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  • 1
    Electronic Resource
    Electronic Resource
    Acceleration of experimental diabetic retinopathy in the rat by omega-3 fatty acids (1996)
    Springer
    Diabetologia 39 (1996), S. 251-255 
    Details
    ISSN: 1432-0428
    Keywords: Keywords Diabetic retinopathy ; rat model ; omega-3 fatty acids.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Omega-3 fatty acids exert several important biological effects on factors that may predispose to diabetic retinopathy. Potential pathogenetic mechanisms include platelet dysfunction, altered eicosanoid production, increased blood viscosity in association with impaired cell deformability and pathologic leucocyte/endothelium interaction. Therefore, we tested whether a 6-month administration of fish oil (750 mg Maxepa, 5 times per week), containing 14 % eicosapentaenoic acid (EPA) and 10 % docosahexaenic acid, could inhibit the development of experimental retinopathy of the streptozotocin-diabetic rat. The efficiency of fish oil supplementation was evaluated by measuring EPA concentrations in total, plasma and membrane fatty acids and by measuring the generation of lipid mediators (leukotrienes and thromboxanes). Retinal digest preparations were quantitatively analysed for pericyte loss, and the formation of acellular capillaries. Omega-3 fatty acid administration to diabetic rats resulted in a twofold increase of EPA 20:5 in total fatty acids, and a reduction of the thromboxane2/3 ratio from 600 (untreated diabetic rats) to 50 (treated diabetic rats). Despite these biochemical changes, diabetes-associated pericyte loss remained unaffected and the formation of acellular, occluded capillaries was increased by 75 % in the fish oil treated diabetic group (115.1 ± 26.8; untreated diabetic 65.2 ± 15.0 acellular capillary segments/mm2 of retinal area). We conclude from this study that dietary fish oil supplementation may be harmful for the diabetic microvasculature in the retina. [Diabetologia (1996) 39: 251–255]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00418338
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  • 2
    Electronic Resource
    Electronic Resource
    Diabetic retinopathy risk correlates with intracellular concentrations of the glycoxidation product Ne-(carboxymethyl) lysine independently of glycohaemoglobin concentrations (1999)
    Springer
    Diabetologia 42 (1999), S. 603-607 
    Details
    ISSN: 1432-0428
    Keywords: Keywords Diabetic retinopathy ; prediction ; lymphocytes ; glycation.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Aims/hypothesis. We investigated whether either the amount of diabetes-induced intracellular oxidative stress or the concentration of hyperglycaemia-induced advanced glycation endproducts is associated with the risk of diabetic retinopathy. Methods. We measured concentrations of the glycoxidation product Ne-(carboxymethyl)lysine and two non-oxidation-dependent advanced glycation endproducts (methylglyoxal-derived and 3-deoxyglucosone-derived) in CD45RA+ T-cells from 21 Type I (insulin-dependent) diabetic patients with and without diabetic retinopathy and from age-matched non-diabetic control subjects. Results. Intracellular concentrations of both oxidation-dependent Ne-(carboxymethyl)lysine and oxidation-independent advanced glycation endproducts were increased in memory T-cells from diabetic patients. Ne-(carboxymethyl)lysine: diabetic median-24 176 arbitrary units/mg protein (95 % confidence interval 18 690–34 099 arbitrary units/mg protein); nondiabetic-9088 arbitrary units/mg protein (confidence interval 6994–10 696 arbitrary units/mg protein; p 〈 0.0001). Methylglyoxal-derived advanced glycation end products: diabetic-5430 arbitrary units/mg protein (confidence interval 3458–13 610); nondiabetic-271 arbitrary units/mg protein (confidence interval 61–760 arbitrary units/mg protein; p 〈 0.0001). 3-Deoxyglucosone-derived advanced glycation end products: diabetic-8070 arbitrary units/mg protein (confidence interval 7049–16 551 arbitrary units/mg protein); nondiabetic-1479 arbitrary units/mg protein (confidence interval 1169–3170; p 〈 0.0001). Only Ne-(carboxymethyl)lysine concentrations, however, inversely correlated with the duration of retinopathy-free diabetes (r = –0.51; p 〈 0.02). Diabetes-dependent Ne-(carboxymethyl)lysine accumulation did not correlate with age, diabetes duration, or averaged glycohaemoglobin concentrations. In vitro experiments wih menadione and lymphocytes confirmed that Ne-(carboxymethyl)lysine concentrations reflect intracellular oxidative stress. Conclusion/interpretation. Monitoring intracellular concentrations of increased oxidative stress in long-lived CD45RA+ lymphocytes by markers such as Ne-(carboxymethyl)lysine possibly identifies a subgroup of patients at high risk for microvascular complications. [Diabetologia (1999) 42: 603–607]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250051201
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  • 3
    Electronic Resource
    Electronic Resource
    The relationship of glycaemic level to advanced glycation end-product (AGE) accumulation and retinal pathology in the spontaneous diabetic hamster (1998)
    Springer
    Diabetologia 41 (1998), S. 165-170 
    Details
    ISSN: 1432-0428
    Keywords: Keywords Diabetic retinopathy ; chinese hamster ; advanced-glycation end-products ; pericytes.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary To assess the relationship between glucose and advanced glycation end products (AGE) and the relationship between AGE and retinal changes in vivo, we studied the time course of retinopathy over 12 months in trypsin digest preparations and measured glycaemia and retinal AGE in spontaneous diabetic hamsters of mild (MD) and severe (SD) phenotypes. Blood glucose levels were elevated in MD (9.44 ± 0.76 mmol/l) and in SD (3 months: 24.3 ± 1.4 mmol/l; 12 months: 31.7 ± 0.8 mmol/l) over non-diabetic controls (NC: 7.15 ± 0.25 mmol/l; p 〈 0.05 or less vs MD; p 〈 0.001 vs SD). Similar relations were found for HbA1. Retinal AGE in mild diabetes was 405 ± 11.3 arbitrary units (AU) (NC 245 ± 7.7; p 〈 0.01) after 3 months and remained unchanged. A non-linear increase of AGE over time was found in severe hyperglycaemic hamsters (466 ± 21 AU after 3 months and 758 ± 21 AU after 12 months; p 〈 0.001 vs MD). Pericyte loss in mild diabetes progressed from –26 % after 3 months to –41 % after 12 months (p 〈 0.001 vs NC). Whereas the initial pericyte loss in severely diabetic hamsters was identical to the mildly diabetic group, a higher degree of pericyte loss occurred after 12 months (–57 %; p 〈 0.05 vs MD). Endothelial cell numbers remained unaffected by mild hyperglycaemia, but significantly increased over time in severe diabetes reaching 31.7 % above controls after 12 months (p 〈 0.001 vs NC and MD). Microaneurysms were absent in all retinae examined. Acellular capillary segments were increased in mild diabetes (3.83 ± 0.31 per mm2 of retinal area) and severe diabetes (7.83 ± 0.73) over controls (1.0 ± 0.23). These data suggest that a threshold of glycaemia might exist above which AGE removal systems become saturated. Pericyte loss and acellular capillary formation are associated with mild increases in blood glucose and AGE levels while endothelial cell proliferation requires higher glucose and AGE levels. [Diabetologia (1998) 41: 165–170]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250050885
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    Paper (German National Licenses)
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