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Thursday, 28 November 2013

Diabetes Preventions – The Antioxidants

 Diabetes is defined as a condition caused by insufficient insulin entering the bloodstream to regulate the glucose. It is either caused by cells in pancreas dying off or receptor sites clogged up by fat and cholesterol. In some cases, diabetes is also caused by allergic reactions of cells in the immune system.
IV. Preventions
C. Antioxidants to  prevent diabetes
Free radicals are formed disproportionately in diabetes by glucose oxidation, nonenzymatic glycation of proteins, and the subsequent oxidative degradation of glycated proteins. Abnormally high levels of free radicals and the simultaneous decline of antioxidant defense mechanisms can lead to damage of cellular organelles and enzymes, increased lipid peroxidation, and development of insulin resistance. These consequences of oxidative stress can promote the development of complications of diabetes mellitus(63).
1. Vitamin E (Free radical scavenger)
According to the study of Vitamin E: function and metabolism, Vitamin E is the term for a group of tocopherols and tocotrienols, of which α-tocopherol has the highest biological activity(a), and is the most common in the North American diet.
In the study of twenty-eight rats rendered diabetic by streptozotocin injection and fed either with a diet with low (10 mg/kg of chow), medium (75 mg/kg of chow) or high amounts of vitamin E (1300 mg/kg of chow). Nine age-matched nondiabetic rats receiving 75 mg of vitamin E/kg chow served as controls, the results showed that 1) vitamin E has a potential to prevent partially hyperglycemia-induced endothelial dysfunction, 2) under in vivo conditions vitamin E deficiency enhanced diabetic endothelial dysfunction dramatically, and 3) positive effects of vitamin E may be attenuated with a longer disease duration(64).
2. Vitamin C (Free radical scavenger)
Vitamin C or L-ascorbic acid is a water-soluble vitamin needed for the growth and repair of tissues of the body. Epidemiological studies showed that diets high in fruits and vegetables are associated with lower risk of cardiovascular disease, stroke and cancer, and with increased longevity(65).
In the study of 84 patients with type 2 diabetes referred to Yazd Diabetes Research Center, Iran, were included in the study. They received randomly either 500 mg or 1000 mg daily of vitamin C for six weeks, found that daily consumption of 1000 mg supplementary vitamin C may be beneficial in decreasing blood glucose and lipids in patients with type 2 diabetes and thus reducing the risk of complications(66).
3. Vitamin D
Vitamin D is a membrane antioxidant: thus Vitamin D3 (cholecalciferol) and its active metabolite 1,25-dihydroxycholecalciferol and also Vitamin D2 (ergocalciferol) and 7-dehydrocholesterol (pro-Vitamin D3) all inhibited iron-dependent liposomal lipid peroxidation(66a). There is evidence supporting that vitamin D status is important to regulate some pathways related to type 2 diabetes development. Based on available clinical and epidemiological data, the positive effects of vitamin D seem to be primarily related to its action on insulin secretion and sensitivity and secondary to its action on inflammation, according to the study by São Paulo State University(66b). Other study linked vitamin D deficiency as a culprit  to the development of Type I and II diabetes. According yo the study by Laboratory of Experimental Medicine and Endocrinology (LEGENDO), Catholic University of Leuven, vitamin D deficiency has been shown to impair insulin synthesis and secretion in humans and in animal models of diabetes, suggesting a role in the development of type 2 diabetes. Furthermore, epidemiological studies suggest a link between vitamin D deficiency in early life and the later onset of type 1 diabetes(66c).
4. Coenzyme Q10
Coenzyme Q10 (CoQ10) found naturally in the body is necessary for the basic functioning of cells. In the study to investigate the effects of coenzyme Q10 (CoQ10) treatment on insulin secretory response, hearing capacity and clinical symptoms of maternally inherited diabetes mellitus and deafness (MIDD), found that the insulin secretory response assessed by glucagon-induced C-peptide secretion and 24 h urinary C-peptide excretion after 3 years in the CoQ10-DM group was significantly higher than that in the control-DM group. CoQ10 therapy prevented progressive hearing loss and improved blood lactate after exercise in the MIDD patients. CoQ10 treatment did not affect the diabetic complications or other clinical symptoms of MIDD patients(67). Other study suggested that CoQ supplementation may improve blood pressure and long-term glycaemic control in subjects with type 2 diabetes, but these improvements were not associated with reduced oxidative stress, as assessed by F2-isoprostanes(68).
5. Alpha-lipoic acid
Alpha-lipoic acid, an antioxidant made by the body and is is necessary for the basic functioning of cells
to turn glucose into energy. According to the study of Bühl and City Hospital, Baden-Baden, Germany, alpha-lipoic acid (ALA), a naturally occuring compound and a radical scavenger was shown to enhance glucose transport and utilization in different experimental and animal models. Oral administration of alpha-lipoic acid can improve insulin sensitivity in patients with type-2 diabetes. The encouraging findings of this pilot trial need to be substantiated by further(69).
6. L-carnitine
L carnitines, is an antioxidant protected our body against lipid peroxidation and oxidative stress. Supplementation of L-carnitine and antioxidants improve lipid profiles and exercise ability in exercise-trained rats. Also, both exercise training and supplementation of carnitine and antioxidants improved lipid profiles and carnitine metabolism in humans, suggesting that carnitine and antioxidant supplementation may improve exercise performance, according to the study by Faculty of Medicine, University of British Columbia(70).
6. Etc.
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Sources
(63) http://www.ncbi.nlm.nih.gov/pubmed/12616644
(64) http://www.ncbi.nlm.nih.gov/pubmed/12649359
(65) http://www.jacn.org/content/22/1/18.full
(66) http://www.ncbi.nlm.nih.gov/pubmed/18160753
(66a) http://www.sciencedirect.com/science/article/pii/001457939381809E
(66b) http://www.ncbi.nlm.nih.gov/pubmed/22347618
(66c) http://www.ncbi.nlm.nih.gov/pubmed/15971062
(67) http://www.ncbi.nlm.nih.gov/pubmed/9628277
(68) http://www.ncbi.nlm.nih.gov/pubmed/12428181 
(69) http://www.ncbi.nlm.nih.gov/pubmed/10468203
(70) http://www.ncbi.nlm.nih.gov/pubmed/18296364