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  • 1
    ISSN: 1432-0428
    Keywords: Limited joint mobility ; stiffening of connective tissue ; diabetic nephropathy ; non-enzymatic glycation ; lipid peroxide ; dyslipidaemia ; oxidative stress
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Limited joint mobility seen in diabetes mellitus is thought to be the result of stiffening of periarticular connective tissue, which is presumably derived from increased crosslinking of collagen related to advanced glycation end products. In this study the extent of the stiffening of connective tissue was measured by the passive extension angle of the metacarpophalangeal joints in 205 elderly diabetic patients. Association with diabetic nephropathy, with which advanced glycation end products have recently been demonstrated to increase, and metabolic abnormalities were also considered. The angle of the metacarpophalangeal joints was significantly correlated with age (r=−0.24, p〈0.01), and was significantly smaller in men than in women (p〈0.01). The angle demonstrated a decrease in association with diabetic retinopathy and nephropathy, and only the association with nephropathy was significant (p〈0.05). The angle was weakly, but significantly, correlated with serum thiobarbituric acid reactants as a measure of lipid peroxides (r=−0.15, p〈0.05), triglyceride (r=−0.20, p〈0.01) and HDL cholesterol (r=0.19, p〈0.01), but not with blood glucose (r=0.02), HbA1c (r=0.06) or duration of diabetes (r=−0.05). In addition, the angle in 14 non-diabetic patients on haemodialysis was significantly (p〈0.05) smaller than that in age- and sexmatched normal subjects. Thus, it was indicated that the stiffening of connective tissue was associated with diabetic nephropathy, serum lipid peroxide and dyslipidaemia. Stiffening of connective tissue seems to be more affected by oxidative stress than non-enzymatic glycation per se. Factors contributing to the stiffening of connective tissue, such as male sex, ageing, serum lipid peroxide, high triglyceride and low HDL cholesterol resemble those associated with arteriosclerosis.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-0428
    Keywords: Non-enzymatic glycation ; thermal stability of collagen ; tail tendon ; vitamin E ; oxidative stress
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Products similar to non-enzymatic glycation end products are known to arise from the interactions between proteins and lipid peroxides in vitro. In this study, we assessed the effect of vitamin E, which possibly modifies lipid peroxide, on advanced glycation end products or similar products in vivo by measuring the fluorescence and thermal rupture time of tail tendon collagen in streptozotocin-induced diabetic rats. The diabetic rats and non-diabetic rats were fed a vitamin E supplemented diet, and a control diet starting 3 days after the streptozotocin injection. After the 4-week treatment, the serum lipid peroxide levels expressed as thiobarbituric acid reactants in the diabetic rats on control diet (15.9 ± 2.6 μmol/l [SEM]) were significantly (p 〈0.05) higher than in the non-diabetic rats (7.9 ± 1.3 μmol/l on control diet and 3.3 ± 0.4 μmol/l on supplemented diet), but the levels in the diabetic rats on supplemented diet (7.9 + 2.3 μmol/l) were reduced to the normal levels. No significant differences were found in serum glucose and glycated haemoglobin levels within the diabetic rats on control and supplemented diets. Both the fluorescence and thermal rupture time of collagen were significantly (p 〈0.05) increased in the diabetic rats on both diets compared with those in the corresponding non-diabetic rats. Although there was no significant difference in the collagen-linked fluorescence within the diabetic rats on control and supplemented diets, the thermal rupture time was significantly (p 〈0.01) shortened with supplemented diet (10.8 ± 0.7 min on supplemented diet vs 15.0 ± 0.7 min on control diet). The effect of vitamin E on the thermal rupture time was not observed in non-diabetic rats (6.6 ± 0.5 min on supplemented diet vs 6.2 ± 0.5 min on control diet). These results indicate that the formation of advanced glycation end products or similar products seen in hyperglycaemia can be partially inhibited by vitamin E supplementation by lowering lipid peroxide levels or oxidative stress. This study is thought to be the first to show vitamin E as an anti-oxidant agent limiting the formation of advanced glycation end products or similar products in vivo.
    Type of Medium: Electronic Resource
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