Category: Diabetes 101

The American Diabetes Association has announced that it will be awarding major research grants to study bariatric surgery and its effects on Type 2 diabetics. Called the American Diabetes Association Research Award Program in Bariatric Surgery in Diabetes is co-sponsored by Covidien and Ethicon Endo-Surgery and will award grants to A. Gordon Smith, M.D. at the University of Utah and Alyssa H. Hasty, PhD, at Vanderbilt University Medical Center.

The program will grant $1 million in funding through the American Diabetes Association for the two research grants, which will each last three years. One grant will provide funding for Smith’s research into the effects of bariatric surgery in the development of neuropathy while the other grant will fund Hasty’s studies on the effectiveness of bariatric surgery in reducing inflammation of adipose, or fat, tissue.

Covidien and Ethicon Endo-Surgery, two cutting-edge leaders in medical device technology for bariatric and endoscopic surgery, will be working together for the first time along with the American Diabetes Association to provide the funding.

“More research is needed to study the effects of bariatric surgery, particularly its implications for people with type 2 diabetes, especially with the nation’s growing epidemics of type 2 diabetes and obesity,” stated R. Robert Henry, MD, President, Medicine & Science, American Diabetes Association. “Research projects such as these will help further our understanding of these mechanisms.”

“We know many bariatric surgery patients experience remission of type 2 diabetes within days of having surgery, before patients begin losing weight,” said Kenneth Sumner, PhD and Vice President of Worldwide Scientific Affairs at Ethicon Endo-Surgery. “Understanding why and how this happens may help us unlock new ways of treating type 2 diabetes and other comorbidities of obesity. We are delighted to support this important initiative as part of EES’ Metabolic Applied Research Strategy (MARS).”

“A growing body of clinical evidence strongly suggests that bariatric surgery is a potentially life-transforming procedure, drastically improving both the physical and mental well-being of patients, and in many cases, completely resolving diabetes and other obesity-related comorbidities,” according to Xavier P. Lefebvre, PhD, Global Vice-President of Clinical Affairs at Covidien. “We are proud to support these projects that have the potential to uncover new scientific insights into a promising and cost-effective solution for the obesity and diabetes epidemics affecting the global population.”

Covidien is an international health care products company, developing medical solutions through clinical research. The company manufactures and distributes medical devices, pharmaceuticals, and medical supplies. Covidien employs 41,000 people around the globe in over 65 countries and posted revenue of $10.4 in 2010. Covidien’s products are sold in more than 140 countries; more information is available at http://www.covidien.com.

Ethicon Endo-Surgery specializes in the development and marketing of medical devices for both minimally invasive and open surgeries. The company researches and markets devices that aid in the diagnosis and treatment of conditions through both general and bariatric surgical procedures. Ethicon also performs research and development in the fields of surgical oncology, gastrointestinal health and gynecology. More information is available at http://www.ethiconendosurgery.com.

The American Diabetes Association provides grants for research that aims to prevent, cure, and help people manage their diabetes. The Association works to provide trustworthy information, to aid communities affected by diabetes, and to ensure that diabetics receive their full rights. The American Diabetes Association can be reached by calling 1-800-DIABETES or by visiting http://www.diabetes.org.

The Centers for Disease Control and Prevention (CDC) states in its “2011 National Diabetes Fact Sheet” that 25.8 million children and adults in the United States have diabetes. Additionally, 79 million Americans have a condition known as “prediabetes,” meaning that they are very near developing diabetes. In other words, one in three Americans are in danger of developing diabetes in the near future. The CDC defines diabetes and prediabetes as a defect in the body’s ability to use glucose as a source of energy, which results in elevated levels of insulin in the bloodstream.

However, there is hope for people with diabetes. “Diabetes doesn’t have to equal poor health,” according to Toby Smithson, a Registered Dietitian, Certified Diabetes Educator, and also the founder of the website DiabetesEveryDay.com. “Diabetes can be a manageable condition, but challenging responsibilities fall squarely on the patient. It’s called self-management.” Smithson is aware of the challenges facing diabetics in managing diet and blood glucose levels. She has been a diabetes patient for over 40 years herself but has not suffered any of the various severe complications that the disease can cause, such as heart attack and stroke, infections, limb amputation, kidney failure, and vision loss.

Smithson’s reference to self-management is one with which diabetics should be all too familiar. Diabetics must take responsibility for maintaining moderate blood sugar levels through proper diet, especially in regards to carbohydrates, along with medication, exercise, and frequent blood sugar checkups. Maintaining this level of self-management has been shown to drastically reduce the risk of developing severe complications but it’s estimated that under 10% of diabetics actually meet their goals for managing blood sugar, blood pressure and cholesterol.

“Controlled studies almost always show that ‘intensive lifestyle intervention’ brings marked improvements in these key health indicators, greatly reducing the risks of diabetes complications,” Smithson says. “But in our real world a person with diabetes may go for months between visits with physicians or dietitians or educators. The lifestyle can be complicated, time consuming, frustrating, and lacking in short term positive feedback, so many simply lose their daily connection with diabetes management against life’s other demands.”

“I founded DiabetesEveryDay.com to provide accurate information about diabetes and diabetes management, of course. But more importantly, I want to keep people with diabetes interested in, and connected to, this crucial part of their life. It’s easy for them to lose focus, so we were determined to create something interesting and always changing that will keep people who are self-managing diabetes engaged with us, and therefore engaged with improving their own self-care.”

Smithson listened to the complaints and suggestions of her diabetic patients and used them to build DiabetesEveryDay.com. The website offers weekly diet recommendations, lifestyle advice, and instructional videos on healthy living with diabetes. “We are dedicated to providing something completely different that encourages and motivates people with diabetes to take control — other resources just aren’t working for too many,” says Smithson.

Smithson continues, “Our subscribers can develop a personal connection with me through the video medium, and we can relate ‘face-to-face’. Only someone else doing this daily can really know the struggles, and I never promise I can make it easy. But, I’m absolutely convinced that DiabetesEveryDay can help people managing this disease become comfortable and confident with this overwhelming personal responsibility. A consistent focus is necessary, and the stakes are so high.”

Comedian Vic Dunlop has died at the age of 62. An irreverent and wacky stand-up comic, Dunlop began his career as a prop comic and saw a surge in popularity when he joined the cast of the television show “Make Me Laugh.”  Dunlop died of complications from diabetes at Glendale Activist Medical Center.

Dunlop started out as a comic in the 1970s in Los Angeles with an improv group called Natural Gas. The group appeared frequently on “Don Kirschner’s Rock Concert.” Dunlop later acquired individual fame for his role on “Make Me Laugh,” where comedians attempted to make contestants laugh. Dunlop was said to have held the show’s record for making a contestant laugh, at two seconds.

Dunlop achieved the feat by climbing on the ledge near the contestants and acting like a pigeon. His other antics on the show included dressing up like a baked potato. The portly Dunlop, weighing about 280 pounds at the time, was wrapped from head to toe in tin foil with a dollop of sour cream sitting atop his head.

Though Dunlop started out as a prop comic, fate quickly intervened and forced him down a different comic path. One night while Dunlop did a show at a comedy club, his bag of props was stolen from the backstage area. Forced to do a show without his props, he adapted and found a new routine.

Dunlop did keep one prop from his early days, however: a pair of bulging, fake bloodshot eyes that he would put on during shows. “Show up at LensCrafters and say, ‘What the hell happened to my eyes?’” he suggested. Dunlop was an eager entrepreneur; after telling the joke about the fake eyes, he’d say “I know what you’re saying, ‘Where can I get these eyeballs?’ You can I’ll be in the back selling them for $5 a pair.”

“Vic Dunlop’s Crazy Comic Eyes,” as they were called, were not only a staple of his routine but they sometimes outsold it, earning Dunlop more money in sales than he earned for performing his show.

According to fellow comedian Bill Kirchenbauer, Dunlop was “outrageous, he was loud, he’d scream, he’d make fun of people and make fun of himself. It was a real kind of base humor, basically. But the thing is, Vic was really funnier than his material. He got to [audiences] through his charisma and his natural funniness. He could go on stage and do just about anything, and people would laugh.”

Dunlop said of his comedy routines in a 1991 interview with The Times, “I like to have a party, and I include my audience.”  He infused his material with his natural charisma, making him a hit with audiences. Fellow “Make Me Laugh” alum Murray Langston said that “The one funny thing about him was everything was funny about him — the way he delivered lines, the way he looked and the way he gestured. He was a little bit over the top but all just funny.”

Dunlop also regularly appeared on 80s sitcom “Harper Valley P.T.A.” and Richard Pryor’s 1977 comedy-variety show. He had small movie roles in “Meatballs Part II,” “The Devil and Max Devlin,” “Skatetown U.S.A.,” “Night Patrol” and “Martians Go Home,” amongst others.

A longtime diabetic, Dunlop lost a leg to the disease in 2000 yet continued headlining in clubs around the nation. “Vic never wanted pity,” said his wife, Laura. “When people would say it, ‘I’m sorry that you lost your leg,’ he’d smile and say “It’s OK. I got 10 minutes of new material from it.'”

Researchers have found that diets high in fat are responsible for deactivating an important metabolic enzyme, causing a process that starts an organism down the path of Type 2 diabetes.

The findings are the result of a study conducted on humans and mice. The diabetic pathway is activated in the beta cells of the pancreas, leading to operational defects in other organs and tissues. The process affects the liver, muscle tissue, and adipose tissue (fat). When combined, these defects lead to the onset of Type 2 diabetes.

“We were initially surprised to learn how much the pancreatic beta cell contributes to the onset and severity of diabetes,” said Jamey Marth. Marth is a professor of biochemistry, molecular biology and nanomedicine at the University of California in Santa Barbara.

“The observation that beta cell malfunction significantly contributes to multiple disease signs, including insulin resistance, was unexpected,” continued Marth. “We noted, however, that studies from other laboratories published over the past few decades had alluded to this possibility.” Doctors were aware that defects in the functioning of pancreatic beta cells might be contributing to the onset of diabetes, but no one knew for sure until now.

The beta cells of the pancreas, when functioning normally, utilize glucose transporters embedded in their cell membranes to monitor the level of glucose in the blood stream. When they detect elevated levels of blood glucose, especially after meals, the beta cells absorb the extra glucose and release insulin in response. The insulin influences other cells to also take in the glucose, which they use as a source of energy.

The new study found that elevated levels of fat were responsible for interfering with two transcription factors, or proteins that determine whether a gene is active or inactive.

The two transcription factors are known as FOXA2 and HNF1A and they usually stimulate the production of an enzyme called GnT-4a glycosyltransferase. This enzyme modifies proteins that have a certain glycan, or polysaccharide, structure. But if FOXA2 and HNF1A are not activating correctly, GnT-4a’s effect is lessened.

The study tested this process by feeding a high-fat diet to mice, whose pancreatic beta cells became unable to monitor blood glucose and respond to it. When the researchers ensured that GnT-4a continued to function properly, however, the development of diabetes was halted. The defect in the beta cells’ monitoring of blood glucose was shown to have a significant effect on whether or not diabetes developed, and the severity of the disease if it did develop.

“Now that we know more fully how states of over-nutrition can lead to Type 2 diabetes, we can see more clearly how to intervene,” said Marth. Marth’s team is now looking at different methods of preserving the function of the GnT-4a enzyme in humans, which may work to prevent or possibly even reverse Type 2 diabetes.

“The identification of the molecular players in this pathway to diabetes suggests new therapeutic targets and approaches towards developing an effective preventative or perhaps curative treatment,” continued Marth. “This may be accomplished by beta cell gene therapy or by drugs that interfere with this pathway in order to maintain normal beta cell function.” Now that scientists understand the mechanisms by which the pancreatic beta cells become unable to monitor blood glucose levels, they are looking toward developing treatments.

There are more than 24 million people living with diabetes in the United States, or almost eight percent of the nation’s population. Type 2 diabetes, informally called adult onset diabetes, is far more common in adults, accounting for 90 to 95 percent of newly diagnosed cases of diabetes in adults.

A new study published in Annals on Oncology, a cancer-focused research journal, has found that trastuzumab (Herceptin) — a breast cancer drug — increases the risk of heart complications. Women who have diabetes and women with a history of heart disease are especially at risk.

The study analyzed the medical data of 45 women between the ages of 70 and 92 who had been treated with trastuzumab starting in 2005. Researchers found that 26.7% of the patients demonstrated heart problems that were caused by the drug. This rate was slightly higher than the rate demonstrated in younger and healthier women during the drug’s clinical testing phase. Trastuzumab caused 33% of the women with histories of heart disease to develop asymptomatic or symptomatic heart problems while only 9.1% of women without a history of heart disease developed those problems. Similarly, 33.1% of women with diabetes experienced new heart problems compared to only 6.1% of non-diabetic women. All but one of the women recovered fully once treatment with the drug was discontinued; five of the women renewed their treatment with the drug upon the disappearance of the problems.

Trastuzumab is currently the most-used medication for treating women with HER2 positive breast cancer, or the type of cancer that causes expression of the HER2 protein on the surface of the cancer cells. Elderly women are most at risk for breast cancer but trastuzumab has also been tested on younger, healthy women in clinical trials.

The study was conducted by Dr. César Serrano, a clinical fellow in Barcelona, Spain at the University Hospital Department of Medical Oncology Breast Cancer Centre. “This is the first study to specifically assess trastuzumab-related cardiac toxicity and the cardiovascular factors that are associated with an increased risk in a selected population of elderly breast cancer patients,” said Serrano of the study.

“Trastuzumab is generally well-tolerated and, although there are some concerns about it causing heart problems, until now few risk factors have been identified among patients in clinical trials, most of whom are usually younger than 70 years and have good general health,” continued Serrano. “Our study has demonstrated a significantly increased incidence of cardiac events among patients aged 70 and over with cardiovascular risk factors such as a history of cardiac disease and diabetes.

“Approximately 70% of all newly diagnosed cancers occur in patients older than 65 and, given the expected increase in the absolute number of elderly cancer patients over the coming decades in Western countries, there is an unmet need for information about the efficacy and safety of anti-cancer treatments in daily clinical practice. Data obtained in this report can serve to advise clinicians to be aware of symptomatic and asymptomatic cardiac dysfunction in elderly patients. We think that it is reasonable to refer elderly breast cancer patients to a cardiologist if one or more cardiovascular risk factors are present before or during treatment with trastuzumab. Moreover, a closer surveillance of early symptoms and cardiac function is highly recommended.”

Patients developed both asymptomatic and symptomatic cardiotoxicity after administration of trastumuzab. Asymptomatic cardiotoxicity occurs when no obvious symptoms of heart problems are apparent but scanning or echocardiography reveals that the heart’s left ventrible drops in function by 10% or more. Symptomatic cardiotoxicity shows apparent physical symptoms such as swelling of the limbs and shortness of breath; this type of cardiotoxicity includes congestive heart failure.

“One of the main characteristics of trastuzumab cardiotoxicity is its reversibility,” said Serrano. “It is a well-known phenomenon that differs from other chemotherapeutic agents such as anthracyclines. Reversibility normally happens with treatment discontinuation, but also can also occur spontaneously. The decision to reintroduce trastuzumab, or to continue with it, must be taken case-by-case together with a cardiologist.”

A research team at Vienna General Hospital’s University Department of Internal Medicine III has found that preemptive insulin therapy drastically lowers the risk of patients developing diabetes mellitus, or Type 2 diabetes, after a kidney transplant. As of now, up to 30 percent of patients receiving kidney transplants develop diabetes within a year of the transplant.

“We give the patients insulin immediately after the transplant even before diabetes mellitus occurs,” says Marcus Säemann of the Clinical Department of Nephrology and Dialysis. “The new thing about this is that we are giving insulin to non-diabetics and are hereby treating patients preventatively.”

The research group has proven this approach to be successful. A selection of 25 patients who were treated with preventative insulin therapy for three months after the transplant showed about a 75% decrease in their chances of developing diabetes. A control group that was not administered insulin treatment but treated according to the current standards for kidney transplant patients had a 45% chance of developing diabetes within the year following the transplant. “This is sensational data that we have obtained from thousands of blood sugar measurements,” said Manfred Hecking, a supervisor for the study.

The research team’s efforts did not go unnoticed. Their initial results caught the attention of the University of Michigan as a research partner. Starting at the end of 2011 the United States National Institutes of Health (NIH) will sponsor the study and expand upon it across multiple research facilities throughout the world. The study will last three to five years and will be coordinated by Hecking and Säemann. Research facilities in Germany, France, Italy and Spain will contribute to the effort.

Kidney transplant patients often develop diabetes mellitus in the year following the transplant because of increased stress from the surgery and also from the high levels of immunosuppressant drugs given to the patient to prevent acute organ rejection. “The patient shall be, so to say, swept away from a wave of acute disease,” says Säemann. There are currently no effective treatments in use for the development of diabetes following a transplant. Diabetes drastically shortens the patient’s life expectancy and quality of life in addition to reducing the lifespan of the transplant organ. The results of this new study provide hope for those waiting on kidney transplants that they may not have to face diabetes in their lifetimes.
Kidney transplants typically extend the life of patients by 10-15 years. Even elderly patients who receive transplants live four more years on average than if they had stayed on dialysis. Patients who receive kidney transplants see their quality of life improve greatly. They feel less fatigued and can eat a less restrictive diet.

Kidney transplant patients must take a variety of immunosuppressant medications to prevent the body from rejecting the new kidney. The most common combination of medications includes tacrolimus, mycophenolate, and prednisone; patients have to take these expensive medications for the remainder of their lives. Amid the chances of organ rejection and development of diabetes, kidney transplant patients are also at risk of infections and sepsis, lymphoma, hair loss, acne, obesity, and raised cholesterol. Preventative insulin therapy may one day eliminate the development of Type 2 diabetes as a risk that kidney transplant patients must take.

“Our study is a great advance for transplant medicine generally,” said Säemann. The Vienna General Hospital currently treats about 1,100 patients who received kidney transplants with outpatient therapy.

Physicist Aaron Keller and his colleagues at the Helmholtz-Zentrum Dresden-Rossendorf in Germany and at Aarhus University in Denmark have reported a significant advancement in the possibility of treatment for Type 2 diabetes and Alzheimer’s disease. The researchers are studying amyloids, or clumps of proteins that form in the body, which seem to be closely related to the development of these diseases. If doctors could prevent these clumps from forming they might have an effective defense against diabetes and Alzheimer’s.

Amyloids form on the surfaces of different types of cells, namely the cells of the pancreas in diabetes and the brain in Alzheimer’s. Physicians currently do not have imaging technology that can view these processes as they occur, but Adrian Keller and his colleagues are working to recreate these processes artificially in tests at the Interdisciplinary Nanoscience Center in Aarhus, known as “iNano.”

Recreating the processes on an artificial surface is difficult because of the properties of the cell surfaces in organisms. Cells can be hydrophilic or hydrophobic, which means they either attract water or repel water, respectively.

Adrian Keller has used mica crystal to recreate the amyloid-forming process. He has configured the surface of the mica so that positively-charged atoms of argon gas are only able to slightly penetrate into the surface of the material. “This chemically activates the surface without significantly changing the roughness,” said Keller of the first step of the process. The roughness of the surface would also influence the possibility that amyloids could form there.

Next, Keller places the processed mica into boxes and stores them in the lab for several weeks. While stored away, the surface of the mica adsorbs hydrocarbons in the air around it. The surface of the mica gradually becomes hydrophobic instead of hydrophilic; after about three months, the mica is totally hydrophobic (water repellent).

Keller conducts experiments during these three months. He places amylin, a small protein, on the mica. This protein is also produced by certain pancreatic cells along with insulin. When an organism develops Type 2 diabetes, its body’s reaction to insulin becomes less effective. The organism’s blood sugar elevates and the pancreas produces more insulin and amylin in response to the increased blood sugar. Some of the amylin proteins assume a concave “bowl” shape and influence nearby amylin proteins to follow suit.

The misshapen amyloid proteins begin to stick together, forming amyloids. These clumps destroy pancreatic cells and reduce insulin production, which causes the other cells to ramp up their own insulin produciton. The cycle continues and the organism’s insulin production mechanism can be devastated.

In Keller’s experiments, the amylins clump together on the surface of the mica according to the nature of the crystal’s surface. If the experiment has just been started and the surface is still hydrophilic, the amylin proteins form clusters called “fibrils.” However, if the mica has been gathering hydrocarbons and the surface is becoming hydrophobic, the amylins increasingly form clumps called “oligomers.” Both oligomers and fibrils work to destroy the surface of the cells, though they work through different mechanisms. In either case, when the clumps form on pancreatic cells, they inhibit insulin production.

Keller’s experiments have allowed researchers to view the creation of amyloid clumps for the first time in history. This new technology may pave the way for researchers to develop methods of preventing the clumping process and thus preventing diabetes and Alzheimer’s.

Tampa Bay Rays outfielder Sam Fuld made the day of one six-year-old boy when he visited Andrew Cordovez in an examination room. Fuld had one special connection with the young boy: they both have Type 1 diabetes.

Andrew received an autograph picture of Fuld and a baseball. “That was cool,” said Andrew. “He’s a really good player.”

Fuld visited the newly-founded diabetes center at the University of South Florida, taking a two-hour tour of the 10,000 square foot facility. The diabetes center, which opened last month, is part of the Carol & Frank Morsani Center for Advanced Healthcare.

Officials at the University of South Florida hope that the facility will propel them to the forefront of research, education and treatment of diabetes. The disease affects more than 23 million people around the country.

According to the dean of the USF College of Medicine, Dr. Stephen Klasko, the university is quickly becoming a national leader in diabetes research. The university has received more than $400 million for its efforts in studying diabetes but did not have a clinical facility. The new diabetes center cost $2 million; university funds and donations paid for the facility.

Facility officials who met Fuld included Dr. Klasko, Judy Genshaft (USF President) and Drs. Jeffrey Krischer and Henry Rodriguez (heads of the new center). The group all wore Tampa Bay jerseys.

Fuld visited the center with wife, Sarah, and son, Charlie, in tow. Charlie is 20 months old and does not have diabetes but his parents are wary since the disease is hereditary and Charlie is at increased risk.

“It’s a cause near and dear to my heart,” said Fuld of diabetes. He was diagnosed with Type 1 diabetes at only 10 years old. But like Andrew Cordovez, Fuld was visited by an athlete with Type 1 diabetes when as a young boy. Fuld met Bill Gullickson, a professional pitcher who also had Type 1 diabetes, when Fuld was 12 years old.

Gullickson had encouraging words for Fuld. “He told me I could do anything, academically and athletically, I wanted to,” said Fuld of the meeting.

Fuld took the advice to heart and made the best of his situation. Now 29 years old and known as “Super Sam,” Fuld’s athletic style of fielding has garnered attention and adoration from fans. His athleticism belies the fact that his diabetes requires him to perform regular blood sugar checks on himself, six to seven times a day, including two to three times in the middle of games. Fuld also administers his own insulin shots four to five times every day. “I keep those up in the clubhouse in the locker room. So if you see me running up the tunnel to go to the locker room, that’s probably why,” said Fuld.

According to Fuld, he has an advantage in that baseball is more flexible in addressing his diabetes. “All that down time in the dugout. So I get plenty of time to check my sugar. And I give myself shots probably four to five times a day.”

“My outlook on it, all along was just look at it as a challenge,” Fuld said of living with diabetes.

Fuld isn’t the only athlete who achieved success despite being diagnosed with diabetes. Other diabetic athletes include NFL quarterback Jay Cutler, Indy car driver Charlie Kimball, Olympic gold medalist swimmer Gary Hall Jr. and two tennis Hall of Famers: Billie Jean King and Arthur Ashe.

Mannkind (MKND) stock rose more than 20%, showing increased investor confidence after the fledgling pharmaceutical company confirmed that it has received approval from the FDA for clinical trials on its key product. Mannkind received FDA clearance to conduct efficacy trials on a new inhaled insulin product dubbed Afrezza, designed to treat patients with both Type 1 and Type 2 diabetes.

Mannkind has navigated rough financial waters, seeing its stock fall upon news of delays in developing the drug but the company has seen its fortunes reversed in light of the new agreement regarding the design of the clinical trials. One trial will compare Mannkind’s new inhaler design with the MedTone inhaler, subject of previous trials. The FDA has requested data on the impact of various inhalers on the cardiovascular systems of users.

Mannkind’s fortunes have hinged on Afrezza and the market for inhaled insulin. The company has suffered numerous setbacks to the development and approval of Afrezza amidst a general reduction in interest of inhaled insulin. Eli Lilly and Pfizer backed out of the inhaled insulin race; chairman and CEO of Mannkind, Alfred Mann, believes that there is a market for inhaled insulin. Mannkind currently has no products on the market.

“We are very encouraged and pleased with this outcome,” said Mann of the FDA approval. “Our attention now turns to the execution of these trials. The protocol for Study 171 has already been sent to Institutional Review Boards and the protocol for Study 174 is being finalized and will be distributed to our sites shortly,” Mann said, referring to the two recently approved trials.

Mannkind focuses primarily on treating patients with cancer and diabetes. While it has no products on the market, it is hopeful that Afrezza will give it a heady boost. The medication is an meal-time inhaled insulin.

Inhaled insulin was on the market in the United States from September 2006 through October 2007. The first FDA-approved inhaled insulin product, called Exubera, was approved in January 2006 and marketed by Pfizer. Studies determined that inhaled insulin was no more effective than subcutaneously injected insulin. Both Type 1 and Type 2 diabetics would still require injections of long-lasting insulin in addition to inhaled insulin. The possibly of dosing errors with inhaled insulin, along with its prohibitive cost, caused major players Pfizer and Eli Lilly to discontinue their programs and market interest in the product dwindled. Mannkind is the only company still pursuing production of inhaled insulin with its Afrezza product.

Mannkind received notification from the FDA in January that additional clinical trials would need to be performed before Mannkind received the green light for marketing Afrezza. The product was first submitted for approval in March of 2009, when the FDA notified Mannkind that it would need to provide additional data before trial approval was granted.

The approval of the trials is a boon for Mannkind, which saw losses of $44.5 million in the second quarter of 2011 and $42.3 million in the same quarter last year. Per-share losses saw no change at 37 cents. Mannkind did not see any revenue in the second quarter of 2011 compared with revenue of $93,000 in the same quarter of 2010.

In the wake of the news, company shares rose 47 cents to $2.84.

Mannkind has its corporate headquarters located in Valencia, California, with the manufacturing facility for Afrezza located in Danbury, Connecticut. Though technically founded in 1991, the current form of Mannkind was founded in 2003 with a merger between three of Alfred Mann’s companies. Mann has invested over $900 million in the company.

Researchers at York University have discovered a new protein that might hold the answer to the problem of controlling blood sugar and appetite.

The protein is called nesfatin-1 and Suraj Unniappan, an associate professor in the York Department of Biology, Faculty of Science & Engineering, is exploring its characteristics. The protein occurs naturally in large amounts in the brain; Unniappan administered rats with the protein and found that they were more active and ate less while their metabolisms were more likely to use stored body fat to generate energy. The administration of the protein in rats and mice also stimulated pancreatic beta cells into secreting insulin.

“[The rats] actually ate more frequently but in lesser amounts,” said Unniappan, who was chosen by York’s neuroscience graduate diploma program and also received the Canadian Institutes of Health Research New Investigator Award. “In addition, they were more active and we found that their fatty acid oxidization was increased,” added Unniappan. “In other words, the energy reserve being preferably used during nesfatin-1 treatment was fat. This suggests more fat loss, which could eventually result in body weight loss.” The rats’ metabolisms switched to using fat as their preferred energy resource, making it more likely that body fat would be reduced through activity.

Unniappan’s findings were published in the form of two recent articles in Endocrinology and in the Journal of Endocrinology.

A research team from Japan discovered nesfatin-1 in 2006. It has been shown in the past that nesfatin-1 regulates appetite and the storage of body fat when it is injected into the brains of rats and mice.

Unniappan showed through his research that, in addition to regulating body fat, nesfatin-1 stimulates the islets of Langerhans in the pancreas into producing several hormones, including insulin. The pancreas then secretes the insulin into the bloodstream, which works to reduce blood sugar levels.

Unniappan’s research team had previously shown the link between nesfatin-1 and diabetes in mice. Not only could nesfatin-1 be used to stimulate the production of insulin in mice, but the islets of Langerhans in mice with Type 1 diabetes showed decreased nesfatin-1 production while those in mice with Type 2 diabetes displayed increased nesfatin-1 production. In patients with Type 1 diabetes, the destruction of pancreatic cells causes the body to stop producing insulin while Type 2 diabetes sees patients becoming insulin resistant.

Unniappan focuses his research on discovering and analyzing metabolic hormones on fish and mammals. “We call this the gut-brain axis,” he says. “While the brain is involved in many factors that regulate our energy balance, the gut is also responsible for many neural and endocrine signals responsible for regulating hunger, satiety and blood sugar levels. A major question we’re trying to address is how these peptides act and interact with other peptides in the endocrine network – which is so complex – in order to maintain steady blood glucose levels and body weight.”

Unniappan believes that understanding this gut-brain axis is the key to developing new medications and treatments for obesity and diabetes. However, he warns that nesfatin-1 may not be used pharmacologically any time soon. “New hormone-based treatments that would suppress body weight and blood sugar would be very desirable. However, we are far from developing nesfatin-1 as a candidate molecule. Our current research focuses on further exploring the therapeutic potential of nesfatin-1 in metabolic diseases with debilitating complications.”