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Diabetic patients

In terms of membrane area used and doUar value of the membrane produced, artificial kidneys are the single largest appHcation of membranes. Similar hoUow-fiber devices are being explored for other medical uses, including an artificial pancreas, in which islets of Langerhans supply insulin to diabetic patients, or an artificial Uver, in which adsorbent materials remove bUinibin and other toxins. [Pg.88]

The separation of proteins and peptides mixtures is the objective of protein biochemisdy. Albumin (Mr 66 000) concentration in a biological fluid (seaim, urine or cerebrbrospinal fluid) is assayed as markers for a series disease, such as nephritic syndrome or chronic glomuleronephritis. In diabetic patients the progression of microalbuminuria is accompanied by an increase in urinary concentrations of human semm albumen. In normal the excretion of albumin is 20 (tg/ml, in pathology - 20-200 p.g/ml. [Pg.100]

On the other hand, EFN-a may also be involved in the activation of autoreactive T-cells as has been proposed for type I diabetes. An DFN-a inducible superantigen, encoded by the truncated envelope gene of a human endogenous retrovirus and specifically activating V 37 T-cells, has been detected in pancreatic lesions from type I diabetes patients, infiltrated by V 37 T-cells. Since IFN-a expression could be detected in pancreatic (3 cells in conceit with persistent viral infections, there is a clear link between viral infections and autoimmunity via IFN-a-stimulated superantigen expression. [Pg.646]

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. [Pg.1297]

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... [Pg.1298]

Large doses of IValbuterol or IV terbutaline may aggravate diabetes mellitua Diabetic patients may require an increase in insulin dosage or oral hypoglycemic drug. [Pg.345]

Diabetic patients have reduced antioxidant defences and suffer from an increased risk of free radical-mediated diseases such as coronary heart disease. EC has a pronounced insulin-like effect on erythrocyte membrane-bound acetylcholinesterase in type II diabetic patients (Rizvi and Zaid, 2001). Tea polyphenols were shown to possess anti-diabetic activity and to be effective both in the prevention and treatment of diabetes (Choi et al, 1998 Yang et al, 1999). The main mechanism by which tea polyphenols appear to lower serum glucose levels is via the inhibition of the activity of the starch digesting enzyme, amylase. Tea inhibits both salivary and intestinal amylase, so that starch is broken down more slowly and the rise in serum glucose is thus reduced. In addition, tea may affect the intestinal absorption of glucose. [Pg.138]

SCHWARTZ J G, GUAN D, GREEN G M, PHILLIPS w T (1994) Treatment with an oral proteinase inhibitor slows gastric emptying and acutely reduces glucose and insulin levels after a liquid meal in type 11 diabetic patients. Diabetes Care. 17 255-62. [Pg.184]

It has been suggested that sugars such as glucose, which is present in high concentrations in diabetic patients, can... [Pg.132]

TBA, thiobarbituric acid reactivity DCs, diene conjugates MA, microangiopathy LP, lipid peroxides DM, diabetic patients C, controls HDL, high-density lipoprotein. [Pg.185]

Collier et al. (1990) extended their studies relating to oxidative stress and diabetes by demonstrating that the levels of several free-radical scavengers (red cell superoxide dismutase, plasma thiols) were significantly reduced in 22 type 2 diabetic patients (mean age 53 years) in comparison with 15 control subjects (mean age 51 years). No significant diflFerences in red cell lysate thiols or... [Pg.185]

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). [Pg.186]

A more recent study, which measured three established markers of free-radical activity in addition to serum ascorbic acid in two groups of elderly diabetic patients (with and without retinopathy), found no significant differences in any of the markers between patients and age-matched controls despite significant depletion of ascorbic acid in patients with diabetes, especially those with retinopathy (Sinclair et al., 1992). These rather paradoxical findings suggest the existence of a complex interrelationship between the levels of individual antioxidant molecules in cells and tissues. [Pg.186]

Eluorescence of both collagen (Monnier etal., 1986) and IgG (Jones etal., 1988) are associated with diabetic micrOangiopathy. Monnier etal. (1986) found that measured collagen-linked fluorescence in skin biopsies from both patients with type 1 diabetes ( = 41, age range 29-52 years) and controls ( =25, age range 28-41 years) was significantly correlated with the severity of retinopathy as well as arterial and joint stifihess. Jones et al. (1988) found increased fluorescence of serum IgG in diabetic patients with... [Pg.190]

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. [Pg.194]

Several studies have demonstrated that treatment of diabetic patients with the sulphonylurea, gliclazide, is associated with a fall in lipid peroxidation, protein fluorescence and beneficial effects on platelet function (Florkowski et al., 1988 Jennings et al., 1992). These changes were seen to be independent of changes in giycaemic control. [Pg.194]

Bain, S.C., Le Guen, C.A., Lunec, J. and Barnett, A.H. (1991). Comparison of the free radical scavenging activity of captopril versus enalapril a three-month trial in vivo study in hypertensive diabetic patients. J. Human Hypertens. 5, 511-515. [Pg.195]

Collier, A., Jackson, M., Dawkes, R.M., Bell, D. and Clarke, B.F. (1988). Reduced free radical activity detected by decreased diene conjugates in insulin-dependent diabetic patients. Diabetic Med. 5, 747-749. [Pg.195]

Mooradian, A.D. (1991). Increased serum conjugated dienes in elderly diabetic patients. J. Am. Ger. Soc. 39, 571-574. [Pg.197]


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See also in sourсe #XX -- [ Pg.98 , Pg.258 ]

See also in sourсe #XX -- [ Pg.48 , Pg.54 , Pg.57 , Pg.58 , Pg.75 , Pg.158 , Pg.211 , Pg.212 ]

See also in sourсe #XX -- [ Pg.122 ]

See also in sourсe #XX -- [ Pg.103 , Pg.204 , Pg.218 , Pg.223 ]




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