From the Salt Lake City Tribune // Sept. 22, 2005
By Carey Hamilton // The Salt Lake Tribune
What is Glucagon?
Glucagon is a hormone, available by prescription. It is used to treat people with diabetes when their blood glucose levels drop dangerously low and they cannot swallow food or liquid - they may be having a seizure or losing consciousness. It comes in an emergency kit and is administered by injection.
Natalie Rodgers fears school policies could prevent her 6-year-old daughter and other diabetic children from receiving a lifesaving injection.
The Kearns woman has enlisted the help of state Sen. Patrice Arent, D-Holladay, who is sponsoring a bill that would allow trained adults to administer glucagon to children who take insulin and are losing consciousness. Glucagon is a hormone that raises blood sugar levels, staving off diabetic comas and even death.
Rodgers, Arent and health experts believe trained volunteers at Utah schools should be able to give the injections, which do not need to go in a vein. But students are currently forbidden from bringing almost all medications to school, with the exception of asthma inhalers.
"The thing that's great about it is it's hard to do wrong," said Rodgers, who spoke at an Education Interim Committee at the Capitol on Thursday. "There's no risk of overdose; it's a hormone that your body stores naturally. If you gave it to someone who doesn't have diabetes, it wouldn't hurt them."
People who have diabetes do not produce or properly use insulin, a hormone needed to convert sugar, starches and other food into energy. While the cause of diabetes is unknown, experts believe genetics and environmental factors, such as obesity and lack of exercise, play roles.
Nationwide, more than 18 million people - including a growing number of children - have diabetes, and many are unaware they have it. In Utah, about 4,000 children and teens under 20 - roughly .37 percent of all Utah youth - have diabetes, according to the Utah Department of Health. In 1991, the number of youth with diabetes was 1,800.
Rodgers' daughter, Andrea, was diagnosed with Type I diabetes in 2003 at the young age of 3.
"I have friends who have used glucagon on their children," Rodgers said. "We kindly refer to it as the Heimlich maneuver for diabetics. Normally, I wouldn't let my child go anywhere where she doesn't have glucagon available. It's a lifesaver for her."
Mary Murray, an endocrinologist and director of the diabetes program at Primary Children's Medical Center, beseeched the committee to endorse the legislation, which it did unanimously. Lawmakers will consider the bill when the legislative session begins in January.
Murray has treated patients who could have been helped by glucagon.
"Glucagon is safe and easy to administer," she said. "It can be given to a normal individual by accident, and the worst that will happen is nausea or vomiting."
Under the bill, children would get a prescription for the emergency kit from their doctors and carry it with them in their backpacks. School personnel trained in administering the medication would be shielded from lawsuits or criminal charges if they gave the injections in good faith.
"I don't want to have a situation where we have kids die when we can save them," Arent said.
Thursday, September 22, 2005
Wednesday, September 21, 2005
Type 1 diabetes link to bone loss
From AustralianDoctor.com.au // Sept. 21, 2005
By Jill Stein
ALMOST half of adults with type 1 diabetes have low bone mineral density, according to a study reported at the European Association for the Study of Diabetes meeting held in Athens last week.
Rheumatologist Dr Heather McDonald-Blumer and colleagues from the University of Toronto in Canada presented results of a bone mineral density (BMD) assessment in adult type 1 diabetes patients from a large community diabetes practice.
Among 130 people who completed a BMD assessment, 40% had a T score of less than -1.0 in at least one of three measured sites (femoral neck, total hip and lumbar spine).
"In other words, their T scores were in the low bone mass or osteoporotic range," Dr McDonald-Blumer said.
Men were affected more than women, with 46% of male type 1 diabetic patients showing low BMD compared with 34% of women, a trend especially apparent in the quartile with the lowest BMD.
"Overall, a disproportionate number of young male patients had low BMD scores," Dr McDonald-Blumer said.
While low BMD was more common in older age groups, it was also high among younger patients (11 of 30 patients aged 20-34).
In this population, BMD values did not correlate directly with age, BMI, age of onset of diabetes, duration of diabetes, the presence of micro- or macrovascular complications or the presence of traditional osteoporosis risk factors, Dr McDonald-Blumer said.
She said the results suggested undefined mechanisms were likely to be responsible for low bone mass in this population and further research was needed in the broader type 1 diabetic population.
Patients who were pregnant, seeking pregnancy or who had secondary causes of osteoporosis, or those with low BMD using anti-resorptive medications, were excluded from the study.
By Jill Stein
ALMOST half of adults with type 1 diabetes have low bone mineral density, according to a study reported at the European Association for the Study of Diabetes meeting held in Athens last week.
Rheumatologist Dr Heather McDonald-Blumer and colleagues from the University of Toronto in Canada presented results of a bone mineral density (BMD) assessment in adult type 1 diabetes patients from a large community diabetes practice.
Among 130 people who completed a BMD assessment, 40% had a T score of less than -1.0 in at least one of three measured sites (femoral neck, total hip and lumbar spine).
"In other words, their T scores were in the low bone mass or osteoporotic range," Dr McDonald-Blumer said.
Men were affected more than women, with 46% of male type 1 diabetic patients showing low BMD compared with 34% of women, a trend especially apparent in the quartile with the lowest BMD.
"Overall, a disproportionate number of young male patients had low BMD scores," Dr McDonald-Blumer said.
While low BMD was more common in older age groups, it was also high among younger patients (11 of 30 patients aged 20-34).
In this population, BMD values did not correlate directly with age, BMI, age of onset of diabetes, duration of diabetes, the presence of micro- or macrovascular complications or the presence of traditional osteoporosis risk factors, Dr McDonald-Blumer said.
She said the results suggested undefined mechanisms were likely to be responsible for low bone mass in this population and further research was needed in the broader type 1 diabetic population.
Patients who were pregnant, seeking pregnancy or who had secondary causes of osteoporosis, or those with low BMD using anti-resorptive medications, were excluded from the study.
Friday, September 16, 2005
FDA approves new continuous glucose monitor
Many people we talk to ask about the future of a continuos glucose monitoring system that will eliminate the need for the numerous daily fingerpricks. Here's the latest on one company's efforts.
From the Sept. 2005 JDRF Research Frontline Newsletter
Diabetes product providers continue to develop and refine diabetes management devices that could ultimately represent the component parts of an artificial pancreas. In August, the Food and Drug Administration (FDA) approved the Guardian RT Continuous Glucose Monitoring System, a blood sugar monitor that works both as a round-the-clock tracking device, recording a patient's blood glucose for up to three days, and as an alarm, sounding when blood sugar changes precipitously.
Patients wearing the beeper-sized, wireless monitor can get realtime glucose readings every five minutes, and also track how diet, exercise, and medication are affecting their blood sugar levels.
"Continuous monitors represent where diabetes selfmanagement is heading," says JDRF Scientific Program Manager Aaron Kowalski, who has type 1 diabetes.
Manufactured by Medtronic, Inc., the Guardian RT uses a sensor inserted in the abdomen just under the skin. The sensor transmits information to the monitor and records up to 288 readings a day. These data can be downloaded onto a PC to view trends in the individual's blood glucose activity. It also alerts users to high or low blood glucose levels. After three days, the sensor must be replaced.
While the manufacturer continues to evaluate training, education, and reimbursement fees, the Guardian RT is being sold only in selected U.S. cities. It requires a physician's prescription.
Currently, the only other continuous glucose monitors approved for use by the FDA are Medtronic's CGMS System Gold, an earlier model similar to the Guardian RT, and the GlucoWatch G2 Biographer, a wristwatch-like device manufactured by Cygnus.
Clinical trials show continuous monitors are effective, but at this point in their development they don't work well enough to replace conventional fingerstick glucose meters. As a result, the FDA requires that continuous monitors, including the Guardian RT, be used to complement fingerstick testing and give patients additional information about glucose level trends.
But taking a longer view, continuous monitors represent an important step toward an artificial pancreas, which would sense glucose levels and dispense appropriate amounts of insulin automatically.
"Technology will probably be reoriented around identifying trends and taking measures to prevent extreme highs or lows," says Dr. Kowalski. "Ultimately, it may be more important to know which way your glucose levels are heading than what your exact reading may be."
From the Sept. 2005 JDRF Research Frontline Newsletter
Diabetes product providers continue to develop and refine diabetes management devices that could ultimately represent the component parts of an artificial pancreas. In August, the Food and Drug Administration (FDA) approved the Guardian RT Continuous Glucose Monitoring System, a blood sugar monitor that works both as a round-the-clock tracking device, recording a patient's blood glucose for up to three days, and as an alarm, sounding when blood sugar changes precipitously.
Patients wearing the beeper-sized, wireless monitor can get realtime glucose readings every five minutes, and also track how diet, exercise, and medication are affecting their blood sugar levels.
"Continuous monitors represent where diabetes selfmanagement is heading," says JDRF Scientific Program Manager Aaron Kowalski, who has type 1 diabetes.
Manufactured by Medtronic, Inc., the Guardian RT uses a sensor inserted in the abdomen just under the skin. The sensor transmits information to the monitor and records up to 288 readings a day. These data can be downloaded onto a PC to view trends in the individual's blood glucose activity. It also alerts users to high or low blood glucose levels. After three days, the sensor must be replaced.
While the manufacturer continues to evaluate training, education, and reimbursement fees, the Guardian RT is being sold only in selected U.S. cities. It requires a physician's prescription.
Currently, the only other continuous glucose monitors approved for use by the FDA are Medtronic's CGMS System Gold, an earlier model similar to the Guardian RT, and the GlucoWatch G2 Biographer, a wristwatch-like device manufactured by Cygnus.
Clinical trials show continuous monitors are effective, but at this point in their development they don't work well enough to replace conventional fingerstick glucose meters. As a result, the FDA requires that continuous monitors, including the Guardian RT, be used to complement fingerstick testing and give patients additional information about glucose level trends.
But taking a longer view, continuous monitors represent an important step toward an artificial pancreas, which would sense glucose levels and dispense appropriate amounts of insulin automatically.
"Technology will probably be reoriented around identifying trends and taking measures to prevent extreme highs or lows," says Dr. Kowalski. "Ultimately, it may be more important to know which way your glucose levels are heading than what your exact reading may be."
Antibiotic may slow or prevent diabetic retinopathy
From the Sept. 2005 edition of JDRF Research Frontline Newsletter
JDRF-funded researchers at Penn State University have found that an antibiotic used to treat acne may slow or prevent diabetic retinopathy, the most common eye-related complication of diabetes and the leading cause of adult blindness in the U.S. The drug, minocycline, has proved effective in diabetic rats and could begin tests in humans soon.
"We think minocycline could enter clinical trials relatively quickly, given that it is already FDA-approved for another use." said Thomas Gardner, M.D., director of the JDRF Center for Mechanisms and Intervention of Diabetic Retinopathy at Penn State University Hershey Medical Center, where the study was conducted.
The researchers found that minocycline reduces by half the damage caused by diabetes to certain nerve cells, microglia, in the retina. Normally, microglia act as the cleanup crew for the nervous system, disposing of damaged cells by releasing toxins and engulfing them. In the presence of diabetes, microglia in the retinas become activated inappropriately - researchers were unsure how - and release toxins that kill healthy nerve cells critical for normal vision. Treatment with minocycline blocks this activation and the ensuing nerve cell death that leads to retinopathy.
Previous studies have shown that the changes diabetes causes in the body lead to increased production of cytokines, or proteins that cause inflammation of the nerves. The Penn State study, led by Kyle Krady, Ph.D., and published in the May issue of Diabetes, goes a step further to show that in early diabetes, elevated levels of cytokines activate the microglia, setting off destruction of retinal nerve cells.
After confirming that diabetic rats had high cytokine levels, Dr. Krady treated the animals with minocycline and found that it reduced cytokine levels and inflammation. Since nerve cell damage also decreased from the drug, the study draws a strong link between elevated cytokine levels and nerve cell death, suggesting how retinal cells may be damaged or changed by diabetes.
"These results confirm that diabetes causes an early increase in the _expression of inflammatory mediators within the retina, and that minocycline reduces this inflammatory component," said study co-author Steve Levison, Ph.D, professor of neural and behavioral sciences at Penn State College of Medicine.
Dr. Gardner said the Center's data will be introduced as a candidate for therapeutic development to the Diabetic Retinopathy Clinical Research Network, a collaborative network between the JDRF and the National Eye Institute at the National Institutes of Health.
"This is an exciting new development that has great potential for the treatment of this devastating complication," said Antony Horton Ph.D., JDRF Program Director for Diabetes Complications.
Identification of minocycline's potential is the latest payoff from the JDRF Center's unconventional approach to studying diabetic retinopathy, which traditionally has been regarded as a blood vessel disease that damages capillaries supplying blood to the retina.
Researchers at the Penn State Center think retinopathy may also - or even primarily - result from changes in the retinal cells. When researchers can identify and completely understand the sequence of these early retinal changes in various cell types, the information could help medical research intervene earlier in the
course of the disorder.
JDRF-funded researchers at Penn State University have found that an antibiotic used to treat acne may slow or prevent diabetic retinopathy, the most common eye-related complication of diabetes and the leading cause of adult blindness in the U.S. The drug, minocycline, has proved effective in diabetic rats and could begin tests in humans soon.
"We think minocycline could enter clinical trials relatively quickly, given that it is already FDA-approved for another use." said Thomas Gardner, M.D., director of the JDRF Center for Mechanisms and Intervention of Diabetic Retinopathy at Penn State University Hershey Medical Center, where the study was conducted.
The researchers found that minocycline reduces by half the damage caused by diabetes to certain nerve cells, microglia, in the retina. Normally, microglia act as the cleanup crew for the nervous system, disposing of damaged cells by releasing toxins and engulfing them. In the presence of diabetes, microglia in the retinas become activated inappropriately - researchers were unsure how - and release toxins that kill healthy nerve cells critical for normal vision. Treatment with minocycline blocks this activation and the ensuing nerve cell death that leads to retinopathy.
Previous studies have shown that the changes diabetes causes in the body lead to increased production of cytokines, or proteins that cause inflammation of the nerves. The Penn State study, led by Kyle Krady, Ph.D., and published in the May issue of Diabetes, goes a step further to show that in early diabetes, elevated levels of cytokines activate the microglia, setting off destruction of retinal nerve cells.
After confirming that diabetic rats had high cytokine levels, Dr. Krady treated the animals with minocycline and found that it reduced cytokine levels and inflammation. Since nerve cell damage also decreased from the drug, the study draws a strong link between elevated cytokine levels and nerve cell death, suggesting how retinal cells may be damaged or changed by diabetes.
"These results confirm that diabetes causes an early increase in the _expression of inflammatory mediators within the retina, and that minocycline reduces this inflammatory component," said study co-author Steve Levison, Ph.D, professor of neural and behavioral sciences at Penn State College of Medicine.
Dr. Gardner said the Center's data will be introduced as a candidate for therapeutic development to the Diabetic Retinopathy Clinical Research Network, a collaborative network between the JDRF and the National Eye Institute at the National Institutes of Health.
"This is an exciting new development that has great potential for the treatment of this devastating complication," said Antony Horton Ph.D., JDRF Program Director for Diabetes Complications.
Identification of minocycline's potential is the latest payoff from the JDRF Center's unconventional approach to studying diabetic retinopathy, which traditionally has been regarded as a blood vessel disease that damages capillaries supplying blood to the retina.
Researchers at the Penn State Center think retinopathy may also - or even primarily - result from changes in the retinal cells. When researchers can identify and completely understand the sequence of these early retinal changes in various cell types, the information could help medical research intervene earlier in the
course of the disorder.
Adult cells reprogrammed to embryonic state
From the Sept. 2005 JDRF Research Frontline
Researchers at Harvard report they have developed a method for creating therapeutic stem cells by fusing adult cells with embryonic stem cells. This fusion appears to reprogram the adult cell, resetting it to a state that resembles the embryonic stem cell. From that point, it might be coaxed to develop into specialized cells that could be used therapeutically in people.
This technique could be used to create replacement cells that are genetically identical to the donor of the adult cell. In addition, it may permit scientists to derive new human embryonic stem cell lines without the need to use human embryos. The research was led by Kevin Eggan, Ph.D., working with Douglas Melton, Ph.D. JDRF support enabled the research, which is reported in the August 26 issue of the journal Science.
"This research, while interesting and provocative, is still in the earliest stage of development and needs to be confirmed by other groups before we begin to understand its long-range impact," said JDRF Chief Scientific Officer Robert Goldstein, M.D. "It presents another possibility for scientists to explore and demonstrates once again the importance of stem cell research. But it would be a mistake to abandon other areas of diabetes research in general, and embryonic stem cell research in particular, because of this preliminary finding."
Currently, human embryonic stem cells are derived using human embryos either left over from in vitro fertilization procedures or created for research. That process is the major reason why some groups are opposed to embryonic stem cell research.
In the Science study, the researchers combined human skin cells with human embryonic stem cells in the presence of a detergent-like substance that caused the two cell types to fuse. The fused cells were "tetraploid" - meaning they contained the combined chromosomes of both the somatic cells (in this case, skin cells) and the embryonic stem cells, and therefore double the normal amount of DNA as in a human cell.
The fused cells were shown to have the characteristics of embryonic stem cells. They expressed the same genes as embryonic stem cells, even with two kinds of chromosomes (from the adult skin cell, and from the embryonic stem cell). This means that the fused cells must have reprogrammed the skin cell chromosomes so that they expressed the same genes as the embryonic stem cell.
Like stem cells, the fused cells could be grown in culture for long periods. Moreover, these tetraploid cells could be induced to develop into nerve cells, hair follicles, muscle cells, and cells of the stomach lining. This demonstrated the ability of the fused cells to give rise to a variety of different cell types.
Several technological hurdles still remain, with the biggest challenge figuring out a way to eliminate the embryonic stem cell nucleus from the newly created cell so that the fused cell would have a normal number of chromosomes instead of double that amount.
While any therapeutic applications from the new method lie far off, the researchers say that in the short term, it is more likely that the new technique will help to understand how embryonic cells reprogram adult, or "somatic" cells to an embryonic state. But Dr. Eggan told Science he expects that in 10 to 15 years, researchers will be able to use the technique routinely and will no longer need embryos or human eggs to reset adult cells.
"This is another example of how much scientists are learning about human embryonic stem cells in these early years of the research," said Dr. Goldstein.
Researchers at Harvard report they have developed a method for creating therapeutic stem cells by fusing adult cells with embryonic stem cells. This fusion appears to reprogram the adult cell, resetting it to a state that resembles the embryonic stem cell. From that point, it might be coaxed to develop into specialized cells that could be used therapeutically in people.
This technique could be used to create replacement cells that are genetically identical to the donor of the adult cell. In addition, it may permit scientists to derive new human embryonic stem cell lines without the need to use human embryos. The research was led by Kevin Eggan, Ph.D., working with Douglas Melton, Ph.D. JDRF support enabled the research, which is reported in the August 26 issue of the journal Science.
"This research, while interesting and provocative, is still in the earliest stage of development and needs to be confirmed by other groups before we begin to understand its long-range impact," said JDRF Chief Scientific Officer Robert Goldstein, M.D. "It presents another possibility for scientists to explore and demonstrates once again the importance of stem cell research. But it would be a mistake to abandon other areas of diabetes research in general, and embryonic stem cell research in particular, because of this preliminary finding."
Currently, human embryonic stem cells are derived using human embryos either left over from in vitro fertilization procedures or created for research. That process is the major reason why some groups are opposed to embryonic stem cell research.
In the Science study, the researchers combined human skin cells with human embryonic stem cells in the presence of a detergent-like substance that caused the two cell types to fuse. The fused cells were "tetraploid" - meaning they contained the combined chromosomes of both the somatic cells (in this case, skin cells) and the embryonic stem cells, and therefore double the normal amount of DNA as in a human cell.
The fused cells were shown to have the characteristics of embryonic stem cells. They expressed the same genes as embryonic stem cells, even with two kinds of chromosomes (from the adult skin cell, and from the embryonic stem cell). This means that the fused cells must have reprogrammed the skin cell chromosomes so that they expressed the same genes as the embryonic stem cell.
Like stem cells, the fused cells could be grown in culture for long periods. Moreover, these tetraploid cells could be induced to develop into nerve cells, hair follicles, muscle cells, and cells of the stomach lining. This demonstrated the ability of the fused cells to give rise to a variety of different cell types.
Several technological hurdles still remain, with the biggest challenge figuring out a way to eliminate the embryonic stem cell nucleus from the newly created cell so that the fused cell would have a normal number of chromosomes instead of double that amount.
While any therapeutic applications from the new method lie far off, the researchers say that in the short term, it is more likely that the new technique will help to understand how embryonic cells reprogram adult, or "somatic" cells to an embryonic state. But Dr. Eggan told Science he expects that in 10 to 15 years, researchers will be able to use the technique routinely and will no longer need embryos or human eggs to reset adult cells.
"This is another example of how much scientists are learning about human embryonic stem cells in these early years of the research," said Dr. Goldstein.
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