The Effect Of Free Radicals On The Development Of Diabetic Complications

Diabetes is a disease where the body is unable to produce or use insulin effectively. Insulin is needed for proper storage and use of carbohydrates. Without it, blood sugar levels can become too high or too low, resulting in a diabetic emergency. It affects about 7.8% of the population. The incidence of diabetes is known to increase with age. It’s the leading cause of end-stage renal disease in the US, and is the primary cause of blindness and foot and leg amputation. It is known to cause neuropathy in up to 70% of diabetic patients. Individuals with diabetes are twice as likely to develop cardiovascular disease. There are two types of diabetes: Type 1 and Type 2.

Compared to diabetic control rats, total antioxidant levels were significantly increased in GTE supplemented rats. Inversely, malondialdehyde levels and AT(1) receptor were significantly lower in the GTE supplemented diabetic group [77]. Catechin and its derivatives in green tea are shown to be therapeutically very effective.

This indicates that the metabolism of proteins was apparently affected by Ch.t extract. The improvement on the levels of protein and albumin in the diabetic treated groups show that Ch.t extract have significant effect in glucose and protein level because insulin inhibit gluconeogenesis from protein [ ] or could be due to improvement in renal function. This affirmative agrees with the fact that the weight of skeletal muscles was significantly increase in diabetic rats treated with Ch.t extract. The decrease in albumin level documented for diabetic rats may be due to liver massive necrosis, deterioration of liver function, hepatic resistance to insulin and glycogen impairment of oxidative phosphorylation[ ].Under the same experimental conditions serum globulin level revealed an appreciable decrease[ ]. The renal pathogenesis is related to duration of diabetes, the most devastating complication with diabetes is nephropathy[

Superoxide dismutase (SOD) is a free radical scavenging enzyme that catalyses the dismutation of highly reactive superoxide anion O2 to molecular (O2) and to the less reactive species hydrogen peroxide. It has been proposed that poor glycemic control in diabetes is associated with depletion of antioxidant enzymes including SOD.

Type 2 diabetes is a polygenic, complex disease that has become a worldwide health crisis. According to the World Health Organization over 422 million people in the world had this disease in 2014 (1), the Center for Disease Control and Prevention stated that in the United States alone 29 million people had diabetes in 2014 (2). While the genetic predisposition contributing to the diabetes phenotype is not fully understood to date it still remains an area of active research. There are also various environmental factors that contribute stress to the glucose homeostasis system that provide a different approach in understanding this disease. Comprehending the pathogenesis of the disease has been an area of constant research for decades. There is hope that pharmaceutical developments can follow along and find medical treatments that can target the key pathogenic elements of this disease.

Similarly, an increase in the levels of lipid peroxidation was observed in Aβ-induced rat hippocampal cells, confirming previous reports [17]. Enzymatic antioxidants such as SOD, catalase, and GPX act as the cellular antioxidant defense mechanism against free radicals. Since NADPH is required for the regeneration of catalase from its inactive form, catalase activity might be decreased in Aβ induced toxicity due to reduced NADPH levels. In this study, we have reported that Honokiol treatment significantly increased the enzymatic antioxidant activities in APP-CHO cells. In addition, non-enzymatic antioxidants like GSH also exhibited beneficial neuroprotective effects against oxidative stress. GSH is an endogenous nonenzymatic antioxidant that prevents damage to cellular components caused by ROS such as free radicals and peroxides. GSH is oxidized to glutathione disulfide (GSSG) by ROS, thereby causing a reduction in the level of GSH. GR reduces GSSG to GSH via NADPH, which in turn is released by glucose-6-phosphate dehydrogenase [18]. Honokiol treatment upregulated the activity of these antioxidants in APP-CHO cells. In addition to oxidative stress, a strong association between insulin resistance and the development of AD has been demonstrated. Several studies have reported that insulin resistance (IR), an underlying characteristic of type 2 diabetes, is an important risk factor for AD

Several possible mechanisms have been explained regarding diabetes induced neurodegeneration. Diabetes mellitus and the accompanying hyperglycemia is a chronic endogenous stressor that is accompanied with increased oxidative stress in brain, particularly the hippocampus, by accelerating free radical generation. These radicals contribute to increased neuronal degeneration by inducing oxidation to proteins, DNA alterations and lipids oxidation in cell membranes .

Diabetes mellitus (DM) is a condition in the body that is related to a faulty metabolism. It means that the body’s metabolism is not functioning properly, which leads to adverse effects in the health. The food we ingest, gets broken down into blood sugar (glucose), which is what fuels our body in the form of energy. This converted glucose needs to enter our cells so that it can be used for energy and growth. And in order for the glucose to enter our cells, there needs to be insulin present, which the beta cells of the pancreas is responsible for producing. This hormone is responsible for maintaining glucose level in the blood. It allows the body cells to use glucose as a main

Indeed, American consume a very high amount of flour and sugar daily because almost every food contained sugar and flour. Although I know it is the misconception of diabetic, I still view diabetic as one of the adult’s disease when I heard the word diabetic. Somehow, I do not expect that teenagers would suffer from it. I agree with Dr. Mark Hyman that most of us do not know how to feed our brain due to the lack of education. Obviously, I am the first generation who go to the college in my family and I have never thought about how my diet affect my brain. Moreover, I do not realize that sugar can contribute to depression. I also have no idea how to feed my brain with healthy foods until I saw the video of “How to Eat Right for Your Brain” by

As a reducing sugar, fructose reacts with protein molecules to form toxic advanced glycation end-products (AGEs) to a much greater extent than other sugars, which appears to contribute not only to the aging process but also play a role in the pathogenesis of diabetic complications in diabetic patients such as nephropathy, retinopathy, neuropathy and others. Supplementing the diet of healthy male volunteers with 3g of fructose per kg of body weight per day resulted in insulin resistance developing in as little as six days. A study carried out in non-diabetic rats fed a diet containing 68% carbohydrate, provided as fructose, shows that almost all retinas from the rats showed pathologic changes that were histologically indistinguishable from diabetic retinopathy. [1]

High blood glucose levels and enhanced oxidative stress, found in both clinical and experimental diabetes, are thought to be the main cause of chronic diabetic complications.

Glutathione helps to protect cells from reactive oxygen species. GSH checks free radical damage and helps detoxification by conjugating with chemicals. Increase in reactive oxygen species protection causes GSH depletion. GSH acts as cofactor for Glutathione Peroxidase (GPx) and Glutathione-S-transferase (GST). Glutathione-S-transferase is thought to play a physiological role in initiating the detoxification and these enzymes catalyse the reaction of such compounds with the -SH group of glutathione, thereby neutralizing their electrophilic sites and rendering the products more water-soluble. GPx is present throughout the tissues as four different isoenzymes, cellular, extracellular glutathione peroxidase, as phospholipid hydroperoxide glutathione peroxidase and gastrointestinal glutathione peroxidase (Alam et al 2013). GPx low activity is one of the early consequences of a disturbance of the prooxidant or antioxidant balance due to toxic exposure. Glutathione reductase plays an important role in maintaining a basic GSH pool, via catalysing the reduction of glutathione disulfide (GSSG) to GSH in NADPH-dependent reaction (Yao Chen et al

Toll-like receptor 4 (TLR-4) plays important roles in innate immunity. Changes in the reduction-oxidation balance of tissues can lead to a pro-inflammatory state and insulin resistance. An action thought to be mediated by TLRs. Omega-3 fatty acids and Peroxisome Proliferator Activated Receptor gamma (PPAR-γ) agonists as pioglitazone are used for decreasing inflammation. The aim of this study is to investigate the anti-diabetic effects of combining omega -3 fatty acid with pioglitazone on type 2 diabetes, and the modulating effects on TLR-4. Type 2 diabetes was induced in male Sprague-Dawley rats by combination of high fat diet and low dose streptozotocin (35 mg/kg). Diabetic rats were treated with omega-3 fatty acids (10% W/W diet), pioglitazone (20 mg/kg), and their combination for 4 weeks. Omega-3 fatty acids and the combination treatment significantly decreased TLR-4 activation. Omega-3 fatty acids, pioglitazone, and their combination significantly decreased TLR-4 mRNA expression, hepatic malondialdehyde, total cholesterol and triglycerides levels, compared to diabetic group. Pioglitazone and the

Diabetes Mellitus is “a group of metabolic diseases characterized by hyperglycemia resulting from defects in insulin secretion, insulin action or both. It is a disease which is caused by the insufficient insulin secretion or decrease in the peripheral effects of insulin. It is a serious problem in terms of morbidity and mortality. The hyperglycemia is associated with long term damage, dysfunction and failure of various organs especially the eyes, kidneys, nerves, heart and blood vessels. It’s associated with many complications which includes blindness of the eyes and amputations of the extremities. It is also associated with neuropathy, retinopathy, and cardiovascular diseases which lead to mortalities.

Korean black ginseng (Panax ginseng C. A. Meyer), three to nine times-steamed and dried ginseng, has biological and pharmacological activities. In this study, the antidiabetic effects of black ginseng ethanol extract (BGE) in typical type 2 diabete model db/db mice was investigated. The effect of BGE in Type 2 diabetic mice was investigated by their blood analysis, biological mechanism analysis, and histological analysis. The mice group treated with BGE showed decreased fasting blood glucose and glucose tolerance compared to the nontreated BGE group. In the blood analysis, BGE decreased main plasma parameter such as HbA1c, triglyceride, and total-cholesterol levels related to diabetes and improved the expression of genes and protein related to glucose homeostasis and glucose uptake in liver and muscle. Moreover, BGE increased the phosphorylation of the AMPK in liver. Through histological analysis, the result showed that BGE decreased lipid accumulation in liver and damage in muscle.