Tag Archives: curing diabetes

How I cured my Diabetes

Got your attention? good, If you have been reading my blog then you know I have been going through a tough time with my daughter almost being killed in an auto accident. After almost 9 weeks in the hospital she came home, we had to keep running for doctors appointments and then more appointments. A little at a time she has gotten better and just a week ago she had taken a shower and forgot to put on her eye patch and later realized that her vision had come back !! Another small miracle, small compared to the other ones she already received.Then my wife took sick and after 2 weeks of misery they finally decided that her gallbladder had to come out. No sweat easy scope operation but painful. Well when they inserted the scope and pumped her up with co2 her heart rate fell and went lower and lower so they stopped and reduced the pressure. Her heart rate came back so they restarted the procedure only this time her heart stopped! Continue reading

Regulating the sugar factory in diabetes

Scientists in Sydney and Boston believe they may have identified a gene that controls abnormal production of sugar in the liver, a very troublesome problem for people with diabetes.

The liver is the sugar factory for the body – when blood sugar (glucose) levels fall, the liver makes and releases more. In people with diabetes, especially Type 2 diabetes, the liver doesn’t stop making sugar when it should, so blood sugar levels can rise overnight while they sleep even though they haven’t eaten.

Dr Jenny Gunton, diabetes specialist and endocrinologist from Sydney’s Garvan Institute of Medical Research, in collaboration with Dr Xiao Hui Wang and Professor Ronald Kahn from Harvard Medical School and Joslin Diabetes Centre in Boston, have published their findings in the journal Cell Metabolism, now online.

“A lot of my patients will complain that they go to bed with a blood sugar of 5 and wake up with a blood sugar of 12,” said Dr Gunton.

“It upsets people when their blood sugar behaves as if they’re getting up in the night and having a really big snack. I have to tell them it’s just one of those unfair things about having diabetes.”

People with Type 2 diabetes do not produce enough insulin in the pancreas after a meal. At the same time, they are less able to use that insulin to move glucose into fat and muscle cells, a condition known as ‘insulin resistance’.


With her colleagues in Boston, Gunton has been studying a transcription factor, or kind of ‘master regulator’, called ARNT, which controls expression of other genes involved in processes like glucose breakdown and insulin production. In an earlier study, the group showed that there is 90% less ARNT in insulin-producing cells of people with Type 2 diabetes.

The current study looks at how ARNT might be affecting the liver, and its results confirmed Dr Gunton’s suspicions. “We’ve shown that there’s likely to be decreased ARNT in the liver of people with Type 2 diabetes compared to people without Type 2 diabetes,” she said.

“Working with mice, we found that glucose levels were elevated and there was glucose production from a ‘precursor’, a source not normally metabolised.”

Other results in the study show that to some extent ARNT is regulated by insulin, so that insulin resistance in itself will contribute to a decrease in ARNT. If liver cells are treated with insulin, there will be a small increase in ARNT protein. The insulin will also help move the ARNT into the nucleus of the cell, where it does its job as a master regulator.

The paper concludes that a decline in ARNT isn’t limited to the beta cells of people with Type 2 diabetes. ARNT is also reduced in other important diabetes-related tissues like the liver.

Dr Gunton believes that if a new drug could be developed to increase ARNT activity in the liver, then it may be possible to shut down abnormal sugar production and improve blood sugar control in people with diabetes.

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ABOUT GARVAN

The Garvan Institute of Medical Research was founded in 1963. Initially a research department of St Vincent’s Hospital in Sydney, it is now one of Australia’s largest medical research institutions with nearly 500 scientists, students and support staff. Garvan’s main research programs are: Cancer, Diabetes & Obesity, Immunology and Inflammation, Osteoporosis and Bone Biology, and Neuroscience. The Garvan’s mission is to make significant contributions to medical science that will change the directions of science and medicine and have major impacts on human health. The outcome of Garvan’s discoveries is the development of better methods of diagnosis, treatment, and ultimately, prevention of disease.

All media enquiries should be directed to:
Alison Heather
Science Communications Manager
+61 2 9980 1224
+61 434 071 326
a.heather@garvan.org.au

New evidence of how high glucose damages blood vessels could lead to new treatments

AUGUSTA, Ga. – New evidence of how the elevated glucose levels that occur in diabetes damage blood vessels may lead to novel strategies for blocking the destruction, Medical College of Georgia researchers say.

They found a decreased ability of blood vessels to relax resulted from increased activity of a natural mechanism for altering protein form and function, says Dr. Rita C.Tostes, physiologist in the MCG School of Medicine.

The researchers suspect increased modification of proteins by a glucose-derived molecule is a player in vascular problems associated with hypertension, stroke and obesity as well.

One aftermath of high glucose levels is low levels of the powerful vasodilator nitric oxide in blood vessels, a shortfall that increases the risk of high blood pressure and eventual narrowing of the vessels, researchers reported at the American Society of Hypertension 24th Annual Scientific Program in San Francisco during a joint session with the Council for High Blood Pressure.

IMAGE: This is Dr. Rita C.Tostes, physiologist in the MCG School of Medicine and Victor Lima, a graduate student at the University of Sao Paulo.
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“We know diabetes is a major risk factor for cardiovascular disease and we think this is one of the reasons,” Dr. Tostes says.

Diabetes increases the risk of cardiovascular disease such as heart disease and stroke, even when glucose, or blood sugar, levels are under control. In fact, about 75 percent of people with diabetes die from some form of heart or blood vessel disease, according to the American Heart Association.

Most of the glucose in the body goes directly into cells where it’s modified to produce the energy source ATP. However about 5 percent of all glucose is converted to another sugar moiety, O-GlcNAc, one of the sugar types that can modify proteins.

Inside the blood vessel walls of healthy mice, MCG researchers found increased activity by O-GlcNAc competes with another mechanism for modifying proteins called phosphorylation. In blood vessels, phorphorylation modifies the enzyme that produces nitric oxide, called nitric oxide synthase, so that it makes more of the blood vessel dilator. But add more O-GlcNAc to the mix and it seems to beat phosphorylation to the punch so there is the opposite result. The longer O-GlcNAc levels were high, the worse the resulting problem, says Victor Lima, a graduate student at the University of Sao Paulo working with Dr. Tostes.

An animal model of hypertension seemed to confirm the finding that the more O-GlcNAc, the more blood vessels contract because these animals had higher O-GlcNAc levels. “Now we are trying to see why this is happening and what comes first. Is increased blood pressure leading to changed O-GlcNAc or are augmented levels of O-GlcNAc contributing to the change we see in the vasculature of hypertensives?” Dr. Tostes says. “If we know how this changes vascular function, we can understand some of the dysfunction that we see in diabetes.”

To make sure they were targeting the O-GlcNAc sugar and not dealing with other effects of glucose on blood vessels, the researchers blocked the enzyme OGA, an enzyme that normally removes O-GlcNAc from proteins so they can revert to their normal state.

If the findings continue to hold true, drugs similar to those they use in the lab to inhibit OGA or OGT, the enzyme that adds O-GlcNAc to the protein, could one day help reduce the significant cardiovascular risk associated with diabetes, Mr. Lima says. “I think it looks very promising,” Dr. Tostes adds.

Future studies will include blocking the pathway for adding O-GlcNAc in hypertensive animals to study the impact on blood pressure and vascular function.

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Old diabetes drug teaches experts new tricks

Research from the Johns Hopkins Children’s Center reveals that the drug most commonly used in type 2 diabetics who don’t need insulin works on a much more basic level than once thought, treating persistently elevated blood sugar — the hallmark of type 2 diabetes — by regulating the genes that control its production.

Reporting in the May 15 issue of Cell, investigators say they have zeroed in on a specific segment of a protein called CBP made by the genetic switches involved in overproduction of glucose by the liver that could present new targets for drug therapy of the disease.

In healthy people, the liver produces glucose during fasting to maintain normal levels of cell energy production. After people eat, the pancreas releases insulin, the hormone responsible for glucose absorption. Once insulin is released, the liver should turn down or turn off its glucose production, but in people with type 2 diabetes, the liver fails to sense insulin and continues to make glucose. The condition, known as insulin resistance, is caused by a glitch in the communication between liver and pancreas.

Metformin, introduced as frontline therapy for uncomplicated type 2 diabetes in the 1950s, up until now was believed to work by making the liver more sensitive to insulin. The Hopkins study shows, however, that metformin bypasses the stumbling block in communication and works directly in the liver cells.

“Rather than an interpreter of insulin-liver communication, metformin takes over as the messenger itself,” says senior investigator Fred Wondisford, M.D., who heads the metabolism division at Hopkins Children’s. “Metformin actually mimics the action of CBP, the critical signaling protein involved in the communication between the liver and the pancreas that’s necessary for maintaining glucose production by the liver and its suppression by insulin.”

To test their hypothesis, researchers induced insulin resistance in mice by feeding them a high-fat diet over several months. Mice on high-fat diets developed insulin resistance, and their high blood glucose levels did not drop to normal after eating. Once treated with metformin, however, CBP was activated to the levels of nondiabetic mice, and their blood glucose levels returned to normal. However, when given to diabetic mice with defective copies of CBP, metformin had no effect on blood glucose levels, a proof that metformin works through CBP.

Researchers further were able to determine that metformin worked on one particular section of CBP by studying the drug’s effects in mice with normal CBP and in mice missing this section of their CBP. The mice with normal CBP responded to metformin with a drop in their fasting blood glucose — much like diabetes patients do — while the mice missing that section in their CBP had no decrease in their blood sugar.

Because CBP is involved in growth and development and a variety of metabolic processes in other organs, this newly discovered pathway may hold therapeutic promise for conditions like growth retardation, cancer and infertility, investigators say.

Another important finding in the study: Investigators have discovered a biomarker that can predict how well a person will respond to treatment with metformin and help doctors determine the optimal therapeutic dose, which can vary widely from person to person. The Hopkins team has found that in mice, metformin changes CBP in white bloods cells — just as it does in liver cells — creating a molecular marker that is easily measured via a standard blood test.

“This is the quintessence of individualized medicine: We have found an easily obtainable biomarker with great predictive power that can tell us whether and how well an individual will respond to treatment and help us determine the best dose right away instead of trying to do it by trial and error,” Wondisford says.

Researchers caution that, while promising, their findings must be first replicated in humans.

Diabetes (type 1 and type 2) is a leading cause of kidney failure, eye disease and amputations, and one of the main causes of heart disease and stroke. Nearly 24 million Americans have type 2 diabetes, according to the U.S. Centers for Disease Control.

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Lead author of the paper is Ling He.

Other investigators in the study include Amin Sabet, Stephen Djedjos, Ryan Miller, Mehboob Hussain and Sally Radovick, all of Hopkins, and Xiaojian Sun, of the University of Chicago.

The research was funded by the National Institutes of Health and by the Baltimore Diabetes Research and Training Center, a joint endeavor between Johns Hopkins and the University of Maryland for basic science, clinical research and community outreach on diabetes and obesity in both adults and children.

Connections between diabetes and Alzheimer’s disease explored

A special issue of the Journal of Alzheimer’s Disease

Amsterdam, The Netherlands, May 11, 2009 – Modern societies face the increasing burden of age-related diseases, in particular Alzheimer’s disease (AD) and type 2 diabetes (T2D). There is some evidence that the causes underlying both diseases are linked. Continue reading

Researcher develops screening tool to identify patients with prediabetes

Early detection in younger patients can minimize progression to diabetes, morbidity and mortality

IMAGE: Richelle J. Koopman is assistant professor of family and community medicine in the University of Missouri School of Medicine.

COLUMBIA, Mo. – A third of Americans with diabetes do not know that they have it, and many more who have prediabetic conditions are unaware that they are at risk. Continue reading

News from the December 2008 Journal of the American Dietetic Association

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CHICAGO – The December issue of the Journal of the American Dietetic Association features research studies focusing on the everyday eating habits of consumers. Researchers look at why fast foods continue to be a popular meal choice and methods for adding healthier foods to a person’s diet. Continue reading

What Are The Symptoms Of Diabetes? by JohnJames

Ensure that you don’t eat foods that will increase your blood sugar level. That’s a very big mistake lots of diabetic patients make. They still think they are young, gay and without any problems. As soon as you get diagnosed with diabetes, it’s time to eat and drink responsibly and with a great deal of caution, least you worsen the condition. Continue reading