Posts Tagged ‘insulin resistance’

Yet another reason to listen to your mother and slow down and chew your food properly – eating too quickly has been associated with a doubled risk of developing impaired glucose tolerance, or pre-diabetes. As the name suggests, pre-diabetes is the forerunner to developing type 2 diabetes. Most diabetics have type 2 diabetes – a form of diabetes where your body no longer responds properly to insulin (called insulin resistance). Type 2 diabetes used to be described as non insulin dependent diabetes.

Insulin is the hormone that moves sugar (glucose) from the blood to the body’s cells to provide them with energy. If your cells do not use insulin properly, the pancreas produces more insulin that normal to cope with the body’s demands. Eventually, the pancreas cannot keep up, and excess glucose builds up in the bloodstream. Type 2 diabetes is characterized by high levels of glucose in the blood.

A recent Japanese study followed over 170 healthy individuals for three years, monitoring their eating habits. Snacking, eating late at night, skipping meals and eating out were not associated with developing pre-diabetes. The one and only eating habit associated with the development of insulin resistance was eating too quickly. Read the full article

Researchers at the Salk Institute have discovered how a hormone turns on a series of molecular switches inside the pancreas that increases the production of insulin. The finding, published in the Proceedings of the National Academy of Sciences, raises the possibility that new designer diabetes drugs might be able to turn on key molecules in this pathway to help the 80 million Americans who have type 2 diabetes or pre-diabetic insulin resistance.

The molecular switches command pancreatic beta islet cells, the cells responsible for insulin, to grow and multiply. Tweaking these cells might offer a solution to type 1 diabetes, the form of diabetes caused by destruction of islet cells, and to type II diabetes, the form caused by insulin resistance.

“By understanding how pancreatic cells can be encouraged to produce insulin in the most efficient way possible, we may be able to manipulate those cells to treat or even prevent diabetes,” says the study’s lead author, Marc Montminy, a professor in the Clayton Foundation Laboratories for Peptide Biology at Salk.

To read the full article on ScienceDaily, >Click Here.<

MADISON – Ten years of meticulous mouse breeding, screening, and record-keeping have finally paid off for Alan Attie and his lab members. The University of Wisconsin-Madison researchers’ efforts, published Oct. 6 in the journal PLoS Genetics, pinpointed a gene that confers diabetes susceptibility in obese mice.

They also showed that the protein coded by the gene, called tomosyn-2, acts as a brake on insulin secretion from the pancreas. “It’s too early for us to know how relevant this gene will be to human diabetes,” says Attie, a UW-Madison biochemistry professor, “but the concept of negative regulation is one of the most interesting things to come out of this study and that very likely applies to humans.”

In a properly tuned system, insulin secreted into the blood after eating helps maintain blood sugar at a safe level. Too little insulin (as in type 1 diabetes) or insulin resistance (as in type 2 diabetes) leads to high blood sugar and diabetic symptoms. Too much insulin can drive blood glucose dangerously low and lead to coma or even death in a matter of minutes.

“You can imagine that if you’re in a fasted state, you don’t want to increase your insulin, so it’s very important to have a brake on insulin secretion,” says Angie Oler, one of the lead authors. “It needs to be stopped when you’re not eating and it needs to start again when you do eat.”

The group honed in on tomosyn-2 while searching for genes that contribute to diabetes susceptibility in obese animals. Why study fat mice?  To read the entire Press Release on FierceBiotech, >Click Here.<

A study published in the American Journal of Clinical Nutrition found that the more red meat people eat, especially processed meat, the higher their risk of developing type 2 diabetes.

Processed meats include the American staples bacon, sausage, hot dogs and most packaged sandwich meats. The study did not establish why red and processed meats increased the risk of developing diabetes. One theory is that the high amount of nitrates used as preservatives in processed meats may increase insulin resistance.

Others theorize that the large amount of iron in red meat leads to high iron stores in the body, which have been associated with an increased risk of type 2 diabetes. A third theory is that high meat consumption may contribute to obesity – a major risk factor for diabetes. The answer may lie in a combination of these factors.

To read more about the issue on WebMD, >CLICK HERE.<

Photo: Julius Schorzman

Add your daily cup of java to the list of things that can make it more difficult to control your diabetes. A growing body of research indicates that caffeine disrupts glucose metabolism and increases insulin resistance, even in people that don’t have diabetes.

The findings raise concerns that caffeine’s tendency to increase insulin resistance could increase the risk of developing diabetes, or lead to poor control of the disease in those that already have it.

In people with type 2 diabetes, the expected rise in blood sugar after eating carbohydrates is exaggerated if they also drink a caffeinated beverage. This larger than anticipated rise in blood glucose could throw off diabetics’ calculations of the required dosage of diabetes medication, including insulin injections.

This is further complicated by the fact that people metabolize coffee at different speeds, and that both slow and fast metabolizers are common in the general population.

Caffeine is not only found in coffee, but also in tea, soft drinks and in energy drinks. Caffeine’s impact on glucose metabolism was reported on in the inaugural issue of the Journal of Caffeine Research: The International Multidisciplinary Journal of Caffeine Science.

“The links that have been revealed between diabetes and the consumption of caffeine beverages – especially coffee – are of monumental importance when it is acknowledged that more than 80 percent of the world’s population consumes caffeine daily,” says the new journal’s editor in chief, Jack E. James.

Credit: Gutenberg Encyclopedia

Researchers from the Max Planck Institute for Neurological Research (MPINR) claim to have proven that insulin has direct effects on the reward centers of the brain.  In a recent article in Cell Metabolism outlining their work the MPINR team explained that they set out to better understand the “reward” aspects of food and how insulin influences brain function.

Unlike earlier studies that had focused on insulin’s effect on the feeding behavior related hypothalamus, the team focused on neurons in the brain that release dopamine, a brain chemical that plays a role in reward and motivation. They found that insulin causes the dopamine-releasing neurons to fire more frequently.

Mice whose insulin receptors were inactivated to no longer respond to insulin overate and became obese. They also showed an altered response to sugar and cocaine when their food supply was limited, further suggesting that the brain’s reward centers require insulin to function normally.

The findings suggest that insulin resistance may help to explain why many obese individuals find it so difficult to resist food and lose weight. “Insulin resistance may drive a vicious cycle,” explains MPINR’s Jens Bruning, “There is no evidence that this is the beginning of the road to obesity, but it may be an important contributor to obesity and to the difficulty we have in dealing with it.

The next step is to conduct functional magnetic resonance imaging (MRI) scans in human subjects who have had insulin artificially delivered to the brain to observe its effects on their reward centers.

To read the article in Cell Metabolism, >CLICK HERE.<

Researchers at the Salk Institute for Biological Studies have discovered a mechanism that stimulates glucose production in the liver in response to a drop in blood sugar. Histone deacetylasses (HDACs) are a group of enzymes that respond to what researchers call “fasting signals”.

Fasting signals kick in after long periods without food, such as overnight. HDACs are situated in liver cells, usually outside of the nucleus. The Salk researchers discovered that they move rapidly into the cell in response to fasting signals, and turn on the genes that produce glucose.
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Doctors and researchers have known for a while that excess weight, diet and lack of exercise can all be contributing factors in the development of type 2 diabetes and insulin resistance. Unlike type 1 diabetes, which is known as an immune disease, type 2 diabetes is generally considered a metabolic disorder, and is attributed to poor lifestyle choices. A new study shifts some of the responsibility for the development of their condition away from the patients by shedding light on other possible influences.

For this study, the results of which were published in Nature Medicine, researchers tested blood samples of 32 obese people, and found that the half who had insulin resistance had antibodies that were not present in the half who were obese but not insulin resistant.  This suggests that type 2 diabetes may be an immune disorder, and that there is a possibility of developing a vaccine for the condition. Read the full article

dna

Photo credit: jscreationzs

An international study found that nearly ten percent of Europeans with Type 2 diabetes have a mutation in a gene called HMGA1.  HMGA1 regulates how the body responds to insulin. The gene mutation causes insulin resistance, a condition where the body can no longer use insulin effectively.

This finding, which was published in the March 2011 Journal of the American Medical Association, has important significance in screening for and treating type 2 diabetes in the future, and may lead to better diabetes medications. To read the whole story online at WebMD, click >HERE<.

empty alcohol bottle

Photo credit: nkzs

Actos, an oral diabetes medication used to treat type 2 diabetes, may play a future role in combating alcohol addiction. Actos belongs to a class of medications called thiazolidinediones, or TZDs (also known as glitazones). TZDs reduce insulin resistance by binding to peroxisome proliferator-activated receptors, or PPARs. They also activate PPAR-g, a sub-class receptor which may play a role in the brain’s reward circuits involved in addiction.

“As we learn more about the brain, we are seeing a growing number of examples where medications developed initially for purposes unrelated to psychiatry may have new and otherwise unexpected applications,” writes Dr. John Krystal, the Editor of Biological Psychiatry, “New data in animal models suggest that TZDs might be promising agents in the fight against addiction.”

Research is also ongoing in the use of commonly prescribed cholesterol medications in fighting nicotine addiction.  To read the whole article in Science Daily, click >HERE<.