Diabetes Research

My favorite neighbor Mrs. Lindbergh has type two diabetes. For several years, she has suffered from this disease. She told me that her love for sweet desserts like delicious Mango Pudding and chocolate chip cookies caused her diabetes. After years of treating and battling her type two diabetes, there are only a few improvements on the health condition of Mrs. Lindbergh. In fact, her left kidney failed because of diabetes. We are all so sad to hear that her health slowly falling apart. I also felt sad because whenever there's a neighborhood party, Mrs. Lindbergh can't eat a lot of delicious food that she likes since it's forbidden.

Last night when I was browsing the internet, I came across an article about low fat vegan's diet for diabetic people. In the article, it says there that the researchers discovered that the standard diet is less effective for diabetic people. They highly recommend that they follow low fat vegan's diet. It's healthy and good for people. Whoever follows this will lose fats and cholesterol. It can also help control your blood sugar.

After I read this article, I immediately went to my neighbor and let her read this article. I told her to consult her doctor and ask him whether she can take the low fat vegan's diet. Her doctor told her that it's okay for her to follow this type of diet. I was so happy to find out that there's still hope for my favorite neighbor.

We all know that diabetes can be a deadly disease because apart from the disease itself, what is more worrisome are the many possible complications that it ultimately brings. There are many diabetic patients who, in the later phase of life, have gone on to lose their eyesight, or a foot or a limb because of complications due to diabetes.

However, aside from the eyes and the upper and lower extremities which are the usual targets of diabetes-related complications, the ears are also prone to being affected, though not really as a result of complications but rather an accompanying disability of the disease that only presents itself later in the life of a diabetic. In many such cases, the deafness will often be exhibited before the person becomes 40 years old. As with diabetes, the deafness is also inherited, often from the maternal side of the family. The degree of the deafness is usually varied, but will most likely result in the use of hearing aids.

Nevertheless, there is still too few cases of deafness being actually due to complications brought about by diabetes. The data available present deafness and diabetes as a single disorder with one following the other later in life due mainly to genetic make up. Yet, with diabetes' propensity to give rise to complications, it may not be a surprise if a large body of information relating deafness to diabetes soon becomes available.

Diabetes is a disorder that has largely been considered as hereditary. In other words, the disease is usually passed on from one generation to another. However, few people are aware that diabetes can also be acquired through non-hereditary means. Ingestion of certain harmful substances, particularly those contained in products which are designed to kill household pests like rats, can also cause diabetes. There was the case of a 7-year-old boy who accidentally ingested Vacor,a known rodenticide, and died within 14 hours. An autopsy made on his body revealed a non-reduction of his glucagon levels, a condition known as insulinopenia.

Other than accidents, diabetes or its more specific form, diabetes insipidus, can also be acquired through other ways. This can come about when vasopressin, a human hormone is not secreted in its proper amounts. The hormone is released when the body is low on water, enabling the kidneys to conserve the liquid by reducing urine volume. A decrease in vasopressin secretion can lead to diabetes insipidus, a condition characterized by hypernatremia or an increase in blood sodium count.

Nevertheless, whether diabetes can be artificially acquired or genetically determined, the fact remains that it is a serious disease. Hence, it needs to be given serious attention and treatment.

Researchers in Canada have identified an unsuspected role of a protein named SHP-1 in controlling blood glucose that could constitute a new therapeutic path against Type 2 Diabetes. It is known that SHP-1 plays a role in regulating the immune system, but the researchers verified if this protein was involved in the regulation of metabolism. The study involved a series of genetically modified mice producing little or no SHP-1 indicated extreme sensitivity to insulin and, consequently, they are very effective in metabolizing glucose at the level of the liver and the muscles. SHP-1 inhibits the decomposition of insulin by the liver which could explain the increase in the insulin concentrations of certain metabolic disorders associated with obesity.

It would perhaps be possible to restore better control of blood glucose by inhibiting the activity of SHP-1. But the difficulty is to reach that point without blocking the essential part played by this protein in the immune system. Although SHP-1 protein is present in humans, its role in the regulation of the metabolism of glucose and in the development of Type 2 Diabetes remains to be shown. But considering the findings in the study, this could lead to further research regarding diabetes.

Treatment for nerve damage caused by diabetes has been subjected to preclinical and early patient trials and has shown promising results. Experts at the University of Manchester have discovered that the injection of a novel therapeutic that works by stimulating a person's genes may prevent nerve damage - primarily to the hands and feet - caused by the disease. This sheds a significant hope for the development of a new treatment for diabetic nerve damage or 'neuropathy' that will be able to manage the condition and prevent thousands of unnecessary foot amputations each year.

The said test had shown that a single injection of a DNA-binding protein protected nerve function stimulated nerve growth and prevented tissue damage that in humans can lead to limb loss. Neuropathy causes numbness and sometimes pain and weakness in the hands, arms, feet and legs and occurs to an estimated 50 per cent of patients with long-term diabetes. The new gene therapy is quite very different compared to previous attempts at treatment for this one made use of a DNA-binding protein called ZFP TFTM to poke life into the patient's own genes and produce a growth factor that has a role in nerve protection and regeneration.

A new research show that children with type 1 diabetes, who have to take multiple injections of insulin, can safely mix rapid-acting and long-acting insulin analogs in the same syringe without compromising long-term control of their blood sugar levels. Type 1 diabetes is typically diagnosed in childhood and it is due to loss of insulin-producing cells in the pancreas.

After six months of comparing blood sugar control in 55 children who mixed insulin glargine and a rapid-acting insulin analog with that seen in 55 children who took separate injections, it was found that sugar control was nearly the same in each group and low and high blood sugar complications were uncommon and occurred with similar frequency in each group. The ability to give rapid-acting insulin analogues (such as Apidra, NovoRapid) and long-acting insulin glargine (Lantus) in the same syringe has the potential to decrease the number of daily injections and increase use of insulin glargine. The experts are saying that the findings will be very encouraging for patients who wish to minimize the number of total daily injections because of needle fear, forgetting injections, or other injection-related issues. Even if I am not diabetic, I can say I have a slight fear of syringes.

A recent study showed that about 2.8 percent of U.S. adult--one-third of those with diabetes--still don't know they have it, and type 2 diabetes accounts for up to 95 percent of all diabetes cases and virtually all undiagnosed diabetes cases. Experts analyzed national survey data from two periods--1988 to 1994 and 1999 to 2002 and over those periods, about 26 percent of adults age 20 and older continued to have impaired fasting glucose (IFG). Here, the blood glucose measured after an overnight fast is high but not yet diagnostic of diabetes, increases heart disease risk as well as the risk of developing type 2 diabetes.

The researchers also found that nearly 22 percent of people age 65 and older had diabetes, IFG and undiagnosed diabetes were about 70 percent more common in men than in women, and nearly 40 percent of people age 65 and older had IFG, which becomes more common with age. Doctors stressed the importance of knowing if you have pre-diabetes or undiagnosed type 2 diabetes by talking to your health care professional about your risk. If your blood glucose is high but not high enough to be diagnosed as diabetes, losing weight and increasing physical activity will greatly lower your risk of getting type 2 diabetes, and if you have diabetes, controlling your blood glucose, blood pressure, and cholesterol will prevent or delay the complications of diabetes.

A recent study confirms that mutations in an enzyme called glutamate dehydrogenase can cause congenital hyperinsulinism, which is a group of genetic disorders that cause hypoglycemia in infants and children. Hypoglycemia is considered dangerous for it can cause seizures and permanent brain damage if not promptly diagnosed and treated. Congenital hyperinsulinism, in its various forms, is the most common and most difficult cause of hypoglycemia in young infants.

Majority of congenital hyperinsulinism cases appear to be due to defects in insulin secretion by pancreatic cells. At the moment it is thought that mutations in any of four different genes can cause the disorder. Serving as a code for an enzyme called glutamate dehydrogenase is one of the four genes. It is stimulated by the amino acid leucine, meaning that protein meals that contain leucine lead to activation of glutamate dehydrogenase, which in turn triggers the release of insulin from pancreatic cells.

The findings can provide potential targets for development of new drugs, such as inhibitors of the enzyme, which might be used to treat patients. The result also provide support for using genetic mutation analysis of glutamate dehydrogenase to help diagnose children with hyperinsulinism. The study can provide better understanding of the possibility that glutamate dehydrogenase or enzymes in the pathways of amino acid stimulated insulin secretion could serve as targets for drugs to treat diabetes.

Chris Jarvis is a member of the Canadian rowing team has had diabetes since he was 14. He tested his blood sugar level 20 times a day when he competed for the 2004 Athens Olympics. But now, Jarvis wears a new device that tests his blood sugar levels continuously and provides a stream of information that allows him to know when and how much insulin he needs. The device shows whether his glucose level is rising or falling, and gives a picture of how fluctuations occur around the clock. This helps him anticipate changes in blood sugar levels and helps him decide how to adjust his insulin doses to correct for them.

Two devices of the Continuous Glucose Monitoring Systems have been approved by the Food and Drug Administration and a third is expected by year's end. The technologies are said to be a key step toward development of what doctors call "the holy grail of diabetes," which is an artificial system that mimics the human pancreas. Clinical tests have shown the new monitors increase by 26% the amount of time each day patients' blood sugar levels are in the normal range and reduce long-term high sugar levels. Diabetes research aims to develop a three-part device. This includes an insulin pump, an accurate and reliable continuous glucose monitor, and a computerized formula that will take the monitoring data and tell the pump how much insulin to give.

Experts know very well that diabetes claims a limb every 30 seconds, that's why they are focusing their study more about the mechanisms that cause foot ulcers in the first place. This may help them design such interventions as casting and footwear more precisely to prevent foot ulcers or help them heal faster. Based on studies, it was found that increased plantar loading in diabetic patients seems to increase the risk of plantar ulcers. It was observed that the more plantar loads are reduced in diabetic patients, the better their chances for avoiding amputation.

Experiments showed that footwear affords a more even distribution of load on the plantar foot and may also facilitate forward transfer of body weight. Also, using a bivalved total contact cast attained the greatest degree of plantar pressure reduction in the forefoot and in the heel. But evident drawbacks showed that plantar loads increased in the midfoot region which may be a problem for patients with Charcot foot. Their midfoot collapses which will lead to increased pressure and ulceration. Preventive foot care socks were also found to have been successful in reducing plantar foot pressures in patients with diabetic neuropathy. Although there's no conclusion yet on how much pressure reduction is needed to prevent diabetic ulcers, the general consensus is that rest and such devices as the total contact cast is the best treatments for plantar foot ulcers.

Researchers say they have smuggled genes that produces insulin into the pancreas of mice by hiding them in a tiny "bubble." Then by bursting the bubble with sound waves, the researchers were able to free the insulin genes to infiltrate the pancreas, which normally produces insulin. Once they are there, the genes went to work protecting the organ against the ravages of diabetes. This new technique was considered to be less invasive than other strategies that require direct injections into the pancreas and could be an advancement in the use of gene therapy against diabetes.

In the study, human genes that produces insulin were hid in gas-filled "micro-bubbles" that they injected intravenously into the body. When the bubbles have reached the pancreas, they are blown open by sound waves produced by an ultrasound machine. The said technique succeeded in boosting the ability of the mice to tolerate higher glucose levels and showed no evidence that the pancreas was damaged. But the researchers said they are still in the early stages of their study, and it is still a long way to go before they can prove that gene therapy is safe and evident on large animals. Only then that the test can be conducted with human subjects.

Diabetes is the result of the reduction in the number of islet beta cells in the pancreas, which leads to insufficient insulin secretion and high blood glucose levels (hyperglycemia). Currently, insulin secretion is used as a surrogate measure of beta cell mass but however, serum insulin concentrations provide an imprecise measure of beta cell mass and no reliable non-invasive measure of beta cell mass has been available. But a recent study report that positron emission tomography (PET)-based quantization of pancreatic radio-labeled VMAT2 receptors in diabetic rats is a reliable and non-invasive way to measure beta cell mass.

Paul Harris and colleagues from Columbia University in New York exploited the finding that type 2 vesicular monoamine transporters (VMAT2) are expressed in human islet beta cells within the pancreas. It is also expressed in tissues of the central nervous system. Currently used in clinical imaging of the brain, the radioligand [11C]Dihydrotetrabenazine (DTBZ) binds specifically to VMAT2. Then the researchers were able to use DTBZ to estimate beta cell mass in rats with type 1 diabetes. In longitudinal PET studies, Harris and his colleagues saw a significant decline in pancreatic uptake of DTBZ that preceded the loss of glycemic control in the diabetic rat. The result suggest that PET-based quantization of VMAT2 receptors could provide a non-invasive measurement of beta cell mass. This could be used to study the pathogenesis of diabetes and to monitor therapeutic interventions.

Based on an earlier Nobel-Prize winning research, scientists have seen for the first time a key step in the complex molecular processes whereby pancreas cells release insulin into the bloodstream. This could have implications for the treatment of diabetes which is caused when not enough insulin is released by the pancreas to meet the body's demands, and could also be important in understanding other diseases, as hormone and protein secretion is an important function of all types of cell.

The team of scientists explained that large numbers of proteins, including hormones such as insulin, are constantly being produced by our cells and carry out essential body functions. In order to work, these proteins have to be transported to the right place and it is this process - of fundamental importance to all living organisms - that the scientists are interested in.

That hypothesis was devised and proven by Doctor Gunter Blobel, who received the Nobel Prize in Physiology or Medicine in 1999. His finding provided a framework of how the system worked. The scientists visualized the structure using a technique called cryo-electron microscopy and has confirmed that many of the earlier proposals of the model were in fact correct. The aim is to understand how these specialized secretary cells release insulin and why this process goes wrong in type-2 diabetes.

It was found in a study that insulin uses two distinct mechanisms to control glucose and the metabolism of blood fats (lipids) in the liver. Failures in each of these networks can lead to the breakdown of glucose metabolism that can lead to type 2 diabetes, and the malfunction of lipid metabolism contributing to metabolic syndrome. Metabolic syndrome puts people at increased risk of heart disease, vascular disease and type 2 diabetes.

People with metabolic syndrome condition have high levels of both glucose and lipids in the blood. However, Doctor Ronald Kahn said that the insulin that controls the pathways that control glucose levels are different from those that regulate lipid levels. Targeting these specific pathways might aid researchers to improve problems with glucose metabolism, lipid metabolism or both. The liver keeps glucose levels in the blood constant between meals while insulin tells the liver to stop producing glucose. The food you have just eaten will, for a while, supply an adequate amount and also tells the liver how to handle lipids.

Insulin drives the liver's metabolic functions by activating phosphoinositide 3-kinase (PI3K), which then recruits other enzymes to carry out its orders. There were increased glucose production in the liver, impaired glucose tolerance, and increased levels of insulin in the blood of mice that could not activate the protein kinase AKT. These are all contributors to type 2 diabetes while those mice with defects in the atypical forms of the enzyme protein kinase C (PKC) had decreased lipids in the blood. Researchers can begin to look for ways to specifically target just the lipids or just the glucose.

Obese individuals often have excessive fatty tissue in and around their abdomen, high cholesterol, elevated blood pressure, and an inability to utilize insulin or blood sugar (insulin resistance). These symptoms that put them at high risk for coronary heart disease and stroke. The molecular mechanisms linking obesity and insulin resistance are the subject of intense investigation and are not completely understood.

In a study conducted in Kobe University, Japan, the concentration of monocyte chemoattractant protein-1 (MCP-1) in fat cells and blood plasma was increased both in genetically obese diabetic mice as well as healthy mice in which obesity had been induced by feeding them a high-fat food diet. Mice expressing an MCP-1 transgene in fat cells manifested insulin resistance, increased infiltration of macrophages into fatty tissue, and high cholesterol levels.

The said effects were not observed in mice lacking MCP-1 even when fed with the high-fat diet. The results suggest that MCP-1 links obesity and insulin resistance by the induction of an inflammatory response (macrophage infiltration) in fatty tissue. The authors also suggest that blocking the interaction of MCP-1 and its receptor, known as CCR2, might provide the basis for development of new therapies for this syndrome.

Researchers said in a recent report that ghrelin, a hormone long considered a key player in obesity, may instead take a major role in maintaining the balance between insulin and glucose and the development of diabetes. They said companies have been developing ghrelin antagonists as anti-obesity drugs, and now these drugs may have a value in treating diabetes.

The study involved mice bred to be deficient in both ghrelin (which stimulates appetite) and leptin (associated with controlling obesity) could be expected to be thin or of normal body weight. But their glucose levels were lower than in leptin-deficient mice. They found much lower levels in the animals that did not produce either ghrelin or leptin. The mice were more resistant to glucose because they secreted more insulin in response to the glucose challenge.

They found lower levels of uncoupling protein-2 (Ucp2) in cells called pancreatic islets (where insulin is made). Reducing Ucp2 improves the cell's ability to make ATP, the cell's energy molecule, thereby increasing the sensitivity of the pancreatic beta cell (the cell in the pancreas which produces insulin) to glucose-induced insulin release. Animals lacking ghrelin also showed increased sensitivity to insulin, meaning glucose was cleared more efficiently.

But caution was advised by the scientists use of drugs that block ghrelin in treatment of type 2 diabetes (which usually occurs in adulthood and is often associated with obesity). If through this process, ATP production is increased by the beta cell, you may in the long-term get oxidative stress which could eventually destroy the beta cell.

In a multi-center study of young people with diabetes, results reveal that fewer than half of children and young adults who took part in the study were able to meet the current dietary recommendations for particular nutrients. This potentially makes treatment and management of their diabetes much more difficult and complicated.

The research was conducted by the University of South Carolina which looked into the nutrient intakes of nearly 1,700 10- to 22-year-olds who have either type 1 or type 2 diabetes for at least 12 months. The researchers have found that less than half of the participants met the current dietary recommendations for total fat, vitamin E, fiber, fruits, vegetables and grains, although a majority met recommendations for vitamin C, calcium and iron.

The dietary recommendations for youth with diabetes, according to the researchers, are based on strong scientific evidence regarding intake of specific nutrients and foods in relation to physiologic health outcomes. This include appropriate growth and development through adolescent years and optimizing metabolic status. The researchers have expressed urgency for further studies to better understand the barriers to healthful dietary habits and to identify effective approaches to improving dietary intake in youth with diabetes.

New analysis at the University of Washington shows that nearly 2.8 million teenagers in the United States could be on the brink of developing Type 2 diabetes, which used to be almost exclusive to adults. Another 39,000 teens might already have the disease. The findings support the growing concerns of public-health authorities nationwide over the increasing number of kids who are overweight. This is a major factor in the development of Type 2 diabetes which can eventually lead to kidney failure, limb amputations, blindness, heart disease, strokes and high blood pressure.

Health agencies in the US say about 18.2 million people in the country have diabetes, including 210,000 people under 20 years old. Another 1.3 million new cases a year are being diagnosed, and the majority are Type 2, which was formerly almost exclusive to people older than 40. Type 2 diabetics are not able to use the insulin made by their bodies to metabolize glucose in the body, while those with Type 1, formerly called juvenile diabetes, are not able to make insulin.

Experts spoke about their observance in the reduction in physical activity and an increase in the prevalence of overweight kids. Weight loss and exercise have been shown to prevent pre-diabetes from progressing to full diabetes among adults. This is also believed to be true for young people as well. Family physicians and health officials in the country have been campaigning about keeping young people trim.

The condition known as gastroparesis or delayed gastric emptying happens when the stomach takes too long to expel its contents. It happens often to people with type 1or type 2 diabetes. The nerves in the stomach, collectively known as the vagus or pneumogastric nerves, are either damaged or they ceased working that's why gastroparesis results. The vagus is responsible for controlling food movement in the digestive tract.

The relation between gastroparesis and diabetes has long been recognized in the field of medicine. Diabetes speeds up gastroparesis by damaging the vagus nerves because the sugar level in the blood remains high even for a long period of time. And because the nerves carry blood, high glucose can cause rupture to the nerves.

But a groundbreaking study by the Cork University Hospital found that an electrical implant can help treat gastroparesis in diabetics. The gastric stimulators, as they are called helped sooth the stomach problem and reduce its symptoms. The implants were tested on two Irish patients who have been suffering a severe form of gastroparesis that is linked to type one diabetes. After being implanted, the patients achieved a more improved condition and their vagus nerves were restored back to normal.

In Canada, the number of people living with chronic diabetes is roughly two million. It is quite saddening that one out three diabetics does not know that she or he is diabetic. With the help of the Integrated Strategy on Healthy Living and Chronic Disease, funds which will benefit diabetics, greatly improved. I feel for these people especially to those who seem to be unaware that they are diabetics. It is also my utmost hope that such funds will be appropriated accordingly and properly to improve public safety and health.

It sounds so great that the Canadian government through its Canadian Diabetes Strategy, helps prevent, promote, and supervise diabetes and awareness. As such, development of the risks of diabetes can be minimized. Well, I hope it will be implemented religiously. This program created the first system of surveillance based on the data from territorial and provincial health units.

In addition, this program helps bring together communities, stakeholders, territories, and provinces to develop ways and strategies on how to combat the disease. This government program works on system of surveillance for diabetes, management and prevention, public information and programming, and proper coordination. In this manner, this program helps improve both the physical and mental health of the people.

An effective way to maintain one's physical health is to keep an eye on sugar intake. We all know that too much sugar intake might lead to the development of diabetes, one of the most feared diseases in the whole world today. Diabetes is a hormonal disease that may generate certain complications in the body.

To further keep us abreast with the latest development in diabetes, Dr. Walter M. Bortz II wrote "Diabetes Danger". In this book, the author stresses that inactivity and obesity are the main causes of this disease that has been devastating the lives of many Americans and the world in general. The author further explains that among the many dreadful and incurable diseases, diabetes has the most numbers of complications. Such complications may include heart and kidney malfunctions, strokes, impotency, blindness, skin irritations, and even depression or psychological disorder.

In addition, this disease does not only ravage the body. Deadly diabetes necessitates huge amount of money in order be treated well. This valuable book tells us to be in total control of ourselves. A healthy body entails the fusion of balanced diet, proper exercise, and right stress management. You can actually help prevent the occurrence of diabetes if you adhere to the basics of healthy living.

Just like the dreaded cancer disease, diabetes is one of the plagues of America in the new millennium. As such, nonprofit organizations like American Diabetes Association or ADA, in short, were formed to provide the public with information on diabetes and increase their awareness of the disease. Alongside these efforts, ADA also wants to help diabetes patients and their families by looking for a cure for this illness.

In line with the mission of information dissemination and disease prevention, ADA funds various research programs. These would benefit not only the people affected by diabetes in the present, but also the next generations to come. The research programs ADA funds range from clinical studies that involve transplants and biological methods to basic research that aims to address actual behavior and instructional issues of diabetics and people around them.

It is evident that ADA's programs garner wide support from all sectors of society and works well with other studies of research bodies like National Institutes of Health or NIH. In fact, there was a significant increase in the research funding since 1999. Last year, ADA has allotted about forty million dollars, a number that hopefully obtained new ideas and investigators for diabetes research.

Diabetes is a genetically determined disease like the dreaded cancer. The disease, however, can be prevented and controlled through lifestyle modification. Unlike viral infections such as HIV infection or herpes simplex infections, diabetes is not contagious. However, the predisposition in acquiring diabetes can be transferred from parents to offspring. Hence, there is a higher risk for a person to develop diabetes if one of his parents or grandparents or any blood relatives have history of diabetes. Diabetes is actually a hormonal disease that has many complications including optic nerve defects, kidney malfunction, heart disease, gangrene of the extremities and diabetic coma.

Continuous subcutaneous insulin infusion or insulin pump therapy has become a common treatment for young people with type1 diabetes in recent years. Recent studies suggest that insulin pump therapy is more effective than the normal insulin therapy, which involves multiple insulin shots everyday. The effectiveness of insulin pump therapy is only shown in short-term clinical studies. Long-term clinical studies on the effects of insulin pump therapy are scarce or virtually inexistent. Insulin pump works by mimicking normal insulin secretion of the pancreas. The insulin is delivered continuously in the body through a catheter in precise doses under the skin.

Fish may not be such a healthy diet after all, especially if you want to avoid developing diabetes. POPs are persistent organochlorine pollutants, which can come from the fish you eat. POPs are highly toxic and include pesticides such as DDT.

According to Swedish researchers, POPs which are well-retained in fatty fish like salmon. A group of 200 fishermen and their family were analyzed for chemicals in their blood. The research showed that in diabetic individuals, higher levels of these industrial poisons have been found. POPs according to studies may reduce the body's ability to absorb sugar.

The study, however, pointed out that the Baltic coast, where the fishermen fish, was more heavily contaminated by industrial pollutants compared to other fishing areas.

Researchers have discovered a molecule that could be the cause of vision loss in Diabetics, also called Diabetic Retinopathy, in which an overgrowth of blood vessels in the eye affects vision, and even destroys it.

The molecule, called erythropoietin, is thought to stimulate blood vessel growth. Levels of this protein hormone were found to be 12 times higher in the eyes of those with Diabetic Retinopathy than those who did not suffer from it.

But the role of erythropoietin is said to be but part of the overall cause of Diabetic Retinopathy in Diabetics. Although it can cause Diabetic Retinopathy on its own, it is thought that erythropoietin works in conjunction with other factors to cause damage.