetes. Artificial sweeteners such as saccharin, sucralose, and aspartame are commonly used in weight loss strategies because they do not add calories while still satisfying sweet cravings. However, artificial sweeteners are not always effective in managing weight and glucose, and scientists at the Weizmann Institute of Science may have figured out why.

Through experimentation they observed that adding artificial sweeteners to the diets of mice caused significant metabolic changes, including increasing blood sugar levels more than mice fed regular sugar. It didn’t matter whether the mouse was obese or at a normal weight, they all reacted the same. Dietary changes can alter the populations of bacteria in our guts, so the study addressed whether those changes affected blood glucose levels as well. After being treated with saccharin for nine days, the populations of gut bacteria in the mice shifted dramatically and corresponded with an increase in their glycemic index. Specifically, the bacterial group Bacteroidetes increased while the group Clostridiales decreased. These changes in bacterial populations is associated with obesity in mice and people.

When they administered antibiotics to reverse this and return the bacterial populations to a healthy state, it also countered the effects of saccharin, returning glucose levels to normal. To take it a step further, researchers took feces from saccharin-consuming mice showing glucose intolerance and transplanted them into other mice that had never consumed saccharin. Remarkably, those mice started showing signs of glucose intolerance.

In a study of 400 people, those who consumed artificial sweeteners had a gut microbiome that was vastly different from those who did not. They had a group of people consume high levels of artificial sweeteners for seven days, and like the rats their glucose levels increased and their microbiomes changed.

Overall, these studies show that artificial sweeteners may induce glucose intolerance instead of preventing it due to the intimate connection between the bacteria that live in our digestive systems and our metabolic state. In the future, expect to see diagnostic and therapeutic procedures that utilize our microbial friends.

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Sweet Guts

November 29, 2014 by

Nov. 21, 2014

By Medical Discovery News

Sweet guts

Your tongue isn’t the only part your body that can taste sweetness. Three years ago, scientists discovered that our intestines and pancreas have receptors that can sense the sugars glucose and fructose. This could revolutionize treatment for diabetics, who must closely monitor their blood sugar levels. A drug called New-Met, made by Eleclyx Therapeutics in San Diego, that is now in phase II clinical trials is attempting to do just that by targeting those sugar receptors in the digestive system.

It appears these taste receptors are basically sensors for specific chemicals that can serve functions other than taste in other parts of the body, although we don’t know what all those functions are yet. We do know the function of the T1R2/T1R3 taste receptor found on some cells in the intestine. When they detect sugar molecules, these cells secrete hormones called incretins, which in turn stimulate insulin production in the pancreas.

This neatly explains a phenomenon that had mystified scientists for over 50 years: eating glucose triggers significantly more insulin than injecting it directly into the bloodstream. When intestinal cells with sweet receptors detect sugar, they trigger neighboring cells to make a glucose transporter that allows the sugar to be absorbed by the body. The faster sugar is absorbed, the more signals are sent to the pancreas, and the more insulin it releases. Signals are also sent to the brain to tell us we are satiated. Artificial sweeteners can trigger the same effect. Understanding these signals is critically important in the control of blood sugar levels.

Metformin is a drug commonly prescribed to those with type 2 diabetes. It regulates blood sugar levels by decreasing the amount of glucose produced by the liver. Metformin may also modulate multiple components of the incretin signaling system. In combination with insulin, it increases the use of glucose in peripheral tissues like muscles and the liver, especially after meals, reducing blood sugar levels even further. Metformin is usually taken orally, so that it dissolves in the stomach and travels through the bloodstream to the liver.

New-Met is a novel formulation of metformin that dissolves when exposed to the pH in the intestine rather than the stomach. There, it binds to those sweet receptors and activates the release of incretins that stimulate the release of insulin, thereby regulating blood sugar levels. This mimics the natural signaling process triggered by sugars and is fast and direct. This reduces the amount of drug required to be effective by 70 percent. Patients on New-Met had fewer gastrointestinal side effects than those taking the standard metformin, which is the primary reason diabetics choose not to take it.

The number of people with diabetes will soon climb to 592 million, so the demand for better medications to treat them will continue to climb as well.

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A Teaspoon of Agavin

September 13, 2014 by

Sept. 12, 2014

By Medical Discovery News

Agave plant

Next time you have a bitter pill to swallow, think about reaching for a spoonful of agavin instead of sugar to help the medicine go down. You might not know what agavin is yet, but you’ve probably noticed that a number of alternative natural sweeteners like Stevia have been added to grocery store shelves next to traditional sugar. These products sweeten foods but often do not add calories or raise blood sugar levels. Recent research suggests that a sweetener made from agave, the same plant used to make tequila, may lower blood sugar levels and help people maintain a healthy weight.

Agavin is a natural form of sugar, fructose, called fructan. With fructan, individual sugar molecules are linked together in long chains. The human body cannot use this form of fructose, so it is a nondigestible dietary fiber that does not contribute to blood sugar levels. But it can still add sweetness to foods and drinks. Alternatively, agave syrup or nectar, while made from the same plant, contains fructan that has been broken down into individual fructose molecules so it does affect caloric intake and blood sugar levels.

Studies of mice prone to diet-induced obesity and type 2 diabetes found that when they consumed agavin, they ate less and had lower blood glucose levels, increased insulin, and more glucagon-like peptide-1 (GLP-1). GLP-1 is a hormone that inhibits gastrointestinal motility, which causes people to eat less because they feel fuller. It also stimulates the production of insulin. GLP-1 appears to be a regulator of appetite and food intake, and so it is being evaluated as a therapy for type 2 diabetes.

Further testing showed that when agavin was added to the water supply of mice eating a normal diet, they ate less, lost weight, and had lower blood glucose levels compared with mice that consumed other sugars such as glucose, fructose, sucrose, agave syrup, and the artificial sweetener aspartame. While these results are encouraging, the studies need to be replicated and then done using humans for agavin’s effectiveness to be proven. The possible long-term consequences of its use must also be examined. So far, the only known down sides are that agavin is not yet widely available and that it is not as sweet as sucrose or artificial sweeteners.

Agavin would join other natural sweeteners that do not add calories or affect blood sugar such as stevia, which is currently found in a variety of products. The stevia plant is native to Paraguay, where its leaves have been used as a sweetener for over a century. Stevia has been the subject of biological and toxicological studies for more than 50 years and its safety is well-established. It stimulates the pancreas to secrete insulin, a benefit to diabetics, and does not alter the naturally-occurring, beneficial bacteria in the digestive tract.

Thanks to agavin and other natural sweeteners, people with diabetes (or anyone watching their caloric and sugar intake) now have more choices than ever for sweeteners and products made with them, so they can eat or drink without raising their blood sugar levels. Agavin: it’s not just for tequila anymore.

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Bring on the Milk

June 22, 2014 by

June 20, 2014

By Medical Discovery News

Milk

Drinking milk might seem perfectly natural, but it’s actually anything but. Humans are the only species who retain the ability to digest milk after childhood, or at least some of us do. Up to half of adults worldwide don’t have the ability to break down lactose, the main sugar in milk, because their bodies stop producing the enzyme lactase after the age of five.

About 65-75 percent of the population has some degree of lactose intolerance, the most common cause for digestive issues with dairy. Lactase breaks down lactose into simpler forms of sugar that can be absorbed by the bloodstream. Without this enzyme, lactose is fermented by bacteria, causing symptoms like abdominal pain, bloating, flatulence, nausea, and diarrhea 30 minutes to two hours after eating. Populations that have long relied on unfermented milk have the lowest rate of lactose intolerance – only five percent among the Swiss.

Humans’ ability to drink milk actually began as a genetic mutation, like the superheroes of X-Men comics. According to the leading theory, 7,800 years ago humans began to move northward. Since the sun is not out as long in northern latitudes, they could not absorb enough vitamin D from sunlight and needed another source to thrive. Milk is high in vitamin D, which aids in calcium absorption. Humans adapted to this change in their diets and developed a variant of the lactase gene that allowed them to continue synthesizing the enzyme throughout their lifetimes. Since humans with the gene variant had the advantage of consuming more vitamin D, they were successful in passing that gene on to future generations.

But new research suggests that this theory is either wrong or other factors were involved. Scientists in northeastern Spain discovered well-preserved skeletons of people who lived 5,000 years ago. DNA testing revealed that none of these eight skeletons carried the genetic mutation for lactase production. Further testing also showed that these ancient humans are indeed related to modern Spaniards. Next, computer simulations determined that over 5,000 years, chance alone would not have allowed one-third their descendants to digest milk. Strong selection for this trait would have been necessary.

These scientists developed a theory that early farmers began eating fermented dairy products such as cheeses, which have lower levels of lactose. But when food was scarce, they ran out of fermented dairy products and began to consume unfermented milk as a food source. Then, those who acquired the mutated gene for lactose production would have thrived. Those without the mutation would have suffered from diarrhea, making their situation worse, perhaps even life-threatening if they were already starving.

While the need for vitamin D from milk may have been a factor in the spread of lactase persistence, these new findings show that other factors may have also been a part of the selection process that drove this mutation into the population. Now if we could only figure out a way to turn on lactase genes again during adulthood, everyone with lactose intolerance could enjoy a pain-free ice cream cone.

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How Much Sugar Is Safe?

January 31, 2014 by

Jan. 31, 2014

By Medical Discovery News

Sugar

Former Mayor Michael Bloomberg of New York City caused a controversy when he tried to ban the sale of sugary drinks more than 16 ounces. Thus the “Big Gulp” rebellion was born and the ban was later overturned by the courts. Yet the rates of diabetes, heart disease, and obesity remain out of control in the U.S.

In the U.S., 24 million people over age 20 have diabetes. Another 78 million have pre-diabetes with blood glucose levels higher than they should be – the start of glucose intolerance.  And down the road, this may lead to life-threatening heart disease (the No. 1 killer of adults), which is also linked to obesity affecting more than 80 million Americans.

Much of the obesity epidemic has been blamed on unhealthy eating and poor nutrition. Refined sugar has been identified as a source of excess calories. According to the U.S. Departments of Agriculture and Health and Human Services, almost 50 percent of sugar in the diets of Americans comes from sugary drinks and sweetened fruit drinks. The debate over just how much sugar is too much in terms of our health was addressed by a recent study and the results are sending shock waves through the medical community. 

In the experiment, one group of mice ate a normal diet and another group ate a diet where one quarter of the calories came from sugar similar to that in high fructose corn syrup. This level of sugar is pretty equal to that consumed naturally by 15 to 25 percent of the U.S. population. This is equivalent to a person consuming three cans of a sugary beverage a day in an otherwise sugar-free diet. Current nutrition guidelines consider this to be at the top of the safe level of sugar for people.

After 26 weeks of a monitored diet, all the mice were released into an experimental natural environment. Over the next 32 weeks, twice as many sugar-fed female mice died compared to the control group. The sugar-fed male mice produced 25 percent fewer offspring and held 26 percent less territory than mice from the control group. Overall, dietary sugar was linked to a shorter life span, limited reproduction, and lowered competitive success. 

Metabolic measurements on the sugar-fed mice showed changes in glucose clearance and increases in cholesterol levels, but these were considered minor. Nevertheless, life outcomes called Organismal Performance Assays were significantly affected. This may represent a new way to gauge important changes in overall life parameters without corresponding physiological changes.

This certainly raises the question of how much sugar is too much, and the debate over the appropriate level of refined sugar for good human nutrition will continue. It will be interesting to watch in the coming months and years to see if these results are substantiated and if they lead to new nutritional guidelines. Who knows – maybe Mayor Bloomberg was right after all!

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Insulin by Nanoparticle

November 22, 2013 by

Nov. 22, 2013

By Medical Discovery News

Diabetes is a life-changing diagnosis that can mean several injections of insulin and several tests of blood glucose levels every day. Some people with diabetes say they feel like a pin cushion, and children with Type 1 diabetes often find it particularly challenging. However, there may be some relief in sight thanks to nanoparticles.

Researchers have developed a new insulin delivery system that involves a network of nanoparticles. Nanoparticles range in size from one to 2,500 nanometers. For an idea, the width of a strand of human hair is 100,000 nanometers. Once injected, the nanoparticles release insulin in response to increases in blood sugar levels for up to a week. They have been tested in mice and if they perform similarly in people, this may be a better solution than multiple daily injections.

Nanoparticles used to deliver insulin consist of an insulin core, modified dextran, and glucose oxidase enzymes. When glucose levels rise in the blood, the glucose oxidase enzyme in the nanoparticle activates and converts the blood glucose into gluconic acid. This in turn dissolves the modified dextran, releasing the insulin in the core of the nanoparticle.

The more sugar in the blood system, the more insulin is released, mimicking what the pancreas does in those without diabetes. Insulin is a hormone produced by the pancreas that is required to get glucose into cells.

Those with Type 1 diabetes must estimate the amount of carbohydrates in the foods they intend to eat, test their blood sugar levels, and then calculate the amount of insulin that will hopefully keep them in the normal range. The body uses carbohydrates to make glucose, which is the primary fuel for cells. Carbohydrates include simple sugars like lactose, fructose, and glucose that are found naturally in foods such as milk, fruits, and vegetables. However, natural and artificial sugars like corn syrup, sweeteners, and dextrose are also added to many processed foods. Everyone, especially diabetics, is encouraged to limit foods that are high in added sugars.

Complex carbohydrates such as starch and dietary fiber are broken down to glucose but much more slowly. Dietary fibers are in vegetables, fruits, beans, peas, and whole grains. Most Americans don’t get enough dietary fiber because they eat too much bread and dough made from refined flour. Most people, including diabetics, benefit from increasing the amount of whole grains such as brown rice, quinoa, whole wheat, rye, and oats they eat. 

According to the American Diabetes Association, in 2011 there were 25.8 million diabetics, 8.3 percent of the population. An estimated 7 million more have not been diagnosed and another 79 million are prediabetic. In 2012, treating diabetes cost $245 billion.

While it is also important to control the number of new cases of diabetes, devising new methods to more precisely control blood sugar will reduce complications from diabetes and make the lives of diabetics easier.

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Rise of Cavities

August 9, 2013 by

August 9, 2013

By Medical Discovery News

By 65, 92 percent of Americans have cavities in their permanent teeth, and an average of 3.28 teeth missing or decayed. The answer to why this is may not concern toothpaste ingredients or brushing time, but the lifestyles of ancient humans, as two new studies have discovered.

Humans used to live as hunter-gatherers, meaning they hunted for game and foraged for plants to eat. They were mainly nomadic, following herds to keep their food source. That changed about 10,000 years ago when agriculture was invented. They began to settle down in one place, raising livestock and growing crops for food. The human diet changed as it now included more starch from the grains they harvested.

The breakdown of starch begins with enzymes in the mouth that split the starch into shorter chains of sugars. The process continues in the stomach and the small intestine until the sugar chains are broken down into individual sugar molecules. This leaves a residue of sugar in a film on and between teeth, creating an ideal environment for the growth of bacteria. Two recent studies have documented how this change in diet caused bacteria associated with cavities and periodontal disease to emerge and eventually become widespread.

One group analyzed the bacterial DNA in samples of tarter from ancient teeth to monitor the changes in the types of bacteria that were present. What they found was a record of how humans have wrecked the bacterial ecosystem in their mouths. The increase in starchy foods caused sugar-loving bacteria to flourish.

With new DNA sequencing technologies, scientists isolated bacterial DNA from 34 teeth of Northern Europeans that are 7,000 to 400 years old, including the last hunter-gatherers from Poland and early farmers from Germany. Hunter-gatherers’ teeth harbored fewer types of cavity-causing bacteria, while early farmers’ teeth revealed a sharp increase in bacteria that cause tooth decay and periodontal disease. 

One bacterium, called Streptococcus mutans, contributes to cavities, diabetes, and cardiovascular diseases. In the mid-1800s, Strep mutans became even more dominant in the oral microbiome. This change correlates with the Industrial Revolution, which introduced refined grains and sugars. The simple sugars from these processed foods are the basis for microbial fermentation, which lowers the pH of the mouth and causes damage to tooth enamel.

The second study focused on changes in the DNA of Strep mutans alone from the present then going back in time. They sequenced the genomes of the bacterium from 57 people worldwide, then used some clever genetics modeling to calculate when the Strep mutans started expanding and diversifying. They think that occurred about 10,000 years ago, which correlates to the start of agriculture. 

Both studies show that the oral microbiome changed with the development of agriculture. What neither group has dealt with are the influences of modern behaviors like using toothpaste, adding chlorine and fluoride to drinking water, and more changes to the human diet, particularly the shift to fast food.

 For a link to this story, visit http://www.medicaldiscoverynews.com/shows/351-rise.html.

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