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November 28, 2007, 9:56 PM CT

Transporters and diabetes-related retinal damage

Transporters and diabetes-related retinal damage
Two transporters that deliver alternative energy sources to the eye may help delay retinal damage that can occur in diabetes, scientists say.

The transporters, SMCT1 and SMCT2, can circumvent the eye's protective blood-retinal barrier, delivering energy sources lactate and ketone bodies to a healthy eye, says Dr. Pamela Martin, biochemist at the Medical College of Georgia.

In diabetes, characterized by plenty of glucose but the inability of cells to use it, the retina may turn to those alternate sources for survival.

"Glucose is your primary energy source," says Dr. Martin. "But in diabetes, the retina undergoes a lot of stress, there is oxidative damage and a lot of other things going on. These transporters, we believe, may be instrumental in bringing in additional substrates which the cells can use for energy to try and prevent death." .

Diabetic retinopathy, the leading cause of blindness in working-age adults, results in death of retinal neurons, at least in part because glucose availability is compromised for this high-energy-consuming tissue, says Dr. Martin.

She suspects the two transporters work harder in diabetes to increase levels of lactate and ketones bodies, which may help explain why diabetes' impact on the eye may go undiagnosed for years. "I think what fascinates me so much about the eye is you can have diabetes for more than 20 years before you or your doctor realize that you have diabetic retinopathy," says Dr. Martin.........

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September 6, 2007, 5:10 AM CT

How insulin TORC2 blood sugar levels

How insulin TORC2 blood sugar levels
Mice on the left: During fasting, the CREB/TORC2 switch turns on glucose production in the liver. Salk researchers made this process visible with the help of luciferase, which normally produces the glow of firefly tail but in this case lights up the livers of mice actively producing glucose. Mice on the right: In response to feeding, mice produce insulin, which shuts down glucose production in the liver.

Credit: Courtesy of Dr. Renaud Dentin, Salk Institute for Biological Studies
La Jolla, CA With the help of genetically engineered mice whose livers turned into glowing light bulbs, scientists at the Salk Institute for Biological Studies have illuminated the underpinnings of an insidious and growing health concern type II diabetes.

In the study reported in the September 5 advanced online edition of Nature, the scientists report that a protein called TORC2 serves as a key biochemical control point linking feeding, insulin, and elevated blood sugar production in the liver. The findings highlight TORC2 and an enzyme called SIK2 as potential drug targets for treating type II diabetes.

An estimated 21 million Americans have adult-onset, or type II diabetes, and another 54 million have a condition called pre-diabetes where blood sugar levels remain abnormally high even after fasting. As per the Centers for Disease Control and Prevention, one in three Americans born in 2000 will develop diabetes, an incurable disease that can lead to blindness, kidney failure, heart disease, and other serious debilitations.

The problem starts during gluconeogenesisa process by which blood sugar is produced in the liver, explains Marc Montminy, Ph.D., a professor in the Clayton Foundation Laboratories for Peptide Biology, who led the study. During fasting, gluconeogenesis maintains blood sugar levels by increasing glucose production. After a meal, the hormone insulin normally turns down gluconeogenesis ensuring that blood sugar levels dont rise too high. But in people with insulin resistance, blood sugar levels are elevated because gluconeogenesis continues when it shouldnt, increasing the risk of developing type II diabetes, Montminy says.........

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September 6, 2007, 5:08 AM CT

How insulin secreting cells maintain their glucose sensitivity

How insulin secreting cells maintain their glucose sensitivity
Researchers at the leading Swedish medical university Karolinska Institutet have now disclosed the mystery how the insulin-secreting cells maintain an appropriate number of ATP sensing ion channel proteins on their surface. This mechanism, which is described in the latest number of Cell Metabolism, explains how the human body can keep the blood glucose concentration within the normal range and thereby avoid the development of diabetes.

Blood sugar absorbed from food has to timely enter muscles as energy supply as well as the liver and fat tissue for energy storage. Otherwise, diabetes occurs. Such glucose transport is precisely controlled by insulin, the bodys only hormone capable of lowering blood sugar. This hormone is released from insulin-secreting cells in the pancreas.

The ion channel proteins that are regulated by ATP and that transport potassium ions (KATP channels) are situated on the surface of the insulin-secreting cells to sense blood sugar and control sugar-stimulated insulin secretion. However, it has been a long-standing mystery how the insulin-secreting cells keep an appropriate number of KATP channels on their surface. Researchers at the the Rolf Luft Research Center for Diabetes and Endocrinology, Karolinska Institutet, have now disclosed a new traffic route whereby sugar promotes the insulin secretion controller KATP channel to march to its post.........

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July 19, 2007, 10:40 PM CT

Shielding the brain from too much insulin can prolong life

Shielding the brain from too much insulin can prolong life
Morris White, PhD
One route to a long and healthy life may be establishing the right balance in insulin signaling in the body and brain, as per new research from Children's Hospital Boston. The study, reported in the July 20 issue of Science, not only reinforces the value of exercising and eating in moderation, but also helps explain a paradox in longevity research.

Insulin sends a vital signal in the body, telling cells to use sugar from the blood. When cells become less sensitive to insulin, which often happens as we age and gain weight, the body makes more insulin to compensate. For a long time, scientists thought that "more insulin signaling was good," says Morris White, PhD, a Howard Hughes Medical Institute investigator in Children's Division of Endocrinology, who led the new study. "But this insulin is also hammering the brain, and we now believe that's probably a bad thing".

Recent studies in the worm C. elegans and in fruit flies have shown that reducing insulin signaling lengthens lifespan. But in mammals, reducing insulin signaling can lead to fatal diabetes. White suspected that the key to explaining this paradox -- and to maximizing both health and longevity -- is to reduce insulin signaling only in the brain.

To test this hypothesis, White's team measured longevity and other characteristics in three types of mice. One group had normal insulin signaling in their brains. The other two groups were genetically engineered to have reduced brain insulin signaling, having less of a protein called Irs2 that carries insulin's message inside cells.........

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July 17, 2007, 10:51 PM CT

Rosiglitazone for type 2 diabetes

Rosiglitazone for type 2 diabetes
New studies are needed to assess the trade-offs between potential benefits and potential harms when rosiglitazone is used by people with type 2 diabetes.

This Cochrane Systematic Review analysed data from 18 trials that involved a total of 8432 people and found no evidence that rosiglitazone led to better patient outcomes when compared with other therapies. Diabetic control (as measured by levels of HbA1c) was no better in patients given rosiglitazone when in comparison to other antidiabetic drugs. Patient oriented outcomes such as mortality, diabetes related morbidity, or quality of life were not addressed in most studies.

In addition to confirming the known risk of edema (people taking the therapy are at twice the risk of developing this condition) and an increase in body weight up to 5.0 kg, the authors found evidence from one large study indicating increased cardiovascular risk and an enhanced risk in women of having broken bones.

In people with type 2 diabetes, their body has a reduced ability to cause cells to remove glucose from the blood. The resulting high levels of blood-glucose can cause considerable damage particularly to the eyes, nerves and kidneys. Rosiglitazone is one of a range of drugs that increase cells sensitivity to insulin and therefore may restore some of the normal function.........

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July 5, 2007, 9:44 PM CT

Pharmacists To Help Diabetes Sufferers

Pharmacists To Help Diabetes Sufferers
A new Wesley Research Institute project aims to make it much easier for people to manager their Type 2 Diabetes by using community pharmacists.

There are more than one million Australians with Type 2 Diabetes who are at an increased risk of developing serious health problems including heart disease, stroke, kidney disease and blindness.

Chief investigator of the project, Mr David Brand of The Wesley Pharmacy, said this study had the potential to benefit sufferers by enabling them to better understand and manage their own blood glucose levels, thus helping to prevent long-term health problems.

With around 600 new cases of diabetes diagnosed every week in Australia, it is imperative that we continue to look for better, more user friendly ways of managing this condition, he said.

A major problem in Type 2 Diabetes management is the lack of understanding of how lifestyle influences day to day variations in blood glucose levels. If the particular cause of the unhealthy level is better understood, it may be corrected through changes in lifestyle.

Funded by the MBF Foundation, the project is providing participants with education and advice about the control of their blood glucose levels based on individual glucose meter uploads during the day. The study will then determine whether lifestyle advice from pharmacists has a positive impact on participants' glycaemic control.........

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June 27, 2007, 5:27 AM CT

Cord blood may preserve insulin levels in children with type 1 diabetes

Cord blood may preserve insulin levels in children with type 1 diabetes
Insulin-secreting beta cells
Umbilical cord blood may safely preserve insulin production in children newly diagnosed with type 1 diabetes, as per findings from a small national pilot study presented Monday (June 25) at the American Diabetes Associations 67th Scientific Sessions in Chicago.

University of Florida scientists sought to determine whether it is feasible to use a patients own cord blood stem cells to neutralize the bodys autoimmune attack on the pancreas and help restore the organs ability to make insulin, which regulates how the body uses sugar and other nutrients for energy.

This is the first attempt at using cord blood as a potential treatment for type 1 diabetes. We hope these cells can either lessen the immune systems attack on the pancreas or possibly introduce stem cells that can differentiate into insulin-producing cells, said pediatric endocrinologist Dr. Michael Haller, an assistant professor of medicine at UFs College of Medicine.

While this is a relatively small study we can confidently say this is safe, and we have seen metabolic and immunologic changes to suggest there may be benefit, Haller said. Its not curing diabetes, but this is a first step to help us learn more and get us moving in the right direction.

Scientists got the idea in part from a patients father who had read that researchers elsewhere were able to reverse diabetes in mice by taking bone marrow from one animal and infusing it into its identical sibling without using chemotherapy or radiation treatment. And in the lab, researchers have been able to coax stem cells isolated from cord blood into making insulin. The man asked UF scientists whether giving a patient his or her own cord blood could have a similarly positive effect.........

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June 25, 2007, 9:20 PM CT

helping obese diabetics lose weight

helping obese diabetics lose weight
A plate and cereal bowl with markers for proper portion sizes appear to help obese patients with diabetes lose weight and decrease their use of glucose-controlling medications, according to a report in the June 25 issue of Archives of Internal Medicine, one of the JAMA/Archives journals.

Between 1960 and 2000, the proportion of U.S. adults who were obese increased from 13.4 percent to 30.9 percent, according to background information in the article. Most cases of type 2 diabetes can be attributed directly to obesity. Restricting calories has been shown to improve blood sugar control in diabetics, partially by contributing to weight loss. The increasing prevalence of obesity is paralleled by increasing portion sizes in the marketplace, the authors write. Portion sizes are an important determinant of energy intake; the number of calories ingested by subjects at a meal has been directly correlated with the serving size offered.

Sue D. Pedersen, M.D., F.R.C.P.C., and colleagues at the University of Calgary, Alberta, Canada, conducted a six-month controlled trial of commercially available portion control plates and bowls in 2004. The plates were divided into sections for carbohydrates, proteins, cheese and sauce, with the rest left open for vegetables. The sections approximately totaled an 800-calorie meal for men and a 650-calorie meal for women. The cereal bowl is designed to allow a 200-calorie meal of cereal and milk. Half of 130 obese patients with diabetes (average age 56) were randomly assigned to use the plate for their largest meal and the bowl when they ate cereal for breakfast. The other half of the participants received usual care, which consisted of dietary assessment and teaching by dieticians.........

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June 10, 2007, 8:54 PM CT

Potential New Target For Type 2 Diabetes

Potential New Target For Type 2 Diabetes
Researchers at the University of Pennsylvania School of Medicine have discovered a potential new target for treating type 2 diabetes, according to a new study that appeared online this week in Nature. The target is a protein, along with its molecular partner, that regulates fat metabolism.

“Over the last 10 years, we have begun to understand the importance of fat metabolism in diabetes,” notes lead author Morris J. Birnbaum, MD, PhD, the Willard and Rhoda Ware Professor of Diabetes and Metabolic Diseases at Penn and an Investigator of the Howard Hughes Medical Institute. “Type 2 diabetics are at a higher risk for cardiovascular disease because they also have disorders in fat metabolism as a result of obesity and abnormal insulin action.” Birnbaum is also the Associate Director of the Type 2 Diabetes Unit for Penn’s Institute for Diabetes, Obesity, and Metabolism.

When a person eats a meal, the pancreas usually responds by secreting insulin that signals the liver to stop making glucose and burning fat. When a type 2 diabetic eats a meal, insulin cannot stop the manufacture of glucose in the liver, but it can stop the burning of fat stores. This gives the diabetic person a “double whammy:” fatty acids accumulate from food and from the liver. Consequently, more fat is deposited in tissues and obesity worsens.........

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May 23, 2007, 7:52 PM CT

When it comes to preventing amputation

When it comes to preventing amputation
Scientists at Scholl College's Center for Lower Extremity Ambulatory Research (CLEAR) at Rosalind Franklin University of Medicine and Science, Leiden University in the Netherlands, and Texas A&M University have presented important new information that could help physicians and their patients predict dangerous recurrent wounds that precede amputations in persons with diabetes. The study, conducted over a several-year period, identified two simple items that helped predict recurrence.

"The study was surprising and promising in that, out of a whole lot of data, some simple truths emerged," noted David G. Armstrong, DPM, PhD, Professor of Surgery at Scholl College and a principal investigator on the study. "The location of the ulcer (under the big toe) and the presence of poor blood flow were the key factors that dramatically increased the risk for recurrent wounds in these patients, thereby increasing their risk for gangrene and amputation. These findings could go a long way to help us predict and prevent the unnecessarily high rate of complications in persons with diabetes, worldwide".........

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May 21, 2007, 11:43 AM CT

Sleep apnea may increase risk of diabetes

Sleep apnea may increase risk of diabetes
Scientists at the Yale University School of Medicine have observed that patients with obstructive sleep apnea are at increased risk for developing of type II diabetes, independent of other risk factors. The findings are being presented at the American Thoracic Society 2007 International Conference, on Monday, May 21.

The study looked at 593 patients at the VA Connecticut Health Care System referred for evaluation of sleep-disordered breathing. Each patient spent a night in a sleep laboratory to undergo a sleep study, called polysomnography.

The scientists followed the subjects for up to six years and observed that patients diagnosed with sleep apnea had more than two-and-half times the risk of developing diabetes compared with those without the nighttime breathing disorder. The patients were then divided into groups based on the severity of their sleep apnea, and the more severe a patients sleep apnea, the greater the risk of developing diabetes.

In obstructive sleep apnea, the upper airway narrows, or collapses, during sleep. Periods of apnea end with a brief partial arousal that may disrupt sleep up to hundreds of times a night. Obesity is a major risk factor for sleep apnea. Emerging evidence also exists that sleep apnea is linked to hypertension, stroke and heart disease.........

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May 16, 2007, 5:19 PM CT

Illuminating Cause Of Diabetes

Illuminating Cause Of Diabetes
Any photographer can vouch for the difficulty of capturing a clear picture of a moving target.

When it comes to molecules, however, sometimes the motion is exactly what researchers want to see - for example, to understand the pathological protein mis-folding and assembly that seem to underlie a host of human disorders, including diabetes and Alzheimer's disease.

Now, chemists at the University of Wisconsin-Madison have designed a powerful analytical tool capable of measuring molecular structures quickly and accurately enough to catch moving proteins in mid-fold and see the shapes of intermediate steps. As described in this week's online issue of the Proceedings of the National Academy of Sciences, the first applications of the technique offer a glimpse into the contorted form of a human protein that is implicated in type II diabetes.

Pancreatic damage in type II diabetes has been associated with toxic clumps of the protein hIAPP (human islet amyloid polypeptide), which is normally produced by the same cells that make insulin. An unknown trigger prompts the protein to fold into sharp fibers that poke holes in pancreatic cells, killing them.

Though researchers already have a good idea of the healthy "before" and dangerous "after" hIAPP structures, the steps in between remain somewhat of a mystery and may hold clues to what drives the transition, says UW-Madison chemistry professor Martin Zanni, who led the new study.........

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May 14, 2007, 10:34 PM CT

Supplement Inhibits Multiple Sclerosis, Type 1 Diabetes

Supplement Inhibits Multiple Sclerosis, Type 1 Diabetes
A glucosamine-like dietary supplement has been found to suppress the damaging autoimmune response seen in multiple sclerosis and type 1 diabetes mellitus, as per University of California, Irvine health sciences researchers.

In studies on mice, Dr. Michael Demetriou and his colleagues with the UC Irvine Center for Immunology observed that N-acetylglucosamine (GlcNAc), which is similar but more effective than the widely available glucosamine, inhibited the growth and function of abnormal T-cells that incorrectly direct the immune system to attack specific tissues in the body, such as brain myelin in MS and insulin-producing cells of the pancreas in diabetes. Findings from the study are published on the online version of the Journal of Biological Chemistry.

"This finding shows the potential of using a dietary supplement to help treat autoimmune diseases," said Demetriou, an assistant professor of neurology, and microbiology and molecular genetics. "Most importantly, we understand how this sugar-based supplement inhibits the cells that attack the body, making metabolic treatment a rational approach to prevent or treat these debilitating diseases".

The UC Irvine study defines how metabolic treatment with the sugar GlcNAc and other related nutrients modifies the growth and autoimmune activitiy of T-cells. Virtually all proteins on the surface of cells, including T-cells, are modified with complex sugars of variable lengths and composition. Recent studies have shown that changes in these sugars are often linked to T-cell hyperactivity and autoimmune disease.........

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March 15, 2007, 9:23 PM CT

Erectile dysfunction in diabetics

Erectile dysfunction in diabetics
A new study sheds additional light on how erectile dysfunction (ED) interacts with diabetes. The study is another step in uncovering the link between the two disorders, and may lead to improved efficacy in therapys.

The study, "Lack of Central Nitric Oxide Triggers Erectile Dysfunction in Diabetes," was conducted by Hong Zheng, William G. Mayhan, and Kaushik P. Patel, Departments of Cellular and Integrative Physiology; and Keshore R. Bidasee, Department of Pharmacology, University of Nebraska Medical Center, Omaha, NE. The results appear in the March 2007 edition of the American Journal of Physiology Regulatory, Integrative and Comparative Physiology, one of 11 peer-reviewed scientific publications issued monthly by The American Physiological Society (APS) www.The-APS.org.

Background

Sexual dysfunction is a well-recognized consequence of diabetes mellitus in men. Erectile dysfunction, retrograde ejaculation and the loss of seminal emission have all been described by such patients. This study examined induced penile erection, yawning and stretch in diabetic rats. Male Sprague-Dawley rats treated with streptozotocin (STZ) to induce diabetes were used as they exhibit sexual and behavioral symptoms similar to those found in diabetic men with sexual dysfunction.........

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March 13, 2007, 9:18 PM CT

Periodontal diseases and pre-diabetes

Periodontal diseases and pre-diabetes
Periodontal diseases may contribute to the progression to pre-diabetes, as per a new study that appears in the recent issue of the Journal of Periodontology.

Pre-diabetes is a condition in which blood glucose levels are higher than normal, but not high enough to be diagnosed as diabetes. The American Diabetes Association estimates 54 million people in the United States have pre-diabetes, and a significant portion of those people will develop Type 2 diabetes within 10 years.

Scientists from Denmark investigated if having periodontal diseases can influence pre-diabetes and contribute to the progression of diabetes. They observed that having periodontal disease can cause someone to develop pre-diabetic characteristics, and probably disturb the glucose regulation of a non-diabetic who has pre-diabetic characteristics, contributing to the progression of Type 2 diabetes. The study, conducted with rat models known to exhibit pre-diabetes characteristics, is thought to bethe first to evaluate the relationship between periodontitis and pre-diabetes.

"This study observed that having periodontal diseases can alter the metabolic conditions which would probably lead to the progression to pre-diabetic characteristics and Type 2 diabetes," said Dr. Carla Pontes Andersen, Department of Periodontology at the University of Copenhagen.........

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March 1, 2007, 10:05 PM CT

protecting against weight gain and diabetes

protecting against weight gain and diabetes
new study from Joslin Diabetes Center may shed light on why some people can eat excessive amounts of food and not gain weight or develop type 2 diabetes, while others are more likely to develop obesity and this most common form of diabetes on any diet. The study, which used two strains of mice with differing tendencies to gain weight and develop diabetes on a high-fat diet, identified genetic and cellular mechanisms that may prevent certain mice on a calorie-dense diet from gaining weight and developing metabolic syndrome.

Eventhough this study was done with mice, it points out new mechanisms that may underlie the ability of genetically different mice -- and perhaps genetically different people -- to not gain much weight on high caloric diets, said lead investigator C. Ronald Kahn, M.D., an internationally recognized researcher who is Head of Joslins Section on Obesity and Hormone Action and the Mary K. Iacocca Professor of Medicine at Harvard Medical School.

The study, reported in the online edition of the Proceedings of the National Academy of Sciences on Feb. 5-9, builds upon years of research at Joslin and elsewhere on energy metabolism and the genetics of fat cells.

It has long been known that people significantly differ in their tendency to gain weight and develop metabolic syndrome, a group of conditions including hypertension, abdominal obesity, high triglycerides and glucose intolerance that can lead to type 2 diabetes. More than 60 million Americans either are obese or have metabolic syndrome, putting them at risk for type 2 diabetes and its frequent complications, including cardiovascular disease and other serious conditions. Currently 21 million Americans have diabetes and approximately one-third of them do not even know they have the disease. Formerly known as adult-onset diabetes, type 2 diabetes is occurring more frequently in young adults and even children.........

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February 27, 2007, 8:18 PM CT

genetic basis of Type 2 diabetes

genetic basis of Type 2 diabetes
Scientists from the Broad Institute of MIT and Harvard, Lund University and Novartis have announced the completion of a genome-wide map of genetic differences in humans and their relationship to Type 2 diabetes and other metabolic disorders.

All results of the analysis are accessible, free of charge, on the Internet to researchers around the world.

The work is the result of a pioneering public-private collaboration known as the Diabetes Genetics Initiative (DGI), which was formed in 2004 and is aimed at deciphering the genetic causes of Type 2 diabetes. Eventhough Type 2 diabetes clearly runs in families, suggesting the importance of inherited factors, its genetic origins remain largely unclear.

"The Human Genome Project, HapMap database and new genomic tools have made it possible for the first time to screen the genome for DNA variations that contribute to common diseases," said principal investigator David Altshuler, the director of the Program in Medical and Population Genetics at the Broad Institute and an associate professor at Massachusetts General Hospital and Harvard Medical School. "Since diabetes and cardiovascular risk factors are influenced by a number of genes, environment and behavior, these powerful new tools are mandatory to pick up the effect of any one genetic risk factor".........

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February 22, 2007, 10:08 PM CT

Insulin Pen Injector

Insulin Pen Injector Via MedGadget
At last there comes a device that reduces more than a few concerns of diabetics dependent on insulin. And it happens to be the digital insulin pen, Huma-Pen Memoir, designed by researchers at the Battelle Memorial Institute, for the Indianapolis-based drug company Eli Lilly.

The insulin pen injector not only allows the user to dial in the dosage of insulin he/she needs to take, but also cleverly records the dosage, and the date-time of 16 injections at a time. Thereby it plainly addresses the critical every-day issues that diabetics face of maintaining the records of their insulin dosages for analysis by physicians and to avoid overdosage. The device is also an inconspicuous way of taking insulin since it resembles an innocuous looking pen once the cap is replaced. Pretty neat.

The injector is designed to last for about 3 years and uses insulin cartridges and half-inch needles which have to be replaced after every use. The Huma-Pen is due to retail in the U.S. at a modest $45.........

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