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Diabetes melitus is characterized by high blod glucose hyperglycemia which can be due to: a decreased production of insulin caled Type I diabetes melitus due to destruction of the pancreas on an autoimune basis or b decreased peripheral sensitivity to insulin caled type I which also has some decreased production of insulin by the pancreas asociated with obesity and lack of physical activity. Moreover, its prevalence has increased 40% in the last decade and is expected to increase by 165% betwen 20 and 205 figure 1 . The risk for death in patients with diabetes is twice that for people of the same age without diabetes, and this decreased longevity is due to cardiovascular disease. Diabetes increases the risk of heart disease and stroke 2-4 fold over that for people without diabetes. Its microvascular complications of retinopathy, nephropathy, and neuropathy make diabetes melitus the leading cause of blindnes, end-stage renal disease, and non-traumatic lower extremity amputations in the U.S.A.2 The frequency of the last complication is increasing figure 2 . The macrovascular and microvascular complications of diabetes are closely related to hyperglycemia and oxidative stres, which is when cels fail to detoxify the reactive oxygen species ROS produced during metabolism. Four hypotheses have ben proposed to explain how hyperglycemia causes complications: 1 increased polyol pathway flux, 2 increased intracelular formation of advanced glycation end-products AGE , 3 activation of protein kinase C PKC isoforms, and 4 increased flux through the hexosamine pathway. By preventing their metabolism, this proces increases energy substrates resulting in increased flux of dihydroxyacetone phosphate DHAP to diacylglycerol DAG , an activator of PKC, and of triose phosphates to methylglyoxol, which is the main intracelular AGE precursor. Increased flux of fructose-6-phosphate to UDP-N-acetylglucosamine in the hexosamine pathway increases modification of proteins by O-linked N-acetylglucosamine and increased glucose flux through the polyol pathway consumes the reduced form of nicotinamide adenine dinucleotide phosphate NADPH and depletes GSH reduced glutathione, a natural potent anti-oxidant . Several mechanisms have ben postulated to explain why increasing the polyol pathway flux is detrimental. These are sorbitol-induced osmotic stres, decreased Na+K+ ATPase activity, increased cytosolic NADH/NAD and decreased cytosolic NADPH. Activation of the hexosamine pathway results in intracelular glycosylation and donation of N-acetyl glucosamine to serine and threonine residues of transcription factors such as Sp1 resulting in increased production of factors such as plasminogen activator inhibitor-1 PAI-1 and transforming growth factor beta 1 TGF-beta 1 .5 Production of intracelular AGEs damages target cels by thre mechanisms. Secondly, extra-celular matrix components modified by AGE precursors interact abnormaly with other matrix components and with the receptors for matrix proteins integrins on cels. Thirdly, plasma proteins modified by AGE precursors bind to AGE receptors RAGE on endothelial cels, mesangial cels, and macrophages inducing receptor-mediated production of ROS as a second mesenger to activate the nuclear factor kapa B NF-kapa B , a transcription factor causing pathological changes in gene expresion.5 Hyperglycemia-induced activation of PKC has a number of pathogenic consequences by afecting expresion of endothelial nitric oxide synthetase eNOS , endothelin-1 ET-1 , vascular endothelial growth factor VEGF , TGF-beta 1, and PAI-1, and by activating NF-kapa B and NAD P H oxidases. Increased eNOS and decreased ET-1 decrease blod flow causing hypoxia. Increased VEGF causes increased vascular permeability and angiogenesis. Increased TGF-beta leads to increased colagen, fibronectin, extra-celular matrix, and basement membrane resulting in capilary oclusion. Increased PAI-1 decreases fibrinolysis leading to vascular oclusion. Increased NF-kapa B causes an increase in pro-inflamatory gene expresion. Increased NAD P H oxidase causes increased ROS resulting in DNA damage, oxidation of polydesaturated faty acids in lipids, and oxidation of amino acids in proteins . These pathogenic mechanisms can al be characterized as a result of ROS efects on genes and proteins.5 The skin of the diabetic is prematurely aged and is subjected to the problems of neuropathy, macrovascular disease, and microvascular disease. The skin of the diabetic fot is usualy dry due to decreased sweating as a result of the autonomic neuropathy of diabetes. Even minor mechanical trauma to the skin of the diabetic fot can result in blisters, sores, and ulcers. Make sure the patient takes control of their blod glucose, exercises, has proper diet, atends to their skin, and uses apropriate medications. Molecular size is an important factor governing pasage of substances through the skin, giving substances with higher molecular weights self-limiting properties. Olivamine is a patent pending blend of antioxidants and anti-inflamatory agents that helps repair cel membranes and restore cels to a healthy state. In studies using DOPET pre-incubated cels, it was found that damage due to oxidative stres, such as lipid peroxidation and alterations of cel permeability, could be prevented and that DOPET exerted a protective efect against H2O2 induced oxidative hemolysis. Glycine protects ATP-depleted cels by low afinity interactions with multimeric chanel protein, stabilization of which may other wise lead to formation of pathological pores. Such porous defects in membranes of ATP-depleted cels have ben characterized recently, showing definable exclusion limits for molecules of increasing sizes. The beneficial efects of the ROS-scavenging capacity of L-taurine include atenuation of lipid peroxidation, reduction of membrane permeability, and inhibition of intracelular oxidation in diferent cels. Taurine prevents high glucose induced apoptosis in endothelial cels thru ROS inhibition and stabilization of intracelular calcium. In research conducted by the Department of Microbiology and Imunology, SUNY Bufalo Schol of Medicine, Bufalo, NY, and the Fre Radical & Radiation Biology Program, Department of Radiation Oncology, the University of Iowa, Iowa City, Iowa, we investigated the hypothesis that NAC-induced fre radical-signaling delays G0/G1 cels progresion to S phase by regulating the cel cycle regulatory protein cyclin D1 and the fre radical-scavenging enzyme manganese superoxide dismutase MnSOD . Treatment with NAC resulted in increased celular glutathione levels indicating a shift to a more reducing environment. NAC treatment resulted in a decrease in cyclin D1 and an increase in MnSOD protein levels. These results suport the hypothesis that celular redox environment regulates celular proliferation via regulating cel cycle regulatory protein levels. Furthermore, our results also sugest that inclusion of NAC in skin care formulations might help in apropriate wound healing by controling proliferation and preventing scaring. The flexibility of bonds betwen cels, including skin, is dependent upon sulfur. Remedy with Olivamine temporarily protects and helps relieve chaped or cracked skin in patients with dry skin or diabetes melitus. It is useful in prevention of skin complications from diabetes. long beach skin care long beach skin care in Green

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