Vitamin diabetes

Vitamin D metaboUtes may therefore play an active role ia diseases related to these functions, ie, leukemia, cancer (breast, colon, prostate), and autoimmune diseases (AIDS, immune encephaUtis, and diabetes) (51, 141,193—197, 202, 203). 

In addition to direct effects of chemical compounds on the fetus, metabolic disturbances in the mother, such as diabetes or hyperthermia, or deficiencies of calories or specific nutrients such as vitamin A, zinc, and folic acid may lead to teratogenesis. Compounds that inhibit placental functions may also induce malformations, e.g., by inhibiting placental circulation. For example, hydroxyurea disrupts the placental circulation and induces malformations. In addition, it also induces DNA damage. 

Sorbitol is a sweetener often substituted for cane sugar, because it is better tolerated by diabetics. It is also an intermediate in the commercial synthesis of vitamin C. Sorbitol is prepared by high-pressure hydrogenation of glucose over a nickel catalyst. What is the structure (including stereochemistry) of sorbitol ... 

It has been proposed that the development of the complications of diabetes mellitus may be linked to oxidative stress and therefore might be attenuated by antioxidants such as vitamin E. Furthermore, it is discussed that glucose-induced vascular dysfunction in diabetes can be reduced by vitamin E treatment due to the inactivation of PKC. Cardiovascular complications are among the leading causes of death in diabetics. In addition, a postulated protective effect of vitamin E (antioxidants) on fasting plasma glucose in type 2 diabetic patients is also mentioned but could not be confirmed in a recently published triple-blind, placebo-controlled clinical trial [3]. To our knowledge, up to now no clinical intervention trials have tested directly whether vitamin E can ameliorate the complication of diabetes. 

Boshtam M, Rafiei M, Golshadi ID et al (2005) Long-term effects of oral vitamin E supplement in type II diabetic patients. Int J Vitam Nutr Res 75 341—346... 

The salicylates are used cautiously in patients witii hepatic or renal disease, preexisting hypoprotiirombine-mia, or vitamin K deficiency and during lactation. The dragp are also used with caution in patients with gastrointestinal irritation such as peptic ulcers and in patients with mild diabetes or gout. 

Rice bran is the richest natural source of B-complex vitamins. Considerable amounts of thiamin (Bl), riboflavin (B2), niacin (B3), pantothenic acid (B5) and pyridoxin (B6) are available in rice bran (Table 17.1). Thiamin (Bl) is central to carbohydrate metabolism and kreb s cycle function. Niacin (B3) also plays a key role in carbohydrate metabolism for the synthesis of GTF (Glucose Tolerance Factor). As a pre-cursor to NAD (nicotinamide adenine dinucleotide-oxidized form), it is an important metabolite concerned with intracellular energy production. It prevents the depletion of NAD in the pancreatic beta cells. It also promotes healthy cholesterol levels not only by decreasing LDL-C but also by improving HDL-C. It is the safest nutritional approach to normalizing cholesterol levels. Pyridoxine (B6) helps to regulate blood glucose levels, prevents peripheral neuropathy in diabetics and improves the immune function. 

The above scientific information on rice bran phytochemicals indicates that a multitude of mechanisms are operating at the cellular level to bring about specific health effects. Several health benefits of rice bran appear to be the result of the synergistic function of the many phytochemicals, antioxidants, vitamins and minerals which operates through a specific immune response. Their role in the biochemical mechanisms at the cellular level which result in major health effects is shown in Fig. 17.1. A short overview summarizing the effect of the various phytochemicals on major health issues such as cancer, immune function, cardiovascular disease, diabetes, altered liver function and gastrointestinal and colon disease will be given below. 

Ascorbic acid (vitamin C) depletion is the most consistent evidence of compromised antioxidant status in diabetes with reports of reduced levels and altered metabolic turnover in several tissues in experimentally induced diabetes in animals (Rikans, 1981 Yew, 1983 McLennan et al., 1988) and in patients with diabetes (Som et al., 1981 Jennings et al., 1987 Sinclair et al., 1991). 

In a recent study, serum ascorbate concentrations were significantly reduced in a group of elderly diabetic patients (w = 40, mean age 69 years) in comparison with an age-matched group of non-diabetic controls ( = 22, mean age 71 years), and this reduction was more pronounced in those patients with microangiopathy (Sinclair et al., 1991). Diabetic patients were shown to have a high serum dehydroascorbate/ascorbate ratio indicative of increased oxidative stress. Ascorbate deficiency was partially corrected by vitamin C supplementation, 1 g daily by mouth, but the obvious disturbance in ascorbate metabolism in the diabetic patients was accentuated, since serum ascorbate concentrations fell (after the initial rise) despite continued vitamin C supplementation (Fig. 12.3). 

In a recent placebo-controlled study, 2 month s vitamin E treatment in patients with type 1 diabetes resulted in a significant dose-dependent fall in glycosylated proteins independent of changes in plasma glucose (Ceriello et al., 1991). Dose-related falls in both labile and stable fractions of haemoglobin Al also occurred. 

Prevention of vascular disease is one of the goals of a study in progress in Sweden, in which newly diagnosed diabetic children have been randomized in a doubleblind study where one group receives placebo and the other a preparation containing ascorbic acid, )3-carotene, nicotinamide, selenium and vitamin E (Ludvigsson, 1992). Future research with antioxidants may attempt to prevent the onset of pancreatic beta-cell destruction in the prediabetic phase of susceptible individuals. 

Routine antioxidant vitamin supplementation, e.g. with vitamins C and/or E, of the diabetic diet should be considered. Vitamin C depletion is present in all diabetics irrespective of the presence of vascular disease. A recent study demonstrated no significant difference between the dietary intake of vitamin C (the main determinant of plasma ascorbate) in patients with diabetes and age-matched controls, confirming the view that ascorbate depletion is secondary to the diabetic process and su esting that diabetic patients require additional intakes of the vitamin to maintain optimal levels (Sinclair et /., 1994). Antioxidant supplementation may have additive beneficial effects on a wide variety of processes involved in diabetic vascular damage including blood pressure, immune function, inflammatory reactions. 

Behrens, W.A. and Madere, R, (1991). Vitamin C and vitamin E status in the spontaneously diabetic BB rat before the onset of diabetes. Metabolism 40, 72-76. 

Ceriello, A., Giugliano, D., Quatraro, A., Donzella, C., Dipalo, G. and Lefebvre, P.J. (1991). Vitamin E reduction of protein glycosylation in diabetes. Diabetes Care 14, 68-72. 

Sinclair, A.J. Taylor, P.B., Lunec, J., Girling, A.J. and Barnett, A.H. (1994). Low plasma ascorbate levels in patients with type 2 diabetes mellitus consuming adequate dietary vitamin C. Diabet. Med. 11, 893-898. 

The ADA does not recommend low-carbohydrate diets in diabetes management. Although carbohydrates are a primary contributor to post-meal glucose levels, they are also an important source of energy, water-soluble vitamins, minerals, and fiber. Thus, the ADA recommends that carbohydrate intake consists of 45% to 65% of total calories. 

Vitamin B6 (pyridoxine) and its derivative pyridoxamine are apparently able to inhibit superoxide production, reduce lipid peroxidation and glycosylation in high glucose-exposed erythrocytes [353], It was suggested that the suppression of oxidative stress in erythrocytes may be a new mechanism by which these natural compounds inhibit the development of complication in diabetes mellitus. 

At present, antioxidants are extensively studied as supplements for the treatment diabetic patients. Several clinical trials have been carried out with vitamin E. In 1991, Ceriello et al. [136] showed that supplementation of vitamin E to insulin-requiring diabetic patients reduced protein glycosylation without changing plasma glucose, probably due to the inhibition of the Maillard reaction. Then, Paolisso et al. [137] found that vitamin E decreased glucose level and improved insulin action in noninsulin-dependent diabetic patients. Recently, Jain et al. [138] showed that vitamin E supplementation increased glutathione level and diminished lipid peroxidation and HbAi level in erythrocytes of type 1 diabetic children. Similarly, Skyrme-Jones et al. [139] demonstrated that vitamin E supplementation improved endothelial vasodilator function in type 1 diabetic children supposedly due to the suppression of LDL oxidation. Devaraj et al. [140] used the urinary F2-isoprostane test for the estimate of LDL oxidation in type 2 diabetics. They also found that LDL oxidation decreased after vitamin E supplementation to patients. 

Diabetes (type 1) 192 48% Islet IA-2, glutamic acid decarboxylase Infectious agents, ultraviolet radiation/vitamin D... 

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