|
|
News Details
|
June, 2004
Source: New England Journal of Medicine 350:664-671 - Impaired mitochondrial activity in the insulin-resistant offspring of patients with type 2 diabetes (Petersen KT, Dufour S, Befory D, Garcia R, Shulman GI).
|
|
The laboratory of Dr Gerald Shulman (Yale University School of Medicine) has reported exciting findings which can at last shed some light as to the basic metabolic problem in type 2 diabetes. They found that the ability of mitochondria (small particles in the cell that specialize in generating energy to drive different cell function) to generate energy through oxidation of glucose in muscle was 30% less in a group of young lean individuals at high risk for type 2 diabetes. The parents of these individuals had type 2 diabetes. This finding tie up insulin resistance which is a forerunner of type 2 diabetes, the tendency of insulin resistant individuals to accumulate fat in their muscles including that in the heart, and the defective function of insulin secreting cells in the pancreas long before blood sugars start rising. Blood sugars rise when those cells have lost 70% of their function.
Apparently exercise and drugs such as Roziglitazone (Avandia) can reverse this metabolic defect. The influence of the metformin on the mitochondrail defect is unknown.
Back top
|
|
Friday January 25
Source: Christopher Doering - YAHOO Health News - http://dailynews.yahoo.com/h/hl/nm/
|
|
WASHINGTON (Reuters) - A synthetic molecule has proven effective in slowing the development of a type of diabetes in mice, leading researchers to believe that similar molecules could be created to block type 1 diabetes and other autoimmune diseases in humans.
Researchers at the National Jewish Medical and Research Center in Denver and the University of Colorado said on Friday a synthetic antioxidant--a molecule used to block the damaging effects of oxidation on body tissue--could slow or prevent the death of cells needed by the body to produce insulin.
A team lead by Drs. James Crapo and Brian Day studied the effects of the antioxidant that mimics a naturally occurring molecule within the body, but lasts longer and can protect the body from a wider range of other antioxidants.
The molecule is now licensed by Incara Pharmaceuticals Corp.
"It does appear to delay and prevent diabetes, but you would have to be on this for quite a long period of time to prevent diabetes," Day told Reuters. "It is possible that people with a history of juvenile diabetes could be put on this or a similar kind of therapy."
The study, which looked at type 1 or juvenile diabetes, was published in the journal Diabetes. Approximately one million Americans, or about 5% to 10% of all diabetics, have type 1 diabetes, according to the American Diabetes Association.
Type 2, or adult-onset diabetes, is by far the most common and occurs when the body loses its sensitivity to insulin. Insulin is used by the body to turn sugars in the blood into fuel for the body.
Type 1 diabetes occurs when the body mistakenly recognizes insulin-producing cells as foreign invaders and the body's T cells attack them.
During the study, the synthetic antioxidant was injected into 10 mice one day before they were given a separate dose of T cells that trigger diabetes. Researchers administered the antioxidant to the mice four more times, with the last injection coming nine days after the study began.
The researchers report that none of the mice given the antioxidant showed any signs of diabetes after 21 days, and five remained diabetes-free when the study ended after four weeks. A 'control' group of five mice that were not given the molecule became diabetic by day 13.
"The drug actually triggers a response in the immune system that is long-lived," said Day, who estimated the drug lasts about 15 hours within the body.
He cautioned, however, that it is too soon to tout the drug as a cure-all without further tests and refining of the drug.
"It appears that the drug is not permanent in all of the responses ... because some of the animals (given the antioxidant) still went diabetic," he said.
Researchers are optimistic that this antioxidant and others like it could be used to treat immune diseases in humans such as multiple sclerosis and rheumatoid arthritis.
Incara Pharmaceuticals is currently studying whether the antioxidant could be used to protect patients receiving new pancreatic cells from other donors. Currently, the body recognizes many of these new cells as foreign and works to destroy them.
Back top
|
|
Thursday January 24
Source: Merritt McKinney - SOURCE: American Journal of Epidemiology 2002;155.
|
|
NEW YORK (Reuters Health) - In a finding that should be reassuring to women who have taken fertility drugs, researchers report that the medications do not increase the overall risk of ovarian cancer.
But the study did find that some groups of infertile women, including those with endometriosis, may have a higher-than-normal risk of ovarian cancer.
"This is a good news-bad news study," according to Dr. Roberta B. Ness at the University of Pittsburgh in Pennsylvania.
"We did not find a relationship between fertility drugs and ovarian cancer," she told Reuters Health in an interview.
But she added that the risk of cancer was elevated in women with endometriosis-related infertility. The risk was also higher than average in women with infertility that did not have a known cause, Ness said.
The possible link between fertility drugs and ovarian cancer has been controversial. Some research has suggested that the risk of ovarian cancer is increased in women who take fertility drugs but do not become pregnant as well as in those who take the drugs for an extended period of time. But other studies have failed to confirm the connection.
To resolve the question, Ness and her colleagues pooled the results of eight ovarian-cancer studies. The studies, which were conducted between 1989 and 1999, included 5,207 women with ovarian cancer and 7,705 women without cancer.
The investigators found that ovarian cancer was more likely to strike women who had a hard time getting pregnant. Among women who had never been pregnant, those who had tried to conceive for more than 5 years were nearly three times more likely to develop ovarian cancer than women who spent less than a year trying to become pregnant.
But there was no statistically significant link between fertility drugs and the overall risk of ovarian cancer, the researchers report in the February issue of the American Journal of Epidemiology. However, the risk of "borderline serious" tumors, but not invasive ones, was higher in women who had taken fertility drugs.
The report should reassure women who have taken fertility drugs, but it may raise concerns among women whose infertility has no known cause or results from endometriosis--a painful and chronic disease that occurs when bits of the endometrium, the lining of the uterus, form outside of the uterus.
The risk of ovarian cancer was increased 73% in women with endometriosis-related infertility and 19% in those with an unknown cause of infertility.
Ness said that she would love to be able to tell these high-risk women to be screened for ovarian cancer, "but unfortunately we don't have a screening test."
Due to the lack of a screening test and the fact that the symptoms of ovarian cancer are vague and nonspecific, the disease usually is not diagnosed until it has already spread beyond the ovaries, Ness said.
But women can take steps to reduce their risk, according to the Pittsburgh researcher. She noted that women who take oral contraceptives may lower the risk of ovarian cancer by 40%. Women who have tubal ligation--getting their "tubes tied"--may also reduce the risk by 40%, Ness said.
Back top
|
|
Friday January 18, 2002
Source: Daniel DeNoon - SOURCE: WebMD Medical News - http://www.webmd.com/
|
|
A drug that cures diabetes in lab animals finally has begun human tests. The radical idea behind the drug -- still unproven -- is that a person's body can rebuild its own broken-down insulin factories.
The drug doesn't even have a catchy name yet. Its inventors -- Lawrence Rosenberg, MD, PhD, of Canada's McGill University and Aaron I. Vinik, MD, of East Virginia Medical School, Norfolk -- call it INGAP peptide. It stands for islets neogenesis-associated protein. Its exact meaning is still unclear.
People with diabetes need insulin when their own insulin-making cells die off. These cells, called beta cells or islet cells, live in the pancreas. The new drug is a chemical messenger that tells normal pancreas cells to turn into islet cells.
"If we could regenerate insulin-producing cells, in theory it would mean that patients would not have to take insulin," Rosenberg tells Web. "We need to know if these cells, too, will die off. We don't have any hard evidence that this will or will not happen."
The discovery of INGAP began accidentally. Working to develop a laboratory model of pancreas disease, Rosenberg and Vinik wrapped an animal pancreas in cellophane. To their surprise, the isolated pancreas began to grow new islet cells. Further research showed that this happened because the pancreas was making INGAP. Later studies showed that only a small portion of INGAP -- INGAP peptide -- was needed to stimulate growth of new islet cells. Eventually, the researchers discovered the INGAP gene and learned how to make large quantities of the INGAP peptide.
What appears to happen is that the pancreas has a large reservoir of cells that act like stem cells. When they get the right signal, they turn into insulin-making islet cells.
"This is an area of active and potentially very fruitful investigation," diabetes expert Leann Olansky, MD, tells WebMD. Olansky, an endocrinologist at the University of Oklahoma, says that several different research teams are working to develop agents that stimulate the growth of new islet cells.
Just making new islet cells might not be enough. The cells still have to act right. They must make insulin when -- and only when -- the powerful hormone is needed.
This seems to happen. Animals with diabetes-like disease had increased insulin production and lower sugar levels in the blood after a single dose of INGAP peptide.
Even if the new islet cells work, they have to survive. The worry is that whatever killed off the original islet cells will kill the new cells, too. But this doesn't seem to happen in the case of islet cells transplanted from an organ donor.
Currently, a major clinical study is exploring the use of islet-cell transplants to treat diabetes. Such transplants could result in a cure -- but there's a big problem. It takes two donors to provide enough islet cells for a single transplant. Only 3,000 donor organs become available each year. There are some 800,000 people with type 1 diabetes.
"The issues surrounding islet transplant are very complex, and the downside is there just aren't enough donors and never will be," Rosenberg says. "The next generation approach will be stem cells, where you could grow your own islets outside the body. The problem is you have to have a source of stem cells. For the foreseeable future, that is not a viable alternative either. The advantage of our approach is that we can generate stem cells so that everything happens in the person's body. We only kick start the process and the body takes care of the rest. That is the beauty of it."
The initial human study will test the safety of INGAP peptide. A planned 62 patients with type 1 or type 2 diabetes will receive increasing doses. The trial is taking place at three medical centers: the University of Texas Health Science Center, San Antonio; the University of North Carolina, Chapel Hill; and the MedStar Research Institute, Washington, D.C.
INGAP peptide is patented by the two universities and licensed to GMP Companies Inc., Ft. Lauderdale, Fla. An earlier licensing agreement with Eli Lilly and Company expired, Rosenberg says.
Back top
|
For Diabetes, Breathe Deeply - Stress-Reduction Techniques Help Lower Blood Sugar Levels in Diabetics
December 28, 2001
Source: Jayne Garrison , MS - WebMD Medical News
|
|
Nearly one in 15 Americans will develop type 2 diabetes. It is the silent epidemic afflicting this country. Many of them will control the disease through diet and exercise; others will need to inject insulin.
Now there's another option to try: Stress reduction. New research shows it may be as effective as some medications in controlling blood sugar levels.
Researchers have long known that stress worsens diabetes. Stress causes the release of hormones "that lead to energy mobilization -- known as the 'fight or flight' response," explains Richard Surwit, the author of a new study from Duke University published in the January issue of Diabetes Care. "Key to this energy mobilization is the transport of glucose [sugar] into the bloodstream, resulting in elevated glucose [blood sugar] levels."
The key question was: If stress raises glucose levels, could stress reduction techniques lower blood sugar levels? A few previous studies hinted that the answer was yes. But they used time-intensive individual therapy, which many people -- and health plans -- cannot afford.
Surwit and his team studied 108 people with type 2 diabetes. All attended five half-hour educational sessions about diabetes. But half of the patients were also taught stress reduction techniques during their sessions, while the other half weren't. One year later, the doctors tested all patients. Of those who learned stress reduction techniques, 32% had lowered their hemoglobin A1c (HbA1c) by 1% or more -- a significant change. HbA1c is a standard blood test used to determine average blood sugar levels in people with diabetes.
Only 12% of the other patients -- who received diabetes education only -- showed similar improvement.
The FDA considers a 1% decrease in glucose levels sufficient when reviewing new drugs for diabetes control.
Now, says Surwit, the answer is clear: "Managing stress can significantly improve a patient's control of diabetes. These techniques are simple, quick to learn, and have been shown to work for multiple conditions, including [preventing heart attack].
Back top
|
|
Nov. 26, 2001
Source: WebMD Medical News, Michael Smith , MD
|
|
In the last few years, science has made some tremendous breakthroughs in the treatment of type 1 diabetes. And now, researchers have shown that an injection of a specific protein can stop this type of insulin-requiring diabetes in its tracks.
Type 1 diabetes, previously known as juvenile-onset diabetes, is caused by destruction of cells in the pancreas that produce and release insulin. Insulin is the hormone that is responsible for keeping blood sugar levels from getting too high.
In people with type 1 diabetes, insulin-producing cells are killed by the immune system for an unknown reason. Insulin levels get progressively lower as the blood sugar rises, and diabetes develops. At that point, people with type 1 diabetes have to start taking insulin injections to survive.
Researchers from Hadassah-Hebrew University Medical School wanted to see if they could reverse or stop this process. They used a substance called DiaPep277, which has been shown to calm the immune systems in mice prone to developing diabetes. This injection was able to save some of the insulin-producing cells in the pancreases of the mice.
In the current study, published last week in The Lancet, the researchers looked at 31 people who had been diagnosed with type 1 diabetes within the last six months. They were all early enough in the disease process that they were still producing some insulin.
Half of the participants were given DiaPep277 shots and the other half placebo injections. Three shots were given -- at the beginning of the study and again one month and six months later.
People who received DiaPep277 were able to maintain their level of insulin production that they had at the beginning of the study. However, those that received the placebo shots continued to see a fall in their insulin production.
In addition, 10 months after the beginning of the study, the diabetics that received the DiaPep277 injections required less insulin therapy than those that received placebo.
Co-author Dana Elias, PhD, says the research shows it's possible to alter the immune system and prevent or stop it from attacking the insulin-producing cells.
DiaPep277 holds the promise of becoming a breakthrough treatment for those already with type 1 diabetes and may perhaps be able to prevent the development of diabetes in people who are at high risk for the disease, she says in a news release.
"If we reach patients early, we may be able to improve the quality of their lives by significantly reducing their dependence on insulin. We may also halt or delay the development of complications and, possibly, extend patients' lives," says Elias.
Back top
|
|
Nov. 20, 2001
Source: Salynn Boyles- WebMD Medical News
|
|
Having an irregular or absent menstrual cycle is one of the dominant characteristics of polycystic ovary syndrome, a hormonal disorder that still is somewhat a mystery today and affects as many as one in 10 women. The condition is known to be associated with reduced fertility, but the evidence is mounting that it also increases a woman's risk of developing diabetes.
Now a newly published study offers the best evidence to date that menstrual cycle irregularity is directly linked to type 2 diabetes risk. Researchers at Boston's Brigham and Women's Hospital and the Harvard School of Medicine followed more than 100,000 women participating in the Nurses Health Study II, the largest ongoing study of risk factors for chronic diseases in women.
Young women with cycles of more than 40 days or cycles that were too irregular to estimate were found to be twice as likely to develop diabetes as those with normal cycles. The increased risk was seen even when the researchers accounted for obesity, which is a common characteristic of polycystic ovary syndrome (PCOS) and a well-established risk factor for diabetes. The findings were reported Nov. 21 in The Journal of the American Medical Association.
"Women and their doctors need to be aware that irregular menstrual cycles could have broader ramifications than those that they normally think of," lead author Caren G. Solomon, MD, tells WebMD. "We know that women with PCOS have higher rates of diabetes ..., independent of their weight. We also know from other data that the majority of women with irregular cycles probably have PCOS."
The findings suggest that maintaining a healthy weight may be even more important for women who have been diagnosed with PCOS or have irregular cycles. Obesity, specifically excess weight around the abdomen, is a characteristic feature of PCOS. Having an 'apple shape' body type is also a specific risk factor for diabetes and heart disease.
A soon-to-be published national study suggests that those at high risk for diabetes can cut that risk in half by losing a modest amount of weight and exercising regularly as little as 30 minutes a day. Researchers found that moderate weight loss and exercise were twice as effective as taking medication at reducing risk.
"We know that no matter what your risk factors are, maintaining a healthy weight and exercising are key to reducing your risk of this disease," diabetes researcher Edward E. Horton, MD, tells WebMD. Horton, is director of clinical research at Boston's Joslin Diabetes Center and a professor at Harvard Medical School.
"No matter what your cycles are, we know that being overweight and being sedentary are risk factors for diabetes," Solomon adds. "But I think the important message here is that obesity clearly exacerbates the risk that is associated with an irregular cycle. Every woman should eat a healthy diet and get regular exercise, but this is group that may stand to benefit from that even more than others."
Back top
|
|
Monday, 14 January, 2002, 02:21 GMT
Source : BBC Health News
|
|
Many diabetics go undiagnosed
A simple blood test given in the doctor's office could identify millions of patients with previously undetected diabetes, research suggests.
The findings also suggest that three easily assessed risk factors can be used to identify the best candidates for the test.
Diabetes may go undiagnosed for years, damaging organs throughout the body, until symptoms appear.
Diabetes UK, one of the UK's leading diabetes charities, says that on average, people have diabetes for between nine and 12 years before it is detected.
As a result many people with the adult-onset form are already in poor condition by the time it is diagnosed.
It is estimated that in the UK two out of three diabetics die unnecessarily from complications which could have been successfully treated.
At any time, an estimated one million people in the UK have diabetes - but do not know it.
Early detection
Therefore, early detection of the condition is vital.
The current blood sugar test requires several hours of prior fasting and cannot always be administered on the spot.
Researchers from Duke University Medical Center, North Carolina, led by Dr David Edelman, tested a new screening technique called HgA1c.
This test accurately indicates blood sugar levels over the previous two to three months and can detect at least 75% of cases of diabetes, but does not require fasting.
The researchers gave the test to 1,253 patients who had never been diagnosed with diabetes.
It was found that 4.5% had diabetes, which had gone undetected even though they were under medical care.
The researchers say the test would detect almost as many cases of undiagnosed diabetes if performed only on patients with one or more of three risk factors:
- obesity
- self-reported high blood pressure
- family history of the disease
Such targeting would make the screening even more cost-effective.
Undiagnosed
A spokesman for Diabetes UK told BBC News Online: "These results are very interesting as the UK has an estimated one million people with undiagnosed diabetes.
"These people need to be found as soon as possible. Without the right treatment people with diabetes are at a serious risk of long-term damage being done to their heart, eyes and kidneys."
Those most at risk include those over 40, who are overweight, have a family history of diabetes or are from an Afro-Caribbean or Asian background.
Diabetes UK is calling for the introduction of an early identification programme targeted at these high-risk groups.
The research is published in the Journal of General Internal Medicine.
Back top
|
|
Friday, 14 December, 2001
Source: BBC Health
|
|
Some diabetes need to take insulin. The government has published a blueprint for improved care for diabetes, a condition which can contribute to early death.
The set of standards, published on Friday, are the first part of a National Service Framework (NSF) on diabetes.
The document sets out pledges to improve care, with many focussing on the treatment of children and young people with diabetics.
The second part of the NSF, to be published next summer, will set out milestones and implementation plans.
Diabetes is a hormone disorder, which comes in two types. Type 1 destroys the cells in the pancreas that produce the hormone insulin, which sufferers then need to replace to control their blood sugars.
Type 2, or non-insulin dependent diabetes is the most common form of the disease, usually occurring in people who are over the age of 45 and overweight.
Sufferers either do not make enough insulin, or are unable to make proper use of it, leading to a build-up of sugar in the cells which causes health problems.
Around 1.3m people in England are affected by the condition which, if not properly treated, can lead to complications such as heart disease, kidney disease, blindness and foot problems that may lead to amputation.
And diabetes is estimated to account for 10% of NHS hospital resources.
This is the fourth NSF to be published by the government, following care blueprints for mental health, coronary heart disease and care of older people.
Improvements
There are 12 standards set out in the Diabetes NSF, including:
- Cutting the risk of developing Type 2 diabetes in the population by preventing and reducing obesity
- Identifying people who do not know they have diabetes, through follow up and regular testing of individuals known to be at increased risk of developing diabetes, and opportunistic screening of people with multiple risk factors
- Children with diabetes will be involved in planning their care. School staff and health professionals will be educated to spot early signs of diabetes
- Young diabetics moving between child and adult services will experience a smooth transition
- Children and young adults will also receive regular surveillance for the long-term complications of diabetes
- Protocols will be agreed for dealing with diabetic emergencies
Launching the document on Friday, health minister Jacqui Smith said: "This new blueprint of care heralds a new beginning for the many thousands of people with diabetes in England.
"There are currently considerable variations around the country in the organisation and quality of diabetes services.
"Our new national NSF standards will make sure that people receive high-quality care at the right time and in the right place."
'Devil in the detail'
Paul Streets, chief executive of Diabetes UK, said: "The publication of these Framework Standards offers a golden opportunity to ensure that people with diabetes finally get the healthcare they deserve.
"However the devil is in the detail of how the standards are implemented.
"Unless we get this detail right, we will not achieve our ambitions of getting decent care for people with diabetes."
Doctors and policy officials will work out how the standards should be implemented, in a group headed by Professor Mike Pringle, of the Royal College of General Practitioners and Dr Sheila Adam, Director of Policy at the Department of Health.
Funding 'crucial'
Dr John Chisholm, chairman of the British Medical Association's GPs' committee, said: "Family doctors want to provide high quality health care for their patients, but at the moment they face an excessive, and for many, unsustainable, workload.
"We hope this two phase approach to implementing the NSF will allow patients to get the care they deserve without increasing the burden on general practitioners."
Dr Michael Dixon, chairman of primary care body the NHS Alliance, welcomed the delay between setting out standards and setting targets.
He added: "With clearly defined and locally agreed protocols, much of the additional work in general practice could be done by nurses. But that will only be possible if the funding is available."
Back top
|
|
Monday, 10 December, 2001
Source: BBC Health
|
|
Type 1 Diabetes affects more than 300,000 Britons Scientists in Manchester say they have found that lines on the hand - dermatoglyphics -could predict a newborn baby's likelihood of developing diabetes as a teenager.
Researchers at Manchester University's Institute of Science and Technology (Umist) studied computer analyses of the hands of 50 young children.
They concentrated on the line on the palm that sweeps down around the thumb to the wrist.
Prints were taken of the children's palms at the age of six years and those children were again examined upon reaching 18.
In those with diabetes, the line joined a second line at a wider angle and at a point 1cm higher in the palm.
Early indications of the possible onset of diabetes give parents and clinicians adequate opportunity to come to terms with the condition.
Bernard Richards, Professor of Medical Informatics at Umist, led the team of researchers.
He said: "The relevance of this work to society is that such studies can be carried out in the poorer countries and in remote communities, such as in desert lands and in the bush.
"This work does not require hospital or medical facilities: just an ink pad and a magnifying glass."
The discovery is among a number of studies that have increasingly shown how dermatoglyphics can predict a range of conditions and diseases.
Scientists have found clues to the development of heart disease, autism, anxiety, schizophrenia and even cot death.
Dermatoglyphics develop at specific times in the foetus at the same time that critical growth in the brain is taking place.
Back top
|
Resistin - Hormone Produced by Fat cells found linked to Diabetes
Source : By Nathan Seppa : http://www.ScienceNews.Org/
The high incidence of obesity among people with type II diabetes suggests a connection between the two conditions. Scientists have sought a link by studying insulin resistance, the trademark symptom of type II, or adult-onset, diabetes. But they still don't know why cells in people with insulin resistance ignore insulin's signals to process blood glucose for use by muscles and other tissues.
Researchers working with mice have now identified a hormone, called resistin, that is secreted by fat cells and appears to play a direct role in type II diabetes. Healthy mice given doses of extra resistin for 2 days develop insulin resistance, researchers at the University of Pennsylvania in Philadelphia report in the Jan. 18 Nature.
Interestingly, obese mice naturally produce copious resistin, says study coauthor Mitchell A. Lazar, a molecular endocrinologist at Pennsylvania. When given drugs that inhibit the effects of resistin, these overweight mice process glucose more efficiently, he says.
The Pennsylvania researchers have identified the human gene that encodes resistin, but they haven't yet gauged the hormone's effects in people.
Roughly four out of five people with type II diabetes are obese. The new findings "indicate that resistin may form at least part of the missing link between obesity and diabetes," says Jeffrey S. Flier of Beth Israel Deaconess Medical Center in Boston in the same issue of Nature.
Lazar's team found resistin in mice while monitoring the effects of a diabetes medication in the family of drugs called TZDs, or thiazolidinediones. Earlier studies in rodents had shown that TZDs slow type II diabetes even though they spur the creation of fat cells, a seemingly contradictory action. The drugs work by activating a receptor molecule, called PPAR-gamma, in fat cells.
When PPAR-gamma becomes active, production rates change for some proteins in the cells. Although most of these rates rise in the presence of TZDs, the researchers focused on the few proteins having rates that dropped. Among these, Lazar and his colleagues identified one that they dubbed resistin.
Further tests showed that TZDs indeed reduce the concentration of resistin in the blood of mice.
"This is a big deal," says Allen M. Spiegel, director of the National Institute of Diabetes and Digestive and Kidney Diseases in Bethesda, Md. Measuring resistin concentrations in blood could help physicians diagnose type II diabetes, both Spiegel and Lazar say.
Resistin shares some qualities with another protein secreted by fat cells and associated with obesity, the hormone leptin. This hormone, discovered in 1995, seems to regulate food intake.
Establishing that fat cells secrete resistin and leptin confirms that these cells are more than just "oily stuff in the body," Spiegel says. Fat in the body "is an endocrine gland, a hormone-producing substance involved in a dialogue with the brain, liver, and muscle in a complex [process] of nutrient metabolism," he says.
Leptin doesn't appear to have a straightforward association with diabetes. In rodents, a leptin deficiency causes severe insulin resistance, but people with type II diabetes actually have high concentrations of leptin in their blood. Some research points instead to a compound called tumor necrosis factor alpha as a trigger for insulin resistance, Flier says.
Resistin "is almost certainly a piece of the puzzle," Lazar says. "Resistin may actually play a big role in explaining why having too many fat cells can induce insulin resistance."
The Pennsylvania researchers have already devised an antibody to resistin, which they used in the mouse tests to inhibit the newfound substance's effects. However, they still haven't found the molecular receptor that allows resistin to bind to cells. Identifying this molecule could give drug makers a target by which to chemically block the effects of resistin, Spiegel says.
Back top
Diabetes and QTL/Modifier Loci Group
Source : Mammalian Genetics Units : http://www.mgu.har.mrc.ac.uk/
The primary research interest of our group is the Genetic aetiology of type 2 diabetes.
Type 2 diabetes is a very common late onset disease with an ever increasing incidence (over 10% aged 65 years or older in the UK population and has a huge healthcare cost as a result of diabetic complications including coronary heart disease, stoke, foot problems, eye disease and kidney disease. The precise cost of diabetes (including type I) is hard to estimate but may be around £4.9 billion a year to the UK NHS alone (see Diabetes UK http://www.diabetes.org.uk/ and Centres for disease Control and Prevention http://www.cdc.gov/health/diabetes.htm).
Our research is aimed at identifying genes underlying the susceptibility to type 2 diabetes. This disease has a strong genetic component and is likely affected by the interaction of many relatively small effect genes. The lifetime risk to first degree relatives of an affected individual is 35% and is 3-4x greater than that of the general population. There is greater concordance among identical homozygotic (50-90%) than between than non-identical dizygotic twins (37%). The incidence of type 2 diabetes varies between ethnic groups in the same population and there is a direct relationship between incidence and degree of genetic admixture. Further segregation analysis suggests complex genetic control.
Back top
MetFormin - Medication to Combat Diabetes
Source : http://www.diabetes.org/
Saturday, 27 January, 2001, 02:02 GMT
Metformin HCl is an oral antihyperglycemic drug used in the management of non-insulin-dependent diabetes mellitus (NIDDM).
Metformin HCl is a white to off-white crystalline compound is freely soluble in water.
Metformin HCl tablets contain 500 mg and 850 mg of metformin HCl. In addition, each tablet contains the following inactive ingredients: povidone, magnesium stearate and hydroxypropyl methylcellulose (hypromellose) coating.
Metformin is Blood Glucose Regulators
BRAND NAMES: Apophage; Benofomin; Dabex; Denkaform; Dextin; Diabetmin; Diabex; Diaformin; Diformin; Diformin Retard; Dimefor; Fornidd; Geamet; Glucaminol; Glucofago; Glucomet; Glucomine; Glucoform; Glucomin; Gluconil; Glucophage; Glucophage 850; Glucophage Forte; Glucophage-Mite; Glucophage Retard; Gludepatic; Glufor; Gluformin; Glumeformin; Glumin; Glupermin; Glyciphage; Glycon; Metforal; Metomin; Miformin; Orabet; Siamformet; Walaphage
(Foreign Brand names outside U.S. in italics)
Metformin is a biguanide that has been used worldwide for the treatment of type 2 diabetes for the past 4 decades. It improves glycemic control by enhancing insulin sensitivity in liver and muscle. Metformin does not stimulate insulin secretion and therefore is not associated with hypoglycemia. Improved metabolic control with metformin does not induce weight gain and may cause weight loss. Metformin also has a beneficial effect on several cardiovascular risk factors including dyslipidemia, elevated plasminogen activator inhibitor 1 levels, other fibrinolytic abnormalities, hyperinsulinemia, and insulin resistance. While metformin reduces insulin resistance, the cellular mechanism of action is incompletely understood. Metformin enhances muscle and adipocyte insulin receptor number and/or affinity, increases insulin receptor tyrosine kinase activity, stimulates glucose transport and glycogen synthesis, and reduces both hepatic gluconeogenesis and glycogenolysis. In addition, metformin has been reported to decrease lipid oxidation and plasma free fatty acid levels, leading to an inhibition of an overactive Randle cycle. Metformin monotherapy decreases the fasting plasma glucose concentration by ~60 70 mg/dl and HbA1c by 1.5 2.0% in patients with type 2 diabetes. The biguanide is completely additive to sulfonylureas and vice versa, as well as to acarbose and probably troglitazone. In insulin-treated type 2 diabetic patients, the addition of metformin improves insulin sensitivity and glycemic control while allowing a reduction in the daily insulin dose. Side effects of metformin are primarily confined to the gastrointestinal tract (abdominal discomfort and diarrhea). These side effects can be minimized by slow titration and administration with food. Lactic acidosis is rare, with an incidence of ~3 cases per 100,000 patient-years of therapy. Most reported cases of lactic acidosis occur in patients with contraindications, particularly impaired renal function (>90% of cases). In summary, metformin is an effective and safe therapeutic agent for the treatment of type 2 diabetes. Its ability to improve insulin sensitivity and the cardiovascular risk profile of type 2 diabetic patients has enhanced its clinical use as first-line therapy. In the U.K. Prospective Diabetes Study, metformin was the only medication that reduced diabetes-related death, heart attacks, and stroke. Metformin recently has been approved for use in poorly controlled, insulin-treated type 2 diabetic subjects. In the future, its indications may expand to insulin-resistant patients at a high risk of developing type 2 diabetes or with other components of the insulin resistance syndrome.
Back top
Source BBC : http://news.bbc.co.uk/hi/english/health/newsid_1139000/1139186.stm
Insulin rules many diabetics' lives
A potential cure for diabetes, which scientists say could conquer the condition in 10 years' time, is to be tested in the UK.
The treatment could end the daily rigours of insulin injections and could potentially help 130m diabetics worldwide.
The charity Diabetes UK, with the University of Leicester, hopes to set up trials at seven centres across the UK by this summer, at an initial cost of £300,000.
The treatment involves transplanting cells into the livers of diabetes sufferers.
It has been developed in Canada by British-born surgeon James Shapiro.
So far, 13 out of 15 Canadian patients who have had the treatment have been effectively "cured", and have not had to inject insulin for two years.
Diabetes stops the body converting blood glucose into energy because the hormone insulin is either not produced or does not work properly.
About 1.4 million people in the UK are diagnosed with diabetes. An estimatedone million more have the condition but are not aware of it.
Half a million people have to give themselves daily insulin injections to maintain their glucose levels.
Around 50,000 have the most serious Type 1 form of the disease, where the islet cells in the pancreas which produce insulin are destroyed by the body's own immune system.
Even with the daily injections, some Type 1 sufferers are unable to control their blood glucose levels and frequently lapse into potentially fatal diabetic comas.
They are also prone to heart attacks, strokes, blindness and kidney failure, and their lives are shortened by an average of 15 years.
Cell treatment
Dr Shapiro, of the University of Alberta in Edmonton, has developed a way of taking islet cells from a donor and injecting them into the diabetes sufferer's liver.
The treatment takes half a day and can be done under local anaesthetic.
After two injections, the cells kick-start the body's insulin production and no more treatment is needed.
Those patients who have already had the revolutionary treatment, have to take a mixture of anti-rejection drugs for the rest of their lives to stop their bodies destroying the transplanted cells.
However, scientists hope developments, particularly in field of stem cell research, mean this will not always be the case.
Scientists hope the trials will enable 10 islet transplants to be performed in a year.
Unsuitable for all
Dr Shapiro said the treatment did involve risks and would not be suitable for all diabetics.
But those with severe diabetes, or who often lapse into comas could benefit.
"We have to balance the risks of the treatment procedure and anti-rejection drugs against the risks these patients face every day. These patients have a 25 times greater risk of kidney failure, heart attacks, strokes and blindness, and have an average of 15 years sliced off their life span."
Islet cells, found in the pancreas, could theoretically be developed from stem cells.
If taken from the patient being treated, they would not be rejected, so that immuno-suppressants would no longer be needed.
"If we can trick them to grow more islets, that's where the ultimate goal will be," said Dr Shapiro.
"There is some preliminary work being carried out already that indicates that it's possible to grow new islet cells, but not to the level where they could be used to treat patients. "It might take five to 10 years or longer to refine these techniques."
Moira Murphy, director of research at Diabetes UK, said: "It is early days yet, but this may well lead to a cure for diabetes.
"We are extremely excited by this opportunity and feel we have to grab it with both hands.
"That is why we have brought together this new research consortium. If this research proves successful, it could revolutionise the lives of people who currently need to take daily insulin injections to just to stay alive."
Back top
The REALITY Project
On 30th June 2000, CUH, held a project launch meeting. The "Creating Model Diabetes Systems in the NHS Eastern Region" meeting was hosted by Professor Don Detmer, Director of Cambridge University Health and Dr Tia Gilmartin, Research Associate with the group. Health care providers and managers from NHS organisations in East Anglia attended the meeting to discuss the challenges associated with diabetes care. The 30th June meeting was the kick off event for a three-phased research project seeking to create new models of diabetes services based on the principles of chronic disease management and continuous quality improvement. The first phase of the study will examine current diabetes services, resources and best practice in the region. Subsequent phases of the project will focus on the development, implementationand outcomes of new models for diabetes services to meet specific community health needs.
Source : University of Cambridge : http://www.jims.cam.ac.uk/
|
Screening Programme held in Birmingham
The World Federation of Khoja Shia Ithna-Asheri Muslim Communities through its Medical Advisory Board organised its most ambitious medical screening programme ever in Birmingham - UK on 27th and 28th November 1999. The Programme was held in the new Syeda Zainab building - 337 people attended. Over 50 Doctors, Dentists, Opticians, Psychiatrists, Psychologists, Health Education Promoters, Physiotherapists, Chiropodists, Dieticians, Nurses, Careers Advisors in Health, Midwives, and many Volunteers took part. 3 Consultant Psychiatrists and Psychologists provided stress screening. A skin specialist from Switzerland (Consultant Dermatologist) conducted a specialist skin clinic and a child specialist (Consultant Paediatrician) held specialist children's clinic.
A part of the screening programme was the first time ever, two-way interactive health seminars held on Menopause, Arthritis and Diabetes Seminars, conducted in Gujarati.
For more information please see : World Federation at http://www.world-federation.org/MAB/Articles/ |
Back top
|
