Showing posts with label Diabetes. Show all posts
Showing posts with label Diabetes. Show all posts

Thursday, February 7, 2008

Antioxidants May Reduce Harmful Complications Of Diabetes

SAN FRANCISCO, CA -- April 20, 1998 -- Duke University Medical Center researchers have found that the depletion of body chemicals called antioxidants may increase the risk of complications from the most common form of diabetes.

The scientists recommend that diabetics take antioxidants supplements, such as vitamin C or E, to help stave off or even forestall the hallmark complications of diabetes, including blindness, kidney failure, amputation and even death.

antioxidants neutralise oxygen free radicals, highly-reactive chemicals that are the potentially-destructive by-products of the body's process of turning food into energy. Normally, the body produces enough antioxidants of its own to keep the reactive oxygen from causing damage.

"We were able to show that patients with poor control of their diabetes who were beginning to show signs of complications had depleted their store of antioxidants ," said Duke researcher Dr. Emmanuel Opara. "Further, we found a significant correlation between high blood-sugar levels and depletion of antioxidants . It appears that this depletion is a major risk factor for developing complications and that antioxidants supplements could lower this risk."

Opara presented his studies yesterday at Experimental Biology `98, the annual scientific meeting of the Federation of American Societies for Experimental Biology (FASEB).
The researchers studied 50 similar people with Type II diabetes -- also known as non-insulin-dependent or adult-onset diabetes. In this form of the disease, insulin produced in the body is unable to trigger the lowering of high blood sugar. Type II diabetes afflicts about 90 percent of the estimated 10.7 million Americans diagnosed with the disease and the 5.4 million believed to have undiagnosed cases, according to the Centers for Disease Control and Prevention.

Insulin is the hormone that normally regulates the level of sugar (glucose) in the blood and is produced by cells in the pancreas. Insulin is secreted when the level of blood glucose rises -- as after a meal.

All diabetic patients in the study were taking only drugs referred to as sulfonylureas, which increase the sensitivity of receptors to insulin throughout the body. Half the patients exhibited microalbuminuria, the excretion of tiny amounts of protein in the urine that is considered a precursor of kidney disease, while the other half did not. T

he researchers took blood samples from all 50 patients, as well as a control group of 20 similar people without diabetes and determined levels of antioxidantsin their blood.
"We found that the non-diabetics' ability to defend against damage from the oxygen free radicals was almost twice that of those patients exhibiting microalbuminuria," Opara explained. "And while the difference between the two diabetic groups was not as pronounced, the difference was still statistically significant. Also, antioxidants depletion correlated with high blood sugar after meals only in the group with microalbuminuria."

The researchers determined antioxidants levels by a new chemical assay developed at King's College in England that enabled them to measure all known antioxidants in the blood and to obtain a more global picture of the body's total antioxidants capacity, Opara said. Other assays are only specific for individual antioxidants.

Using the newly-developed assay, the scientists rated the ability of the non-diabetics to defend against Free radicals damage at 2.7, compared with 1.4 for those with microalbuminuria and 1.7 for the diabetics without microalbuminuria.

Though the exact mechanism of action of the oxygen Free radicals is not yet clear, these findings confirm in humans earlier animal studies of the chemicals' role in damage in diabetes, Opara said. Previous Duke studies by Opara have shown that vitamin E can delay the development of diabetes in obese rats with Type II diabetes and that the depletion of the antioxidants Glutathione caused diabetes in another rat model.

Click here for more about Glutathione and its benefits to our body.

"The results we've been seeing in our animal studies are now being borne out in humans,” Opara said. "I recommend that since the body has many antioxidants , diabetics should take a number of these agents, including vitamins C and E and Glutathione."

The diabetic patients involved in the current study come from Egypt, and their samples were brought to Duke by E. Abdel-Rahman, one of Opara's collaborators.

Glutathione helps to support the proper functioning

Glutathione helps to support the proper functioning of your immune system , and will improve immune system already in retreat.

Glutathione acts as an powerful antioxidant and Free radicals scavenger, thereby protecting our DNA and RDA from damage due to many environmental factors.

Glutathione acts as the regulator of other powerful antioxidant.

Glutathione acts as a detoxifying agent, removing foreign objects, chemicals and toxins from the body. As you age, your levels of Glutathione are depleted, thereby allowing the aging process to accelerate.

Levels of Glutathione can be sucessfully improved by taking a high quality nutritional supplement!

***Among the uses that have been reported for glutathione are:
treatment of poisoning, particularly heavy metal poisons
treatment of idiopathic pulmonary firbosis
increasing the effectiveness and reducing the toxicity of cis-platinum, a chemo drug used to treat breast cancer
treating Parkinson's disease
lowering blood pressure in patients with diabetes
increasing male sperm counts in humans and animals
treatment of liver cancer
treatment of sickle cell anemia
http://www.healthline.com/galecontent/glutathione

Click here for more about Glutathione and its benefits to our body.

Wednesday, February 6, 2008

Dietary supplement helps to keep immune system balanced

Stanford researchers have found that giving patients who are infected with the human immunodeficiency virus (HIV) a daily dose of a dietary supplement can boost their levels of Glutathione­ a nutrient essential for proper functioning of the immune system. Restoring glutathione levels to those found in healthy people may help HIV-infected patients fight the AIDS-causing virus and fend off other diseases.

"The importance here is that Glutathione is a central component of all cells, and Glutathione deficiency is associated with poor prognosis in many, many diseases," said Leonore (Lee) Herzenberg, PhD, professor of genetics. She is senior author of a paper describing the new study, published in the October 1 issue of the European Journal of Clinical Investigation.

Lee Herzenberg and her colleagues conducted a clinical trial in which 31 HIV-infected patients were given daily doses of N-acetylcysteine (NAC) ­ a substance that is turned into Glutathione in the body. Thirty others were given a benign sugar pill. At the start of the trial all patients had Glutathione deficiency ­ some patients had only half the amount found in healthy people. At the end of the two-month trial, those taking NAC had increased the amount of Glutathione in their bodies to near-normal levels.

"What we've proven is that giving people NAC replenishes the Glutathione stores," said Lee Herzenberg.

At the completion of the eight-week trial, most patients chose to take NAC for the following six months while the researchers continued monitoring the safety of the supplement. They found that patients suffered no ill effects that could be attributed to daily NAC ingestion.

Glutathione is not an anti-retroviral drug, stressed genetics professor Leonard (Len) Herzenberg, PhD. It does not decrease the amount of virus in patients' blood or increase their number of virus-fighting T cells, but it does restore the immune system, the researchers said.
Previous findings by the Herzenbergs and others show that T cells perform better in HIV-infected patients when their Glutathione levels are replenished. Reversal of Glutathione deficiency is also associated with improvement in many other diseases including diabetes, influenza and cystic fibrosis.

"The level of Glutathione is tightly regulated in cells. If nature has gone to the trouble of maintaining those levels, logic says it should be restored to that level if you can," said Lee Herzenberg. "It's like a vitamin deficiency. Any vitamin deficiency would immediately be corrected, and we believe that this is equivalent to a vitamin deficiency."

The Herzenberg team hopes that the benefits of maintaining normal Glutathione levels will encourage people suffering from long-term diseases to avoid lifestyle factors that deplete Glutathione, such as exposure to ultraviolet light and alcohol consumption. They also recommend limited use of acetaminophen ­ the active ingredient in common painkillers such as Tylenol ­ because the risk of liver damage is increased for those with low Glutathione levels.
The Herzenbergs are confident that the new findings will speed the introduction into the U.S. market of medicinal-quality NAC that AIDS patients and others can take to maintain normal Glutathione levels. BY KRISTIN WEIDENBACH

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Wednesday, January 23, 2008

Alpha Lipoic Acid

Food sources and dietary supplements that help boost glutathione levels naturally.

Alpha Lipoic Acid

Made naturally in body cells as a by-product of energy release, ALA increases the levels of intra-cellular glutathione, and is a natural antioxidant with free radical scavenging abilities.

It has the ability to regenerate oxidized antioxidants like Vitamin C and E and helps to make them more potent.

ALA is also known for its ability to enhance glucose uptake and may help prevent the cellular damage accompanying the complications of diabetes. It also has a protective effect in the brain.

Click here for more about Glutathione and its benefits to our body.

Monday, January 21, 2008

Glutathione Fact 2 - slow down the aging process

Glutathione has been shown to slow down the aging process, detoxify and improve liver function, strengthen the immune system, and reduce the chances of developing cancer.

Glutathione also works to help improve mental functions, increase energy, improve concentration, permit increased exercise, and improve heart and lung function - just to name a few.

Among the uses that have been reported for glutathione are:
treatment of poisoning, particularly heavy metal poisons
treatment of idiopathic pulmonary firbosis
increasing the effectiveness and reducing the toxicity of cis-platinum, a chemo drug used to treat breast cancer
treating Parkinson's disease
lowering blood pressure in patients with diabetes
increasing male sperm counts in humans and animals
treatment of liver cancer
treatment of sickle cell anemia

Friday, January 18, 2008

GSH has five major functions

Antioxidant:
Antioxidant is a substance that neutralizes destructive free radicals; some are manufactured by the metabolic processes of the body, others are derived from foods, the air we breath, exercise, stress and disease.GSH is the most powerful Antioxidant occurring naturally in the cells of the body. Through its significant reducing power, GSH also makes major contributions to the recycling of other Antioxidant that have become oxidized. Healthy cells homeostatically oppose free radicals through the use of Antioxidant, of which GSH plays a significant role. The effectiveness of other Antioxidant like vitamins C and E depends on the availability of GSH.

Help Prevent Disease:
Oxidative related diseases: accelerated aging, cell destruction, causes damage to DNA cellular patterns which leads to cancer, arteriosclerosis, coronary artery disease, Parkinson’s disease, diseases of the immune system, diabetes, cataract formation, Alzheimer’s, macular degeneration, COPD, allergy/asthma, stroke.

Detoxification:
GSH also plays a main role in detoxification..primarily in Phase II Liver detox. It "binds" to many toxins by its sulfur molecules and aids in forming a complex which the body then rids itself of.

Immune System Support:
When the immune system responds to an invader, it releases a blitz of free radicals to aid in the offensive agent's demise. This could create damage to local tissue and your body, but GSH rallies around the area to quench the free radicals that are produced in excess.

Protection from Radiation:
A recent research article published in the journal Radiology states that “radiation from a single whole-body scan is equal to that from 100 mammograms and is similar to that received by survivors of the atomic bombings of Hiroshima and Nagasaki, Japan – about 1 mile from the explosions – according to radiation biologist, David J. Brenner of Columbia University. The radiation from one scan is enough to produce a tumor in one out of 1200 people, and for those who have annual scans the risk increases to one tumor in every 50 people. With inadequate intracellular GSH the risk is greatly increased.

Tuesday, January 15, 2008

Glutathione, oxidative stress and aging

The theory of aging proposes that the impairment in physiological performance associated with aging is caused by the detrimental effects of oxygen free radicals. This is interesting because it provides us with a theoretical framework to understand aging and because it suggests a rationale for intervention, i.e., antioxidant administration. Thus, the study of antioxidant systems of the cell may be very important in gerontological studies. Glutathione is one of the main nonprotein antioxidant in the cell which, together with its related enzymes, constitute the “Glutathione system.” The involvement of Glutathione in aging has been known since the early seventies. Several studies have reported that reduced Glutathione is decreased in cells from old animals, whereas oxidized Glutathione tends to be increased. Recent experiments from our laboratory have underscored the importance of cellular compartmentation of Glutathione. MitochondrialGlutathione plays a key role in the protection against free radical damage associated with aging. Oxidative damage to mitochondrial DNA is directly related to an oxidation of mitochondrialGlutathione. In fact, aging is associated with oxidative damage to proteins, nucleic acids, and lipids. These molecular lesions may be responsible for the low physiological performance of aged cells. Thus, antioxidant supplementation may be a rational way to partially protect against age-associated impairment in performance. Apoptosis, a programmed cell death, is an area of research which has seen an explosive growth. Glutathione is involved in apoptosis: apoptotic cells have lower levels of reduced Glutathione, and administration of Glutathione precursors prevent, or at least delay, apoptosis. Age-associated diseases constitute a major concern for researchers involved in aging. Free radicals are involved in many such diseases; for instance, cancer, diabetes or atherosclerosis. The key role of Glutathione and other antioxidant in the pathophysiology of aging and age-associated diseases is discussed in this review.

Juan Sastre1, Federico V. Pallardó1 and Jose Viña Department of Physiology, Faculty of Medicine, University of Valencia, Spain Dept. Fisiologia, Facultad de Medicina, Avenida Blasco Ibanez 17, 46010 Valencia, Spain

Sunday, January 6, 2008

Common symptoms of Diabetes

Symptoms:
*Unusual thirst
*Frequent urination
*Extreme fatigue and weakness
*Blurred vision
*Abdominal pains
*Nausea and vomiting
*Rapid weight loss or gain
*Skin infections
*Impotence
*Fluid retention (especially in legs and feet)
*Poor healing of skin wounds
*Decreased tolerance to cold
*Chronic itching
*Irregular or rapid heart rate
*Dry scaly skin
*Numbness or tingling of fingers and toes
*Extreme hunger pangs
*Hot and sweaty with clammy perspiration
*Heart tremors and palpitations
*Apprehensive with no obvious reason
*Shaky and nervous
*Disoriented, confused, inability to concentrate
*Frequent headaches, dizziness
*Mood changes, irritability

All diabetic symptoms are related to chronically high levels of glucose in the blood, which causes the premature aging of all body parts. So all diabetic symptoms can be explained in terms of what happens to the body as it ages. The branch of science that studies the aging process is called Gerontology and much of what happens to people with uncontrolled diabetes. more...

It is well known that aging is accompanied by a precipitous fall inglutathione levels. Lower glutathione levels are implicated in manydiseases associated with aging including cataracts, Alzheimer's,Parkinson's atherosclerosis and others.Journal of Clinical Epidemiology 47:1021-26, 1994.

Click here to demonstrate to you why glutathione is so important to your health and well-being.

If you have any of the symptoms mentioned above, a family history of diabetes, or are aged 45 or above, contact your doctor or healthcare professional and initiate blood and urine tests for diabetes.

Glutathione infusion potentiates glucose-induced insulin secretion in aged patients with impaired glucose tolerance

OBJECTIVE: To evaluate the effect of glutathione infusion on beta-cell response to glucose in elderly people with impaired glucose tolerance (IGT).

RESEARCH DESIGN AND METHODS: Ten patients with normal glucose tolerance and 10 patients with IGT were matched for age (mean +/- SE, 72.1 +/- 2.8 vs. 71.0 +/- 3.4 yr), body mass index (23.1 +/- 1.1 vs. 22 +/- 2.1 kg/m2), and sex (6/4 vs. 5/5, men/women) underwent glutathione infusion (10 mg/min) under basal conditions and during 75-g oral glucose tolerance tests and intravenous glucose tolerance tests (0.33 g.kg body wt-1.3 min-1). Patients with IGT were also submitted to euglycemic-hyperinsulemic and hyperglycemic glucose clamps.

RESULTS:In subjects with normal glucose tolerance, glutathione infusion failed to affect beta-cell response to glucose. In contrast, glutathione significantly potentiated glucose-induced insulin secretion in patients with IGT. Furthermore, in the latter group studied by hyperglycemic clamps, glutathione infusion significantly potentiated the beta-cell response to glucose when plasma glucose levels varied between 10 and 15 mM. This effect disappeared at plasma glucose levels greater than 15 mM. No effect of glutathione on insulin clearance and action was observed.

CONCLUSIONS: Glutathione infusion enhances insulin secretion in elderly people with IGT.

G Paolisso, D Giugliano, G Pizza, A Gambardella, P Tesauro, M Varricchio and F D'Onofrio Institute of Geriatric Medicine, First Medical School; University of Naples, Italy.

Click here to demonstrate to you why glutathione is so important to your health and well-being.

THE EFFECTS OF STREPTOZOTOCIN DIABETES AND DIETARY IRON INTAKE ON CATALASE

THE EFFECTS OF STREPTOZOTOCIN DIABETES AND DIETARY IRON INTAKE ON CATALASE, GLUTATHIONE PEROXIDASE, SUPEROXIDE DISMUTASE AND LIPID PEROXIDATION IN CARDIAC AND SKELETAL MUSCLES OF RATS
Abstract
Catalase, glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD) prevent oxygen free radical mediated tissue damage. Diabetes increases and a low dietary intake of iron decreases catalase activity in muscle. Therefore, the combined effects of diabetes and iron deficiency on the free radical scavenging enzyme system and lipid peroxidation were studied. Male, weanling rats were injected with streptozotocin (65 mg/kg, IV) and fed diets containing either 35 ppm iron (Db + Fe) or 8 ppm iron (Db $-$ Fe). Sham injected animals served as iron adequate (C + Fe) or iron deficient (C $-$ Fe) controls. Heart, gastrocnemius (GT), soleus and tibialis anterior (TA) muscles were dissected, weighted and analyzed for catalase, GSH-Px and SOD activities after 3, 6 or 9 weeks on the respective diets. The TBA assay was used to assess lipid peroxidation in the GT muscle. Diabetes elevated catalase activity in all muscles while it had a slight lowering effect on SOD and GSH-Px activities in the GT and TA muscles. In the C $-$ Fe rats, catalase activity declined and remained depressed in all muscles except the heart. There was an elevation in GSH-Px and SOD in the GT muscles of these animals after 6 weeks but not after 9 weeks of consuming the low iron diet. The Db $-$ Fe animals were unable to respond to the diabetic state with catalase activity as high as observed in the Db + Fe rats. Treatment with insulin or iron returned catalase to control levels. The C $-$ Fe animals had significantly lower levels of lipid peroxidation than the other groups at 6 and 9 weeks. Refeeding an iron adequate diet resulted in an increase in lipid peroxidation levels. These studies indicate that skeletal muscle free radical scavenging enzymes are sensitive to metabolic states and that dietary iron influences lipid peroxidation in this tissue.

SYDNEY REBECCA MORROW, THE UNIVERSITY OF TEXAS GRAD. SCH. OF BIOMED. SCI. AT HOUSTON Date: 1987

Click here to demonstrate to you why glutathione is so important to your health and well-being

Significance of glutathione-dependent antioxidant system in diabetes-induced embryonic malformations

Hyperglycemia-induced embryonic malformations may be due to an increase in radical formation and depletion of intracellular glutathione (GSH) in embryonic tissues. In the past, we have investigated the role of the glutathione-dependent antioxidant system and GSH on diabetes-related embryonic malformations. Embryos from streptozotocin-induced diabetic rats on gestational day 11 showed a significantly higher frequency of embryonic malformations (neural lesions 21.5 vs. 2.8%, P<0.001; GSH in embryonic tissues of diabetic pregnant rats on day 11 was significantly lower than that of normal rats. The activity of y-glutamylcysteine synthetase (gamma-GCS), the rate-limiting GSH synthesizing enzyme, in embryos of diabetic rats was significantly low, associated with reduced expression of gamma-GCS mRNA. Administration of buthionine sulfoxamine (BSO), a specific inhibitor of gamma-GCS, to diabetic rats during the period of maximal teratogenic susceptibility (days 6-11 of gestation) reduced GSH by 46.7% and increased the frequency of neural lesions (62.1 vs. 21.5%, P<0.01) GSH ester to diabetic rats restored GSH concentration in the embryos and reduced the formation of ROS, leading to normalization of neural lesions (1.9 vs. 21.5%) and improvement in nonneural lesions (26.7 vs. 47.4%) and growth retardation. Administration of insulin in another group of pregnant rats during the same period resulted in complete normalization of neural lesions (4.3 vs. 21.5%), nonneural lesions (4.3 vs. 47.4%), and growth retardation with the restoration of GSH contents. Our results indicate that GSH depletion and impaired responsiveness of GSH-synthesizing enzyme to oxidative stress during organogenesis may have important roles in the development of embryonic malformations in diabetes.

Click here to demonstrate to you why Glutathione is so important to your health and well-being

Abnormalities of retinal metabolism in diabetes or galactosemia

PURPOSE: Experimental galactosemia and diabetes are known to result in diabetic-like retinopathy in animals, but the mechanism by which the retinopathy develops remains unclear.

Defects of retinal metabolism that are common to galactosemia and diabetes are closely associated with the development of retinopathy and might play a role in the pathogenesis of the retinal disease.

METHODS: Effects of experimental galactosemia on retinal calcium-activated ATPase [(Ca,Mg)-ATPase], sodium-potassium ATPase [(Na,K)-ATPase], glutathione, ATP, and pertinent ions have been compared with the effects of experimental diabetes in rat and dog models of diabetic retinopathy.

RESULTS: Activities of (Ca,Mg)-ATPase and (Na,K)-ATPase were decreased as a result of either experimental galactosemia or diabetes in both the dog and the rat, and the decreases were accompanied by a diminution of reduced glutathione (GSH) in the retina. Ouabain-insensitive ATPase activity in the retina was not significantly reduced by diabetes or galactosemia, suggesting that the observed defects in (Ca,Mg)-ATPase and (Na,K)-ATPase activities were specific. The decrease of retinal GSH levels was associated with an elevated concentration of oxidized glutathione in diabetes but not in galactosemia. Retinal ATP and ion concentrations remained unaffected by experimental galactosemia or diabetes.

CONCLUSIONS: Comparison of two etiologically dissimilar models of diabetic retinopathy (diabetes and galactosemia) has revealed abnormalities of retinal metabolism that are shared by the two models. Further comparisons of retinal metabolism between these two models should reveal additional sequelae of hyperglycemia that are associated with, and that might play a role in, the development of diabetic retinopathy.

TS Kern, RA Kowluru and RL Engerman Department of Ophthalmology and Visual Science, University of Wisconsin- Madison 53706-1532.
Investigative Ophthalmology & Visual Science, Vol 35, 2962-2967, Copyright © 1994 by Association for Research in Vision and Ophthalmology

Oxidative Stress and Glutathione Synthesis in Type 2 Diabetes: a Stable Isotope Approach

Many of the complications of diabetes are linked to oxidative damage.

We set out to determine whether the reduced antioxidant capacity (as reflected by glutathione concentration) in type diabetes is due to reduced synthesis or increased consumption of glutathione(GSH), and whether short-term dietary supplementation with glycine and cysteine, precursors of GSH, would improve oxidant status.

2H2-glycine was infused for 7 hours to measure glycine kinetics and red blood cell GSH (RBC-GSH) synthesis in diabetic and euglycemic subjects. These same measurements were repeated in a subset of diabetic subjects after 2 weeks of supplementation with glycine and cysteine, the precursors of glutathione. Lipid hydroperoxide and lymphocyte glutathione concentration were also measured.

Twenty euglycemic subjects and 10 subjects with type 2 diabetes participated in the unsupplemented study.

Authors
Reeds, Peter
Jahoor, Farook
Siripoom, Mckay - BAYLOR COLLEGE/MEDICINE
Morlese, John - UNIV. WEST INDIES
Forrester, Terrence - UNIV. WEST INDIES
Jackson, Alan - ROYAL COLLEGE/PHYSICIANTS
Balasubramanyan, Ashok - BAYLOR COLLEGE/ MEDICINE

Hepatic Glutathione Metabolism in Diabetes

Glutathione is important in the regulation of the redox state, and a decline in its tissue level has often been considered to be indicative of increased oxidative stress in diabetes.

In this study of diabetic rats, the level of hepatic glutathione was normal unless food intake was restricted.

Thus, the previous report of a reduction in hepatic glutathione in diabetes is likely to be the result of food deprivation rather than diabetes alone. In contrast to changes characteristic of oxidative stress, the efflux of glutathione in bile from diabetic animals was significantly decreased, whereas hepatic mixed disulfides were unchanged, and the hepatic gamma-glutamyltransferase activity was considerably increased.

These changes were not reproduced by food deprivation. The decrease in biliary excretion of glutathione in diabetes may reflect an attempt to conserve glutathione by activation of the hepatic gamma-glutamyl cycle. We conclude that the disturbances of glutathione metabolism in diabetes are not typical of those seen in oxidative stress or food restriction.

Click here to demonstrate to you why Glutathione is so important to your health and well-being.

Among the uses that have been reported for glutathione are:
treatment of poisoning, particularly heavy metal poisons
treatment of idiopathic pulmonary firbosis
increasing the effectiveness and reducing the toxicity of cis-platinum, a chemo drug used to treat breast cancer
treating Parkinson's disease
lowering blood pressure in patients with diabetes
increasing male sperm counts in humans and animals
treatment of liver cancer
treatment of sickle cell anemia