Category: Diabetes News

Researchers from the Stanford University School of Medicine have discovered that the artificial activation of an important molecular pathway could someday be used to treat various diseases. The pathway is responsible for decreases in the growth of cells that produce insulin, and is activated naturally as an individual grows older. The findings were published in the October 12 edition of the journal “Nature.”

The pathway being studied appears in both mice and humans. It is activated by the expression of a particular molecule called platelet-derived growth factor receptor, or PDGF-receptor for short. Expression of this molecule naturally decreases over time, as does the growth of beta cells in the pancreas, which release insulin that helps removes glucose from the bloodstream and transports it to cells where it can be used as energy.

Scientists have long known that the growth of pancreatic beta cells decreases dramatically over time. In young and newborn humans and animals, beta cell proliferation is abundant.

Another molecule known as Ezh2 appears to be involved in the pathway that reduces production of beta cells, as expression of the molecule decreases over time. Scientists were unaware, however, what caused the change in expression of Ezh2.

Researchers on the study discovered that, in juvenile mice, the expression of PDGF receptors was reduced in the islet cells of the pancreas in a similar pattern to that of the decreases in beta cell production.

Blocking the expression of PDGF receptors in young lab mice—two to three weeks old—caused decreases in Ezh2 production and the number of pancreatic beta cells than control animals whose PDGF receptors were not affected. The mice with reduced Ezh2 production also demonstrated slightly higher blood sugar levels than control subjects and could not remove glucose from the blood stream as effectively when they were given a high glycemic load, such as after a meal heavy in carbohydrates.

A lack of expression in PDGF receptors also affected fully-grown lab mice: their ability to replace beta cells was diminished when the cells were destroyed by a compound that the researchers administered to the animals. They also developed severe diabetes after their beta cells were destroyed.

“We’re hopeful that soon we might be able to manipulate this pathway in a therapeutic way in humans,” said Seung Kim, M.D., Ph.D., senior author of the study and a professor of developmental biology at Stanford University. Kim believes that scientists may one day develop a therapy that activates the pathway to promote the regrowth of beta cells or prevent their destruction.

“Perhaps by rekindling its expression and then activating it through a drug we could give in an injection or through some other route. This could be a kind of one-two punch against diabetes,” continued Kim.

If scientists can develop a therapy that promotes growth of beta cells, it could offer a new method of treating or preventing diabetes that differs from current therapeutics, which mostly focus on maintaining healthy blood glucose levels. Replacing pancreatic beta cells could allow the body to produce its own insulin to regulate blood glucose instead of relying on insulin injections or other medication to control blood sugar.

“This gives us a handhold onto a vaster problem: how to control human beta cell proliferation in a therapeutic way,”

Additionally, the researchers commented that they found other molecular patheways related to the loss of beta cells due to aging that have not yet been explored.

Metformin treatment has been shown in research to provide a significant decrease in risk of cancerous cell growth and thus a decrease in risk of cancer overall. A recent meta-analysis has confirmed that patients with Type 2 diabetes who undergo metformin treatment are similarly at a significantly reduced risk of developing colorectal cancer — a 37 percent decrease in risk. The results were published in the October 2011 issue of the journal “Diabetes Care,” the journal of the American Diabetes Association.

“The results indicate that metformin therapy was associated with an estimated reduction of 37% in the risk of colorectal cancer among patients with type 2 diabetes,” said the researchers on the project.

The meta-analysis was conducted at Shanghai Jiao Tong University in China and was headed by Zhi-Jian Zhang, M.D., Ph.D., with the department of epidemiology and biostatistics at the School of Public Health division of the university. Dr. Zhang’s research team pooled together the existing data from studies that investigated the effects of metformin treatment on colorectal cancer in patients with Type 2 diabetes. Information was pulled from the SciVerse Scopus and PubMed databases, comprising five studies that had been published between January 1966 and March 2011. In all, data from 108,161 patients was identified and used to analyze trends in metformin treatment as it related to risk of colorectal cancer in Type 2 diabetics.

The researchers found that metformin therapy was associated with significantly decreased risk of colorectal neoplasm when compared to patients who received non-metformin treatment (RR=0.63; 95% CI, 0.50-0.79).

The research team did not include one of the identified studies, which had been conducted on colorectal adenoma. After the exclusion of that study, the data of 107,961 diabetes patients remained, with 589 cases of colorectal cancer occurring during the follow-up periods of the four remaining studies. After the findings were adjusted to exclude the study on colorectal adenoma, researchers still found that metformin therapy was associated with significantly reduced risk of developing colorectal cancer (RR=0.63; 95% CI, 0.47-0.84).

The researchers stated that they did not find any evidence which would suggest significant heterogeneity across the studies (P=.30).

According to the research team, metformin may help fight the growth of cancer cells due to its role in the tumor suppressor pathway, where it activates AMP-activated protein kinase (9) and is also a part of the sequence that activates LKB1, a gene that is known to suppress tumors. Additionally, in vitro studies have shown that metformin actually selectively kills cancer stem cells. Those findings have been confirmed in rodent experiments, which also showed that metformin inhibited carcinoma growth in the colon.

The authors noted that previous research has tested the effects of metformin on non-diabetic humans with rectal aberrant crypt foci — one of the earliest warning signs that the individual may develop colon cancer. The findings of that study demonstrated that one month of metformin treatment was associated with a decrease in aberrant crypt foci compared to a control group who did not receive metformin treatment.

The researchers commented that if metformin therapy is definitively proven in further research to significantly reduce risk of colorectal cancer, it will likely be prescribed to most diabetics as a measure to manage blood glucose levels and also to prevent cancer.

“If metformin therapy ultimately proves effective on reducing the risk of colorectal cancer, it would likely be recommended for the overwhelming majority of diabetes patients for both blood glucose control and cancer prevention,” said the researchers.

A recent population-based study conducted by researchers at Columbia University in New York found that patients who had been diagnosed with diabetes for a period of ten years or more were over three times more likely to suffer ischemic stroke. The study, called the Northern Manhattan Study, was a large, longitudinal investigation that allowed researchers to study how risk changed over long periods of time.

Scientists have known for years that patients with diabetes are at an increased risk of ischemic stroke. However, according to Dr. Julio R. Vieira, who presented the findings at the meeting of the American Neurological Association, the ten-year length of the study allowed researchers to look at long-term risks.

The study followed 3,298 participants of varied ethnic backgrounds. The participants had no prior history of stroke. They were tested for diabetes at baseline — the beginning of the study — and then tested again every year, starting in 1993.

The mean age of the participants at the beginning of the study was 69 years, with the ages ranging from 59 to 79. Over half of the participants were Hispanic, while 24 percent were black and 21 percent were white.

At the start of the investigation, 717 patients — 22 percent — had diabetes. An additional 338 patients (10 percent) developed diabetes throughout the course of the study.

Median follow-up among the participants was nine years. Throughout the follow-up period, 244 participants were diagnosed with ischemic stroke.

Researchers used Cox proportional hazards models to determine that the participants who had diabetes at the outset of the study were 2.5 times more likely to experience ischemic stroke throughout the course of the study. Additionally, the risk of suffering an ischemic stroke increased throughout the ten-year follow up period for patients who had diabetes at baseline as well as those were diagnosed with the disease during the study. Participants who had diabetes for five years or less increased their risk of ischemic stroke to 70 percent; those who had diabetes for five to ten years had an 80 percent risk of stroke; and patients who had diabetes for ten years or more were 3.3 times more likely to have an ischemic stroke.

Dr. Vieira stated in an interview conducted after his presentation that most of the participants involved with the study had been diagnosed with Type 2 diabetes. He noted that although diabetics were at an increased risk of ischemic stroke even from the beginning of the study, that risk did not triple until the patients had diabetes for ten years. Risk of stroke was always higher in diabetics but it took a fairly long history of the disease before the risk was significantly elevated.

“Diabetes, like hypertension and all of the other risk factors for cardiovascular disease, takes a while to really cause big damage,” said Dr. Vieira. “That’s exactly what we’re seeing here.” He stressed that patients who had been newly diagnosed with diabetes still had time to make changes to reduce their risk of stroke. “You have a lot of time for intervention,” he said.

However, the risk of stroke may be what compels diabetics to begin managing the disease more effectively. Dr. Vieira commented that even though he warns diabetics of the complications that can occur as a result of the disease, including vision loss and limb amputation, it doesn’t always incur changes. Significantly increased risk of a disabling or fatal stroke, however, may be the catalyst that drives diabetics to better manage the disease.

For individuals with Type 1 diabetes, maintaining healthy blood sugar levels could be not only a necessity for long-term health, but also the key to staying mentally sharp. A study published in the online version of the journal “Diabetes” states that increased exposure to hyperglycemia — elevated levels of blood sugar — is associated with negative effects on brain size, including a decrease in whole brain gray matter. Meanwhile, hypoglycemia is associated with more severe decreases in occipital/parietal white matter volume.

The study was headed by Dana C. Perantie of the Washington University School of Medicine, located in St. Louis, Missouri. Dr. Perantie’s team analyzed physiological changes in brain regions in youths who had Type 1 diabetes when they were exposed to blood sugar levels on both the high and low ends of the spectrum. The control group for the study was comprised of the children’s siblings, who did not have Type 1 diabetes.

At baseline — the beginning of the study — each of the participants underwent brain neuroimaging. Doctors followed up with patients for two years, and patients underwent neuroimaging once again at the end of the follow-up period. Throughout the follow-up, a variety of glucose control measurements were recorded, including HbA1c levels, results from glucose meter readings, and self-reported episodes of severe hypoglycemia. After the neuroimaging was complete at the end of the follow-up, researchers studied whole brain and voxel-wise changes in the volume of gray and white matter in the study participants. Results were also adjusted for age, gender, and the age at which the patients were diagnosed with diabetes.

The findings showed no differences between patients with Type 1 diabetes and the control group in whole brain and voxel-wise brain volume throughout the two-year follow up. However, the patients in the group with Type 1 diabetes who had more hyperglycemia showed a significant decrease in whole gray brain matter than those who had less hyperglycemia. In addition, patients with Type 1 diabetes who experienced severe hypoglycemia showed significant decreases occipital/parietal white matter volume over both the control group and the group of Type 1 diabetics who had not experienced severe hypoglycemia.

“Within diabetes, exposure to hyperglycemia and severe hypoglycemia may result in subtle deviation from normal developmental trajectories of the brain,” commented the authors of the study.

The subject of changes in brain physiology related to Type 1 diabetes has been previously studied in previous research. A 2007 study published in the journal “Diabetes Care” used magnetic resonance imaging (MRIs) to study differences in brain volume among children with Type 1 diabetes and their non-diabetic siblings, age 7 to 17. The study similarly found that volume of grey and white brain matter did not differ significantly between diabetics and non-diabetics, but patients who had a history of severe hypoglycemia displayed reduced gray matter volume in the left superior temporal region. Additionally, patients who had a history of hyperglycemia showed smaller white matter volume in the right posterior parietal region and larger gray matter volume in the right prefrontal region.

The authors concluded that “qualitatively different relationships were found between hypo- and hyperglycemia and regional brain volumes in youth with type 1 diabetes.” They also commented that future research would be necessary to determine what effect, if any, the changes in brain volume would have on cognitive function and whether further exposure to extreme blood sugar conditions would have additional effects on brain matter volume.

The Utah Obesity Study has provided the first prospective, long-term controlled trial on the effects of gastric bypass surgery. The trial discovered that the cardiometabolic improvements associated with recent gastric bypass surgery also persist over long periods of time.

Of the 1,156 morbidly obese participants the Utah Obesity Study, 418 underwent gastric bypass surgery. An additional 417 patients sought to undergo the bariatric procedure but were unable to do so, primarily because of insufficient health insurance. Another 321 patients from the Utah Health Family Tree program were selected to function as community controls.

Doctors followed-up with patients in the Utah Obesity Study for six years. At the end of the follow-up period, patients who had undergone gastric bypass surgery maintained significant total weight loss as well as significant improvements in metabolic and cardiovascular factors compared to the control group, who did not undergo the surgery.

Physical examinations were conducted of all the patients at baseline — the start of the study — then at two years and again at six years. Exams included a wide variety of tests, including interviews with a physician and detailed medical history; submaximal exercise treadmill test and electrocardiogram; resting electrocardiograms and echocardiograms; pulmonary function; limited polysomnography; resting and exercise blood pressure; anthropometry; resting metabolic rate; urinalysis; comprehensive blood tests; and questionnaires analyzing the diet, exercise, and quality of life of the study participants. According to Dr. Ted D. Adams of the University of Utah in Salt Lake City, the six-year follow up with patients was “excellent,” with a 97% rate.

“In the surgical group, nearly all of the clinical measures improved significantly between the baseline and 2-year exams, and they remained significantly improved, compared with baseline at 6 years,” said Dr. Adams. The control groups made far less improvement than those who underwent the surgery, however: “The clinical variables in the combined control groups changed minimally if at all over the 6-year period,” continued Dr. Adams.

The group undergoing surgery showed significant weight loss that persisted throughout the six-year follow up, displaying a total weight reduction of 35 percent at two years out and 28 percent at six years out. In contrast, Dr. Adams noted, the control group displayed minimal weight loss.

The surgery group also fared better in diabetes remission at 75 percent at the six year mark, while the combined control groups were at 1 percent. At the end of the six-year follow-up, incidence of diabetes was at 2 percent for the surgery group and 16 percent for the non-surgery group.

Patients who received surgery appeared to display better cardiovascular health, with cardiac morphology measures being significantly improved just six months after surgery. Echocardiography results demonstrated reduced left atrial volume and left ventricular mass, both factors that could reduce the risk of heart failure related to obesity in the long term. Meanwhile, Dr. Adams reported that the control group displayed increased left atrial volume.

Additional improved health measures displayed by the group receiving gastric bypass surgery included reductions in waist circumference, heart rate, triglycerides, insulin resistance, systolic blood pressure, and low-density lipoprotein cholesterol that persisted through the end of the follow-up period. Higher levels of high-density lipoprotein cholesterol were also reported in the surgery group.

Dr. Adams stated that the results only support previous research on the benefits of bariatric surgery in improving health conditions related to being overweight. The findings will continue to provide insights into the benefits of the surgery and their improvements in the long term.

Dr. Adams did not disclose any conflicts of interest.

A study conducted by researchers at Kaiser Permanente shows that those with Type 2 diabetes would be wise to work at improving their cholesterol. According to the findings of the study, raising HDL cholesterol — or “good” cholesterol — could be associated with a reduction in the risk of stroke and heart disease in Type 2 diabetics. The study was published in the online version of the “American Journal of Cardiology.”

Researchers arrived at their findings after reviewing medical records from 30,067 patients with Type 2 diabetes. The patients had their HDL cholesterol levels measured twice over a time period from 2001 to 2006, with the measurements being conducted from six to 24 months apart. The research team analyzed the records and reviewed the data for hospitalization due to heart disease and stroke among the patients. Then they compared HDL cholesterol data to determine whether those who improved their cholesterol between the two measurements saw any difference in hospitalization rates.

The researchers discovered that, for every 5mg/dL rise in HDL cholesterol, the patients reduced their risk of hospitalization due to heart disease or stroke by 4 percent. Additionally, an increase in HDL of 6.5mg/dL or more was associated with an 11 percent decrease in risk of hospitalization. According to the researchers, this demonstrated “that the prevention of a HDL cholesterol decrease might be at least as important as increasing the HDL cholesterol level.”

About half of all people who have been diagnosed with Type 2 diabetes also have low HDL levels, which are defined as below 40mg/dL for men and below 50mg/dL for women. According to the National Cholesterol Education Program, which is associated with the National Heart, Lung, and Blood Institute, an HDL cholesterol level of under 40mg/dL is considered to be a risk factor for heart disease and stroke.

However, the researchers at Kaiser Permanante noted that studies have still not shown that increasing HDL cholesterol levels causes a direct decrease in risk of heart attack and stroke, “perhaps because safe and effective agents that substantially increase the HDL cholesterol level remain elusive.”

According to Suma Vupputuri, investigator at the Kaiser Permanente Health Research Center in Atlanta, one possible limitation of the study is that researchers did not have access to information about what the patients did to increase their HDL cholesterol levels. It is known that lifestyle changes such as regular exercise, weight loss, and avoiding tobacco can have a positive effect on HDL. However, those changes are also known to reduce the chances of cardiovascular disease; as such, it’s unclear whether the increase in HDL or the improved lifestyles are the main catalyst behind lower risk of hospitalization.

Whether it’s improved HDL cholesterol or lifestyle changes that lead to the lower risk of hospitalization, patients are benefited either way. “I think the general message, certainly, from our paper, is yes, raising HDL is going to improve your cardiovascular outcomes,” said Vupputuri.

Steven Grover, M.D., M.P.A., director of the Cardiovascular Improvement Program at McGill University, agrees that improving HDL reduces the risk of hospitalization. “There’s enough supportive evidence from clinical trials that there’s good reason to believe raising HDL will work” to reduce that risk. Grover conducted a study in 2009 that demonstrated similar benefits in raising HDL cholesterol; however, his findings showed even greater benefits.

Insulin Resistance” src=”https://www.diabeticlive.com/wp-content/uploads/2011/10/Barley-Fiber-Product-Improves-Post-Meal-Insulin-and-Insulin-Resistance-300×300.jpg” alt=”Barley Fiber Product Improves Post-Meal Insulin and Insulin Resistance” width=”300″ height=”300″ />A new study funded by Cargill has demonstrated that beverages fortified with a type of fiber produced from barley could reduce the impact of spikes in blood sugar occurring after a meal and may also increase insulin sensitivity. The findings of the study were published in the journal “Nutrition & Metabolism.”

Branded as Barliv, the fiber was shown in tests to reduce blood glucose levels by 10.2 percent with a three-gram dose. That’s an improvement over the 7.5 percent decrease in blood sugar that study participants displayed when they received a placebo beverage.

Barliv also showed promise as a long-term treatment for decreasing insulin resistance. Participants who consumed a beverage containing six grams of Barliv every day for 12 weeks showed a 19 percent decrease in insulin resistance while a placebo group showed a 42 percent increase. Insulin resistance is the inability of the body to respond to normal levels of insulin and is a common precursor to Type 2 diabetes.

“Because this trial was designed to ensure study subjects underwent protocol-directed maintenance of body weight, it is noteworthy that the metabolic findings occurred without significant weight changes in any of the study groups,” said the researchers. The study was a joint effort conducted by scientists from Louisville Metabolic & Atherosclerosis Research Center, Cargill, the University of Kentucky, ClinData Services, and Frestedt Incorporated.

The study consisted of 50 individuals classified as “generally healthy” according to the researchers. The trial was prospective, randomized, placebo-controlled, and double-blind. Participants were separated into three groups; one group received a placebo beverage to consume daily while the other two received the beverage containing either 3 or 6 grams of Barliv. Both the placebo and Barliv beverages were raspberry-flavored.

Participants receiving the 3 gram dose of Barliv showed a 10 percent reduction in glucose levels; those receiving the 6 gram dose displayed a similar reduction, but the difference was not statistically significant. The group receiving 6 grams of Barliv had an 8 percent decrease in fasting insulin — or insulin levels between meals — while the placebo group actually showed an increase in fasting insulin.

The barley beta-glucan beverage was also associated with a reduction in body fat percentage — a 3.9 percent reduction in fat concentrations in the hips, buttocks, and thighs. However, no weight loss was recorded.

“This study supports that the 6 g/d barley beta-glucan beverage consumed over 12 weeks improves insulin sensitivity among hyperglycemic individuals who have no prior diagnosis of diabetes mellitus and no change in body weight,” said the researchers. “This study suggests barley beta-glucan may slow the deterioration of insulin sensitivity for individuals at increased risk for diabetes mellitus.”

The findings of the study could prove to be a ray of light in the fight against Type 2 diabetes, especially for those who already have pre-diabetes and are at an increased risk. The World Health Organization states that over 220 million people around the world are affected every year by diabetes, while 3.4 million die every year due to diabetes or complications from the disease. Diabetes has been on the rise for decades and the WHO is predicting that the trend won’t stop, stating that deaths from diabetes will double from 2005 to 2030.

Diabetes is a tremendous strain on health care, costing the United States alone up to $174 billion per year. A sizable portion of that number goes directly to medication for diabetes — about $116 billion of it, according to the American Diabetes Association.

According to researchers at the University of Cambridge in the United Kingdom, a rare and serious form of hypoglycemia can be traced back to a hereditary disposition.

The scientists say that the AKT2 gene — or more specifically, mutations in the gene — are responsible for causing this particular type of hypoglycemia, which is serious enough to be considered life-threatening and which deprives the body of the energy it needs to continue functioning normally.

According to the scientists from Cambridge, who published their report in the journal “Science,” there are already cancer drugs in use which are designed to treat a similar process.

Hypoglycemia, or a condition of low blood sugar, can be caused by imbalances between blood sugar levels and insulin, which carries sugar away from the bloodstream and into cells, lowering blood glucose levels. Hypoglycemia typically occurs in individuals who have Type 1 diabetes, when they miss meals, consume alcohol, or inject themselves with too much insulin.

The researchers at the University of Cambridge discovered that one in 100,000 babies is born with a mutation in the AKT2 gene that causes hypoglycemic conditions even when no insulin is present in the blood. In those cases, individuals should exhibit high levels of blood glucose.

Individuals with this mutation must use feeding tubes during periods of sleep to ensure that blood sugar levels do not drop too low. The patient must always be vigilant about maintaining blood sugar levels and ensuring that they don’t dip into dangerous territory, and the condition can be taxing for both the patient and his or her family.

“Fear of low blood sugar has dominated the lives of these patients and their families,” said Dr. Robert Semple, one of the researchers from Cambridge.

In discovering the mutation, the scientists looked at genetic code of three children who had this severe form of hypoglycemia. All of the children exhibited a certain mutation in the ATK2 gene. The mutation causes the ATK2 gene, which functions as an interpreter for insulin, to act as if insulin is always being produced by the pancreas. Blood sugar levels are therefore consistently lowered.

According to Professor Stephen O’Rahilly, lead researcher on the project at Cambridge, there are medications available which target ATK1 and also provide some effect in acting on ATK2. These medications are currently used to treat cancer. Since medications already exist which act on the genes, it may not be long before new treatments are introduced for treating the rare form of hypoglycemia.

“There are actual pills that can be swallowed by humans. There could be a treatment in a year,” said Professor O’Rahilly.

An individual is considered hypoglycemic when his or her blood sugar levels fall below 70mg/dL. If blood sugar levels remain at such a low level for an extended period of time, it can be harmful to the individual. The hormone insulin is normally produced by the beta cells of the pancreas where it works to reduce blood sugar levels, but blood sugar levels can fall too low if too much insulin is produced, exercise is performed at a different time, or alcohol is consumed, among other factors. Hypoglycemia is treated by consuming about 15 grams of carbohydrates and checking blood sugar levels again after about 15 minutes. Hypoglycemia can cause loss of consciousness and even seizures or nervous system damage; as such, it should be treated as quickly as possible, but individuals with low blood sugar should refrain from driving themselves to reach a hospital.

Juvisync, a pill that combines medication for both diabetes and high cholesterol, recently won approval for sale in the U.S. The medication will provide a reduction in both expenses and pill count for users of Januvia and Zocor, both medications developed by Merck & Co., Inc.

Juvisync will be available within a few weeks and will combine Zocor, a statin drug that combats high cholesterol, with Januvia, a Type 2 diabetes medication. Juvisync will be priced about the same as Januvia alone — about $215 for a month’s supply. Generic forms of Zocor cost patients about $30 per month.

The combination pill will likely be attractive to many diabetics who are not currently taking statins, as they will be able to gain the benefits of those medications with little or no extra cost. The American Diabetes Association recommends that diabetics over the age of 40 or who have also been diagnosed with heart disease should take a statin every day.

“This provides a way to simplify their regimen and improve adherence,” says Dr. Susan Spratt of the Duke University Medical Center. According to Spratt, many diabetics already take several pills each day — sometimes six or more — due to the need for different medications for diabetes, high cholesterol, and blood pressure. Taking all of the necessary pills each day can be a chore, and even diabetics who have health insurance can find their medication to be very pricey.

Not only will the patients benefit from fewer pills to take, but the addition of a daily statin could prevent future costs of hospitalization, according to Spratt.

“Anything to reduce the cost is going to be helpful to patients,” says Spratt. “When you improve medication adherence, you actually lower health care costs because patients don’t end up in the ER or the hospital.”

Merck’s shares rose nearly 3 percent on the day of Juvisync’s announcement, up 19 cents to $31.61 at closing.

Type 2 diabetes is a metabolic disorder in which the body does not produce enough insulin or does not use it correctly. The insulin that is produced is unable to bear the load of transporting glucose out of the bloodstream, so blood sugar levels remain elevated and permanent damage to organs and other tissues can result.

A sizable percentage of patients with Type 2 diabetes also have high cholesterol levels: both conditions are related to being overweight or obese. Those with both Type 2 diabetes and high cholesterol are at elevated risk of stroke, kidney disease, heart disease, and other illnesses, as well as complications commonly associated with diabetes such as nerve damage and vision loss.

Though the dangers of high cholesterol combined with Type 2 diabetes are well-documented, Merck says that up to four million patients with Type 2 diabetes are not receiving statins.

“Perhaps one third of the nation’s eligible patients with type 2 diabetes are not being treated with a statin, so here’s a convenient tool for doctors to target glucose as well as cholesterol levels,” said Dr. Seth Reddy, director of clinical affairs for diabetes at Merck.

Merck will offer Juvisync in six different dosages, which will correspond to the variance in severity of diabetes and cholesterol in patients. Side effects include headache, muscle and stomach pain, stuffy nose, and sore throat. The drug will also revitalize Zocor, which saw its market share reduced when it became available in generic forms as simvastatin in 2006.

A study conducted at the University of Wisconsin-Madison has identified a gene that could increase susceptibility to diabetes in those who carry it. Researchers discovered the gene in obese mice; it controls a protein called tomosyn-2, which decreases insulin production by the pancreas. The findings were published in the journal “PLoS Genetics,” which published by the Public Library of Science.

Beta cells in the pancreas are responsible for making and releasing insulin into the bloodstream, where it removes glucose from the blood and carries it into cells so that it can be used as energy. Type 1 diabetes is characterized by a lack of insulin while Type 2 diabetes causes an individual to be insulin-resistant. Both diseases cause a wide variety of complications, becoming more severe if they go untreated.

Alan Attie of the University of Wisconsin-Madison headed the study. He commented that the discovery of the gene could be an important development but it’s uncertain whether the gene can be targeted by therapeutics to effectively combat diabetes in insulin.

“It’s too early for us to know how relevant this gene will be to human diabetes, 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,” said Attie.

Researchers used obese mice in the study, which require more insulin to lower blood glucose levels than mice of a normal weight — and the same is true of humans.

“If you can produce that extra insulin – and most people do – you’ll be okay,” said Attie. “You will avoid diabetes at the expense of having to produce and maintain a higher insulin level.”

According to Attie, however, being overweight means that the body is less able to produce the extra insulin required to eliminate elevated glucose levels.

“Most of the type 2 diabetes that occurs in humans today would not exist were it not for the obesity epidemic,” he said.

Researchers on the study compared diabetes-susceptible and diabetes-resistant mice. They found that a single amino acid accounted for the destabilization of tomosyn-2 in the diabetes-resistant mice. That one mutation allowed the diabetes-resistant mice to produce additional insulin to meet the increased demands of obesity.

While the onset of diabetes is a complex process and it is unlikely that a single gene could be targeted to elminate the disease altogether, genetic research into diabetes can eventually illuminate the processes and allow researchers to develop therapies that cut off diabetes at the source. Many scientists agree that genetic factors play about a 50 percent role in an individual’s risk of developing diabetes.

“This study shows the power of genetics to discover new mechanisms for a complex disease like type 2 diabetes,” said Sushant Bhatnagar, co-lead author of the study.

“Now we know there are proteins that are negative regulators of insulin secretion,” said Attie. “Very likely they do the same thing in human beta cells, and it motivates us to move forward to try to figure out the mechanisms behind that negative regulation.”

The researchers disclosed that they had no competing interests that could have affected the results of the study. Attie and his research team bred mice and kept records of results for over a decade to arrive at their findings.