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  • 1
    Electronic Resource
    Electronic Resource
    Secondary intervention with aminoguanidine retards the progression of diabetic retinopathy in the rat model (1995)
    Springer
    Diabetologia 38 (1995), S. 656-660 
    Details
    ISSN: 1432-0428
    Keywords: Key words Diabetic retinopathy ; rat model ; aminoguanidine ; glycation ; secondary intervention ; islet transplantation.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Primary prevention with aminoguanidine – an inhibitor of advanced glycation end product (AGE) formation – has been successfully employed to prevent diabetic retinopathy in the rat. However, it is unknown whether inhibition of AGE formation is still effective in a secondary intervention strategy. The present study addresses this question by comparing secondary intervention with aminoguanidine with syngeneic islet transplantation in the rat model. After 6 months of diabetes, one group was treated with aminoguanidine (50 mg/100 ml drinking water; D-AG) while another group received syngeneic transplantation of collagenase-ficoll isolated islets by intraportal injection (Tx). After an additional 4 months, both groups were compared to a normal (NC 10) and diabetic (DC 10) control group. Retinal autofluorescence was increased 2.5-fold after 6 months and increased 3.7-fold after 10 months of diabetes (p 〈 0.001). Aminoguanidine and islet Tx retarded the further accumulation of autofluorescence equally (p 〈 0.001 vs DC 10), although the values were higher than those observed in DC at 6 months (p 〈 0.001). Diabetes was associated with a 2.7-fold increase in acellular capillaries after 6 months and a 4.1-fold increase after 10 months. Treatment with aminoguanidine or islet Tx reduced but did not completely attenuate the progression of vascular occlusion (p 〈 0.001 vs DC 10; D-AG vs DC 6, p 〈 0.05; Tx vs DC 6, p 〈 0.01). Both treatments reduced endothelial proliferation (22.4 % after 10 months; p 〈 0.001) and completely arrested pericyte dropout (40 % after 10 months; p 〈 0.001). These data demonstrate that aminoguanidine is as effective as islet transplantation in retarding the progression of diabetic retinopathy in a secondary prevention setting. [Diabetologia (1995) 38: 656–660]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00401835
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
  • 2
    Electronic Resource
    Electronic Resource
    Secondary intervention with aminoguanidine retards the progression of diabetic retinopathy in the rat model (1995)
    Springer
    Diabetologia 38 (1995), S. 656-660 
    Details
    ISSN: 1432-0428
    Keywords: Diabetic retinopathy ; rat model ; aminoguanidine ; glycation ; secondary intervention ; islet transplantation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Primary prevention with aminoguanidine — an inhibitor of advanced glycation end product (AGE) formation — has been successfully employed to prevent diabetic retinopathy in the rat. However, it is unknown whether inhibition of AGE formation is still effective in a secondary intervention strategy. The present study addresses this question by comparing secondary intervention with aminoguanidine with syngeneic islet transplantation in the rat model. After 6 months of diabetes, one group was treated with aminoguanidine (50 mg/100 ml drinking water; D-AG) while another group received syngeneic transplantation of collagenase-ficoll isolated islets by intraportal injection (Tx). After an additional 4 months, both groups were compared to a normal (NC 10) and diabetic (DC 10) control group. Retinal autofluorescence was increased 2.5-fold after 6 months and increased 3.7-fold after 10 months of diabetes (p〈0.001). Aminoguanidine and islet Tx retarded the further accumulation of autofluorescence equally (p〈0.001 vs DC 10), although the values were higher than those observed in DC at 6 months (p〈0.001). Diabetes was associated with a 2.7-fold increase in acellular capillaries after 6 months and a 4.1-fold increase after 10 months. Treatment with aminoguanidine or islet Tx reduced but did not completely attenuate the progression of vascular occlusion (p〈0.001 vs DC 10; D-AG vs DC 6, p〈0.05; Tx vs DC 6, p〈0.01). Both treatments reduced endothelial proliferation (22.4% after 10 months; p〈0.001) and completely arrested pericyte dropout (40% after 10 months; p〈0.001). These data demonstrate that aminoguanidine is as effective as islet transplantation in retarding the progression of diabetic retinopathy in a secondary prevention setting.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00401835
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 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
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
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