Dietary Intevention in Diabetes

INTRODUCTION
Dietary intervention has been regarded to be the safest, most economical and best suited life-long intervention for diabetes. Recently, Katani¹ stated that the intracellular, synthesized antioxidant systems comprised of catalase, superoxide dismutase and glutathione peroxidase provide far more protection to cells than pre-formed vitamin and micronutrient dietary antioxidants. The greatest damage from reactive oxygen species and free radicals is to phospholipids and fatty acids in functional cell membranes.
Medial thickening of arterioles has long been recognized as the hallmark of the microvascular disease associated with diabetes mellitus. Deposits of glycoproteins and glycolipids as seen in early stages of atherosclerosis and accelerated large vessel disease are found in diabetics. More recently the role played by peroxidation of plasma lipids as a contributing pathogenic factor in accelerated atherosclerosis of the diabetic state has been recognized.
Reduced serum antioxidant levels have been documented as contributing to the increased oxidative stress in Insulin Dependent Diabetes Mellitus (IDDM). Antioxidant deficiencies have been shown to be present at diagnosis of Impaired Glucose Tolerance (IGT)/Insulin Resistance (IR) and Non-Insulin Dependent Diabetes Mellitus (NIDDM).
Antioxidant dietary therapy might retard or prevent progression from IGT/IR to NIDDM and decrease the severity of IDDM and diabetic complications by increasing the antioxidant levels of the body's defences against the increased oxidative stress associated with diabetes.
Hyperglycaemia associated with diabetes has been shown to stress the cellular microenvironment and disrupt cell membrane function. Prolonged hyperglycaemia has been shown to reduce the endogenous intracellular antioxidants such as glutathione peroxidase catalase, and superoxide dismutase . Free radicals, formed by the auto-oxidation of glucose and glycosylated proteins, initiate reduction-oxidation reactions and promote oxidative stress which have been implicated in the pathogenesis of diabetes. The degree of oxidation present in chronic diabetics directly parallels the severity of diabetic complications. Free radicals oxidize proteins causing interference with sodium, potassium, and adenosine triphosphate (ATP) ion channels and failure of membrane cell receptors. Deoxyribonucleic acid (DNA) undergoes single and double strand breaks as free radicals attach to phosphate groups, destroying deoxyribose sugars and bases. Excessive oxidation is implicated in mutagenesis, carcinogenesis, diabetes, many other disease processes and possibly aging as it plays a role in tissue degeneration and cell death. The human body has multiple natural antioxidants to manage the ongoing oxidative onslaught. The natural enzyme glutathione peroxidase is regarded as the most important natural enzyme antioxidant in IGT/IR and NIDDM. Persons with IGT/IR are known to have a glutathione deficiency of 15% while NIDDM diabetics have a 20% glutathione deficiency. Glutathione peroxidase activity is enhanced by selenium, but consumes nicotinamide-adenine dinucleotide phosphate (NADPH) in the energy of regeneration of the natural enzyme. In diabetes NADPH is consumed by the competing reduction of glucose to sorbitol in insulin-independent tissues under high glucose conditions. NADPH is also consumed in converting glucose to other monosaccharides.
Glyconutrients are beneficial to wellness in humans.