Category: Diabetes 101

An extended trial of a drug that is commonly used for people who have been diagnosed with type 2 diabetes, an oral DPP-4 inhibitor Linagliptin (Tradjenta) is safe and effective in its ability to lower glucose levels for up to 102 weeks by itself or with a combination of other oral anti-diabetic medication.

The trial consisted of 2,121 people who took part of four recent 24-week randomized, double-blind, and placebo controlled trials and were monitored for 78 weeks more.

During the study, 1,532 people had recently received Linaglipin and continued to do so throughout the study while 589 people received placebo during the 78-week run of the trial.

Participants came from all walks of life, from 231 sites in 32 countries such as Argentina, Austria, Belgium, Canada, China, Croatia, the Czech Republic, Finland, Germany, Greece, Hungary, India, Israel, Italy, Japan, Korea, Malaysia, Mexico, the Netherlands, New Zealand, the Philippines, Poland, Romania, Russia, Slovakia, Spain, Sweden, Taiwan, Thailand, Ukraine, the United Kingdom and the United States.

David R Owens, Professor Emeritus, Centre for Endocrinology and Diabetes Sciences at Cardiff University, Wales, UK said, “Initial 24-week trials showed that linagliptin, either on its own or with other glucose-lowering agents, was effective in improving glycemic control without weight gain or an independent increased risk of hypoglycemia (reduced blood sugar levels). Linagliptin works by blocking the action of DPP-4, an enzyme that destroys the hormone GLP-1, which helps the body produce more insulin when it is needed.”

The drug was given once daily, orally, in all cases. Many times it was given on its own and other times it was used in a combination of others drugs like metformin or metformin plus a sulphonylurea or pioglitazone.

The study found that the average age among the participants was 57.5 years and 75 percent of the participants where younger than 65. 51.8 percent were male and 52.5 percent were diagnosed more than five years ago.

Some participants has side effects, however they were either mild or moderate. A rare few (3.8 percent) were severe and 3.4 percent has to stop use of the drug altogether. Collectively, 14.3 percent has drug-related adverse effects.

Some participants (13.9 percent) also experienced hypoglycemia (low blood sugar as well and 6.9 percent was related to the drug.

Professor Owens concludes, “This is the largest data set of long-term clinical evidence for linagliptin to date. Findings from the 78-week open-label extension involving 2,121 people with type 2 diabetes demonstrate sustained glycemic control for up to 102 weeks treatment duration. They also provide evidence that supports the efficacy and tolerability profile seen in previously reported 24-week studies.

“Therefore this extension study shows that linagliptin is an effective and well tolerated therapy for the long-term management of type 2 diabetes.”

Diabetes is a disease that is sweeping across the globe; so many people have been diagnosed with diabetes. Just in America alone, more than 25 million people have diabetes.

While diabetes has no cure, more drugs have shown a great improvement when it comes to the disease. One of those drugs is called Metformin and it is helping with more than just diabetes. Metformin has also shown great side effects as well, brain cell growth. This particular drug supports the growth of new neurons in the brain.

When studied, the results of Metformin were seen to make mice smarter than they were before, before the drug was administered. The result of the study has brought a great amount of hope the therapies that are designed to help to repair the brain.

Lead author of the study, Freda Miller of University of Toronto-affiliated Hospital for Sick Children said, “The discovery is an important step toward therapies that aim to repair the brain not by introducing new stem cells but rather by spurring those that are already present into action, says the study’s lead author.”

The drug is safe for the use of children who have been diagnosed with diabetes, which makes it a great alternative medication to helping children who are suffering a health issue that deals with the brain.

Recent research by Miller’s team laid out the groundwork for the recent study known as aPKC-CBP, which is well-known for its role in telling neural stem cells where and when to distinguish into mature neurons. The same pathway, aPKC-CBP is important for the metabolic effects of Metformin in liver cells.

Miller says, “We put two and two together.”

It was believed that if Metformin activated CBP in the liver, then it could possibly do that for neural stem cells of the brain and stimulate brain repair. To connect the two, a study was administered to mice. The mice began taking Metformin, which showed an increase in the birth of new neurons.

So far, there is no major evidence to see if this popular drug works in humans but it is very clear that mice are getting brain boosts with it. There is a great hope that Metformin will be a great cure where Alzheimer’s disease is concerned.

Miller says, “ It had been thought those improvements were the result of better diabetes control, but it now appears that Metformin may improve Alzheimer’s symptoms by enhancing brain repair.

Researchers hope that Metformin might be a huge help in curing brain issues that are related to cancer, trauma and even Alzheimer’s disease in the near future.

Recently, researchers have found that fruit flies, who are overeating in the area of carbohydrates and protein not only have a shorter life span but they gain weight and develop insulin resistance as well.

Insulin resistance is a common problem that is linked Type 2 diabetes; poor diet and obesity are also linked to it as well. In the United States alone, more than 25 million people have been diagnosed with type 2 diabetes and another million more will be diagnosed by this time next year. It is a growing disease, despite the strides made from researchers to find a successful cure.

Biologists from the Southern Methodist University in Dallas now say they have developed a tool that could help researchers to understand the disease more.

Researchers have always used mice, rats and other animals when it comes to diabetic genetic and metabolic changes. Now, they are turning to a different species, fruit flies. Recently, fruit flies have been used to investigate an array of human disease such as cancer and Alzheimer’s disease.

Fruit flies have two advantages when it comes to the investigation of these diseases, they don’t live very long and they are inexpensive. Through investigation, an insulin-resistant fruit fly was created in a lab at the Southern Methodist University in Dallas. Feeding fruit flies a high diet in nutrients accomplished it, reported Johannes H. Bauer, the principal investigator for the investigation. It is the same process, which happens in humans, overeating to the point of obesity and then developing insulin resistance.

Since the same process is seen between humans and fruit flies, they can serve as an efficient model for studying type 2 diabetes.

Bauer states, “We learned that by manipulating the nutrients of fruit flies, we can make them insulin resistant. With this insulin-resistant model we can now go in with pinpoint precision and study the molecular mechanisms of insulin resistance, as well as drug treatments for the condition, as well as how to treat obesity, how to block insulin resistance and how metabolic changes from a specific diet develop. The possibilities are endless.”

Carbohydrates and protein are two overfeeding diets that cause insulin resistance. Insulin itself is produced from the pancreas and is a hormone that communicates with our cells, which allows for the absorption of glucose. Glucose is necessary because it helps the brain to function, makes repairs to our bodies and allows us to grow and move.

During the investigation, researchers implemented their testing strategies two separate ways. One, by feeding fruit flies, carbohydrates and two, by feeding fruit flies, protein. Researchers believed that the fruit flies that were fed carbohydrates would develop insulin resistance but were surprised to find that the fruit flies fed the protein diet appeared to develop insulin resistance at a quicker rate. Bauer said, “ Carb-loaded flies gain weight. Protein-loaded flies gain and then lose weight. So the two diets have exactly opposite effects on metabolism. But too much of either one of them causes insulin resistance. That surprised us.”

Diabetes affects more than 25 million people in the United States and plagues its victims with serious medical conditions such as neuropathy, retinopathy and amputation.  As of late, obesity appears to be the leading cause of diabetes.

According to researchers at the Missouri University of Science and Technology, oil derived from the seeds of wild almond trees can help to fight off obesity and diabetes.

Wild almond tree oil, also known as sterculic oil has the ability to influence particular microorganisms that are living within our stomachs.  A study showed that adding sterculic oil to the diets of laboratory mice, who were obese, increased their sensitivity to insulin. This happened due to the effect of wild almond tree oil, it was able to effect three types of microorganisms that live inside the mice’s stomachs.

Shreya Ghosh, PhD and a student in environmental engineering at Missouri S&T said, “That researchers saw a statistically significant improvement in glucose tolerance and insulin sensitivity in the obese mice.”

However when lean mice were given the same sterculic oil, there were no affects.

Previous studies at the University of Missouri of Columbia have found sterculic oil to suppress the bodily enzyme stearoyl-CoA desaturase 1 (SCD1). SCD1 is associated to insulin resistance, which is a huge factor in type 2 diabetes and obesity.

For the experiment, 28 male mice were studied, 14 of them obese and the other 14 normal size and each one about five weeks old. The mice were separated into four groups and fed a standard diet, 0.5 percent of sterculic oil was also added. Recording of weight, food consumptions and glucose levels were taken over a nine-week period.

Once that nine-week period was up, researchers at King Abdullah Institute of Science and Technology in Saudi Arabia looked into the results, comparing diet, improved glucose and the groups of microbes. The obese mice that were fed the sterculic oil did not experience weight loss but researchers did find evidence to support a possible new lead in controlling both weight gain and diabetes.

Many studies have been experimented with to find a cure, or at least an effective treatment for diabetes. While there have been several great herbal remedies pop up in the recent years of medical science, there is no still no common cure or treatment for diabetes. One can help that wild almost tree oil can help to rectify that.

What do these three conditions have in common after a woman is over 60 years of age?

It has been known that there is an increased risk of being diagnosed with breast cancer if a woman is obese, particularly after the age of 60, but new information is being released that there is now a link between breast cancer, obesity and diabetes, with this being the first time that the link with diabetes has clearly been evident.  If a woman is over the age of 60 and obese, she has an increased risk of breast cancer and diabetes, conditions that are life threatening.

Researcher Dr. Hakan Olsson, Professor of Oncology at Lund University in Lund, Sweden, will present his study results the week of December 5, 2011, at the 2011 San Antonio Breast Cancer Symposium.

For his study results, Olsson reviewed the medicals records of more than 2,700 patients.  This review of the 2,700 patients covered up to a 10-year span before the patients were diagnosed with breast cancer.  As well, he studied records for approximately 20,500 patients who never developed cancer.  In essence, the study was looking at the population as a whole and not just women with breast cancer.

If a woman was obese after the age of 60, she had a 55 percent increased risk of being diagnosed with breast cancer.  An example:  While 15 of 100 obese women, at the most, would be diagnosed with breast cancer, less than 10 of the 100 women in the general populace would be expected to be diagnosed with breast cancer, Olsson stated.  Also, up to four years after being diagnosed with diabetes, women of any age had a 37 percent higher risk of being diagnosed with breast cancer.

As far as cholesterol levels, Olsson found a connection between low levels of blood lipids (fat), mostly cholesterol, and a 25 percent higher risk of breast cancer.  Women with higher cholesterol levels had a lower risk of a breast cancer diagnosis, and Olsson stated that this unusual finding needs to be further studied.

Olsson also found that the medication used by a female to control their diabetes also seemed to influence their breast cancer risk.  Lantus (Glargine) was linked with a nearly doubled risk of breast cancer.  But, Metformin (Glucophage, Fortamet and others) was linked with a slightly lower risk.

Olsson stated that the study numbers were not high enough to come to a final determination that there is a direct link between a cancer diagnosis risk and diabetes medication, and if someone were concerned that they should consult with their doctor about what type medication was best for them.

Because Olsson’s study results were present at a medical meeting, the conclusions are considered preliminary until such time as they are published in a journal that has been peer reviewed.

Dr. Suzanne Steinbaum, Director of Women’s Heart Disease at Lenox Hill Hospital in New York City, commented on the new study results:  “The new finding is the diabetes and cancer link.”  But, she added, that it did not surprise her.  “We’ve known that obesity is associated with breast cancer,” and, she noted, “a lot of obese people have diabetes.”

She added a message for women who wish to minimize their breast cancer risk:  “Maintain a healthy weight and avoid diabetes, which will also help their heart health.”

Dr. Olsson plans to continue his research, particularly regarding the cholesterol level results and breast cancer connection.

New findings from the Alpha Omega Trial suggest that low-dose omega-3 fatty acid supplementation could play a role in preventing ventricular arrhythmia-related events in patients who have both diabetes and a history of myocardial infarction.

The trial was conducted by a team headed by Daan Kromhout, MPH, Ph.D., from the division of human nutrition at Wageningen University in the Netherlands. Kromhout and colleagues used a sample of 1,014 patients from the age of 60 to 80, who consumed margarine fortified with recommended daily doses of omega-3 fatty acids. Participants were randomly assigned to three groups, which consumed either placebo or one of three types of margarine fortified with omega-3 fatty acids: 400mg eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA); 2g alpha-linolenic acid (ALA); or a combination of EPA, DHA, and ALA. All patients had a history of myocardial infarction within the past ten years. The trial was conducted over a period of 40 months.

Patients across all the groups consumed an average of 18.6g margarine daily, which included an average additional intake of 223mg EPA, 149mg DHA and 1.9g ALA. The median follow-up period was 40.7 months; during that time, 29 patients experienced a ventricular arrhythmia-related event. Another 27 died of myocardial infarction. According to the researchers, their data suggested that supplementation with omega-3 fatty acids in any combination reduced the patients’ chances of ventricular arrhythmia-related events when compared to the rates associated with placebo. Patients who received a combination of EPA, DHA and ALA supplementation had the lowest incidence at 84 percent less than with placebo. Supplementation with EPA, DHA, and ALA had similar benefits over placebo in reducing cardiac arrest, sudden death, and the placement of cardioverter defibrillators.

The groups receiving supplementation did not appear to differ significantly in rates of fatal myocardial infarction compared to the placebo group. However, after adjusting for potential confounding factors, the researchers found that the group receiving a combination of EPA, DHA and ALA saw a reduced endpoint for ventricular arrhythmia-related events as well as fatal myocardial infarction.

Kromhout pointed out in a press release that, although the findings suggest omega-3 fatty acid supplementation has benefits for patients with both diabetes and a history of myocardial infarction, additional research will need to be conducted before the mechanism underlying the benefits is understood.

“While more research is needed to definitively determine the role of these fatty acids in protecting people from ventricular arrhythmias, they seem to provide a benefit to the heart attack patients who also had diabetes,” said Kromhout. “This is the first study that showed a significant protective effect of omega-3 fatty acids in high-risk patients with diabetes who were on state-of-the-art drug treatment for their heart attack,” he continued.

Myocardial infarction, more commonly known as heart attack, is more common among patients with diabetes and is more fatal. Although the processes that cause heart attack are not different among diabetes patients, scientists believe that the procoagulant and prothrombotic characteristics of diabetes are responsible for the increased rates of heart attack. It is also more difficult to ensure proper blood flow through blood vessels in patients who have diabetes after heart attack than in patients without the metabolic disease. Among patients experiencing myocardial infarction, 10 to 30 percent have Type 2 diabetes. Rates of heart attack are expected to rise in the future along with the increasing rate of Type 2 diabetes.

In addition to Type 1 and Type 2 diabetes, there is another variant of the disease: cystic fibrosis-related diabetes. It differs in some important ways from Type 1 and Type 2 diabetes and it requires different treatment methods.

Patients with cystic fibrosis experience decreased nutritional and pulmonary health several years before they’re diagnosed with cystic fibrosis-related diabetes (CFRD). According to Amanda Leonard, a senior pediatric clinical dietician at the Johns Hopkins Cystic Fibrosis Center, early diagnosis and treatment can significantly improve life expectancy in patients who develop CFRD.

“Screening early and knowing which patients are at risk is really important,” said Leonard at a pediatric nutrition meeting sponsored by Johns Hopkins University.

CFRD does “share some components” with Type 1 and Type 2 diabetes, says Leonard, but it’s also different in some important ways. Patients with CFRD typically experience decline in lung function, protein catabolism, weight loss, and an increased rate of mortality. Ketones rarely appear in patients with CFRD, and the development of the disease does not appear to be related to autoimmune function.

In cystic fibrosis patients at the age of 40, the rate of CFRD is over 50 percent. According to Leonard, more patients develop CFRD in the 20-24 year old range than any other age; meanwhile, Type 1 diabetes usually develops in childhood and Type 2 diabetes usually develops in mid-to-late adulthood.

“In CFRD there is a severe insulin deficiency, but it’s not as complete as in type 1,” said Leonard. Physicians define CFRD as the presence of at least two of the following criteria on at least two occasions: hemoglobin A1c of at least 6.5 percent; fasting glucose level of at least 126 mg/dL; and a two-hour oral glucose tolerance test of plasma glucose at least 200 mg/dL.

Leonard says that CFRD isn’t quite as easy to identify as other types of diabetes. In patients with CFRD, a two-hour oral glucose tolerance test (OGTT) can range from 140 to 199 mg/dL while fasting glucose can range from 100 to 125 mg/dL. According to Leonard, it’s “not quite diabetes, but it’s not quite right either.” The disease is “not an all or nothing kind of thing. It’s not that either you have it or you don’t. It can be transient in nature, and there’s a spectrum,” she continued.

Outpatient OGTTs are the best option for routine CFRD testing in clinically stable patients. Cystic fibrosis patients are recommended to begin OGTT screening for diabetes when they reach 10 years of age.

While HbA1c alone cannot be used as to screen for CFRD due to a high rate of false positives, a low HbA1c can confirm a diagnosis from other symptoms.

Patients who are hospitalized due to pulmonary exacerbation and/or treatment with corticosteroids should be tested with both fasting and two-hour post-meal blood glucose monitoring. The patient is diagnosed with CFRD when fasting or post-meal hyperglycemia lasts longer than 48 hours.

Patients with CFRD are treated with insulin; other treatment methods have not shown benefits for patients and are not recommended over insulin. “Insulin is the treatment of choice. Oral agents do not seem to work as well,” said Leonard.

CFRD patients have the same blood glucose goals as other diabetes patients, with an HbA1c goal of less than 7.0 percent. However, goals are adjusted for each individual patient.

Nutritional recommendations for patients with CFRD are based on those for patients with cystic fibrosis. CFRD patients may also benefit from counting carbohydrates to ensure safe blood glucose levels.

New research conducted at the University of Glasgow, Scotland, suggests that thrombolytic drugs—also called “clot-busting” drugs due to their use in dissolving blood clots—improve outcomes in patients who have suffered from strokes, even when they have a past history of stroke or diabetes. In fact, outcomes were similar to those demonstrated by patients who had experienced neither stroke nor diabetes.

The study was conducted by Kennedy Lees, MD, and colleagues at the University of Glasgow. According to Lees, there is “no statistical justification” for denying such clot-busting medications to patients who have a history of stroke or concomitant diabetes. The research was reported in the November 22 issue of the journal “Neurology.”

The use of clot-busting drugs in patients with a history of stroke or diabetes has been controversial, mainly due to restrictions on the approval of intravenous alteplase (Activase) in Europe. Lees said in a statement that therapy with clot-busting drugs “can limit damage and disability due to blood clots” but that “current guidelines can keep people from receiving the therapy if they have a history of stroke and diabetes.” However, physicians often ignore the restrictions when prescribing thrombolytic drugs to these patients.

Lees and his colleagues analyzed data from two registries of stroke victims. One group (the “T” group) consisted of 23,334 patients from the Safe Implementation of Thrombolysis in Stroke-International Stroke Thrombolysis Register. The other group (the “C” group) consisted of 6,166 patients who had not received treatment with thrombolytic drugs. That data was pulled from the Virtual International Stroke Trials Archive.

The researchers measured outcomes using the 90-day modified Rankin Score, which measures stroke-related death and disability.

In total, the researchers used data from 29,500 patients: 5,411 (18.5 percent) had diabetes; 5,019 (17.1 percent) had a previous stroke; and 1,141 (5.5 percent) had a history of both diabetes and stroke.

Upon analyzing the data, the researchers found that 43.2 percent of the diabetes who received thrombolytic drugs demonstrated a modified Rankin score of 2 or less, which is considered, at worst, a slight disability. Meanwhile, 34.8 percent of patients with diabetes who had not received thrombolytic treatment had a score of two or lower.

Among patients who had a history of stroke and received clot-busting drugs, 48.4 percent showed a modified Rankin score of two or less, compared to 34.5 percent who did not receive the drugs.

Among patients who had a history of both stroke and diabetes, 37.7 percent who received thrombolytic drugs showed a score of two or lower compared to 34.5 percent who did not receive the drugs.

The findings demonstrated that, on average, patients showed improved modified Rankin Scores when they received treatment with clot-busting drugs.

“Better outcomes with therapy show that people with prior stroke or diabetes should not be excluded from receiving thrombolytic therapy,” said Lees. The researchers noted that the study was not randomized; however, they believed that they “attained a reliable statistical result” after adjusting for confounding factors.

According to Bart Demaerschalk, MD, of the Mayo Clinic Hospital in Phoenix, Arizona, noted in an editorial accompanying the study that up to 15 percent of people who arrive at the emergency room with a stroke have a history of previous stroke or concomitant diabetes. Issues surrounding the treatment of these patients with thrombolytic drugs include whether physicians should consider transient ischemic attacks or glucose tolerance in prescribing the drugs. Still, Demaerschalk concluded that “there appears to be no justification for the continued restriction of these patients from receiving thrombolytic therapy.”

A new study found that an enzyme called IKKbeta was linked to increased metabolism in lab mice. When researchers engineered the mice to express the IKKbeta enzyme in their fat tissue, the mice ate more food yet gained less weight, with their bodies using fat and sugar more effectively than mice who had not been treated. The study was published in the online edition of the journal “Endocrinology.”

The researchers working on the study reported that the expression of the enzyme had several positive benefits, including improving the efficacy of insulin, reducing weight gain, and improving metabolism. The mice were also less likely to become obese, though in exchange they experienced significant inflammation. Still, the researchers say that the findings could lead to new discoveries regarding the effect that inflammation and obesity have on insulin sensitivity and insulin resistance.

“Turning on this molecule has a very dramatic impact on lipid metabolism,” says Haiyan Xu, an assistant professor of medicine at the Warren Alpert Medical School of Brown University and a researcher at the Center for Diabetes and Endocrinology of Rhode Island Hospital.

In this study, scientists sought to explore the effects of obesity and inflammation on insulin resistance. Both obesity and inflammation appear to cause insulin resistance, but obesity plays a larger role, and the most popular hypothesis among scientists is that obesity causes inflammation, which contributes to insulin resistance. By expressing the IKKbeta hormone in the fatty tissue of lab mice, the researchers reduced inflammation before they mice were obese; the mice then showed increased metabolism, significantly higher than control mice that did not have the enzyme expressed.

The mice who expressed the enzyme still put on weight, but at a significantly reduced rate. When the mice were fed high-fat diets, altered mice weighed less than 38 gram; control mice weighed over 45 grams. The difference was less pronounced when the mice were fed a healthier diet—called “chow”—but it was still statistically significant. Both male and female mice showed improved metabolism and less weight gain when the enzyme was expressed.

The altered mice actually ate more food, but gained weight more slowly, which demonstrated to the researchers that their metabolic rates were increased over the control mice. Altered mice also displayed lower blood sugar levels after being injected with glucose, and they maintained their lower blood sugar levels after an injection with insulin, which suggests that insulin was more effective for them as well. The altered mice expended more energy than the control mice, which suggests that they successfully metabolized the glucose injections.

The researchers stated that they were not sure about the mechanism by which IKKbeta improves metabolic performance. However, according to Xu, it appears that obesity is a greater factor in causing insulin resistance than inflammation.

“Lower body weight is always a beneficial thing for influencing insulin sensitivity,” said Xu. “Reduced adiposity wins over increased inflammation.”

Previous research has explored the effects of IKKbeta by activating it in the liver, where it seemed to have no effect on weight gain, and in the hypothalamus, where it actually increased weight gain. The findings of the study suggest that IKKbeta’s improvements to metabolic processes are dependent on its expression within fatty tissue.

The study was funded by Brown University as well as the American Heart Association, with a scientist development grant to Xu.