Table 2.
Micronutrient functions in type 2 diabetes.
Trace/macro elements | Functions in type 2 diabetes |
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Sodium and potassium | Na+/K+− ATPase pump is a ubiquitous enzyme that ensures that the transmembrane gradients of sodium and potassium concentrations are maintained. Alterations of this transport system are thought to be linked to several complications of diabetes mellitus [11]. |
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Calcium | Any alterations in calcium flux can have adverse effects on β-cell secretory function and may interfere with normal insulin release, especially in response to a glucose load. The elevated cytosolic calcium will lead to the pathogenesis of complications of T2D which in turn may interfere with normal insulin release, especially in response to a glucose load [26]. |
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Magnesium | The magnesium is an essential ion involved in multiple levels in insulin's secretion and its binding and its activity; and it is also a critical cofactor of many enzymes in carbohydrate metabolism. The magnesium plays an important role to improve insulin resistance [19, 27]. |
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Chromium | The chromium is required for normal carbohydrate metabolism and as a critical cofactor for insulin action and is a component of the glucose tolerance factor (GTF), which plays a role in glucose homeostasis [28]. |
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Cobalt | The glycemia-lowering effect of cobalt chloride (CoCl2) decreased systemic glucose production, increased tissue glucose uptake, or made a combination of the two mechanisms. The action of cobalt results increased expression of glucose transporter 1 (GLUT1) and inhibition of gluconeogenesis [29]. |
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Copper | A deficiency of copper results in glucose intolerance, decreased insulin response, and increased glucose response. It is associated with hypercholesterolemia and atherosclerosis. The copper possesses an insulin-like activity and promotes lipogenesis [20, 22]. |
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Iodine | The role of iodine is correlated with thyroid hormone and it is clear that insulin resistance and β-cell function are inversely correlated with thyroid stimulating hormone which may be explained by insulin-antagonistic effects of thyroid hormones along with an increase in thyroid stimulating hormone (TSH) [30]. |
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Iron | Elevated iron stores may induce diabetes through a variety of mechanisms, including oxidative damage to pancreatic β cells, impairment of hepatic insulin extraction by the liver, and interference with insulin's ability to suppress hepatic glucose production [31, 32]. |
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Selenium | The effect of selenium in diabetes has contradictory effects; the antioxidant property of selenium prevents the development of complications in diabetic patients. While in other studies higher serum selenium concentrations were associated with a higher prevalence of diabetes [33, 34]. |
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Manganese | The enzyme which is activated by manganese plays important roles in the metabolism of carbohydrates, amino acids, and cholesterol and it is required for normal synthesis and secretion of insulin [35]. |
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Zinc | The zinc plays an important role in glucose metabolism. It helps in the utilization of glucose by muscle and fat cells. It is required as a cofactor for the function of intracellular enzymes that may be involved in protein, lipid, and glucose metabolism. The zinc may be involved in the regulation of insulin receptor-initiated signal transudation mechanism and insulin receptor synthesis [36, 37]. |
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Vanadium | The vanadium affects various aspects of carbohydrate metabolism including glucose transport, glycolysis, and glucose oxidation and glycogen synthesis. The vanadium acts primarily as an insulin mimetic agent, although enhanced insulin activity and increased insulin sensitivity have also been noted [38–41]. |