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  • 1
    Electronic Resource
    Electronic Resource
    Renal collagen glucosyltransf erase activity following islet transplantation in streptozotocin-diabetic rats (1981)
    Springer
    Diabetologia 21 (1981), S. 428-429 
    Details
    ISSN: 1432-0428
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00252697
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  • 2
    Electronic Resource
    Electronic Resource
    EASD news section (1993)
    Springer
    Diabetologia 36 (1993), S. 47-53 
    Details
    ISSN: 1432-0428
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00401073
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  • 3
    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
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  • 4
    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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  • 5
    Electronic Resource
    Electronic Resource
    Effect of long-term dietary protein intake on glucose metabolism in humans (2000)
    Springer
    Diabetologia 43 (2000), S. 1257-1265 
    Details
    ISSN: 1432-0428
    Keywords: Keywords Endogeneous insulin, hepatic glucose production, high protein diet, normal protein diet.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Aims/hypothesis. A meal rich in protein stimulates insulin secretion. Long-term effects of dietary protein on insulin release and glucose metabolism are, however, still not known. Our study focussed on the effect of different protein intake on pancreatic insulin secretion capacity, glycogen turnover and gluconeogenesis.¶Methods. Subjects with constant (6 months) dietary protein of 1.87 ± 0.26 g · kg–1· day–1 (1.25–2.41) named high protein group and with 0.74 ± 0.08 (0.57–0.80), normal protein group, were identified by a food questionnaire and were matched (n = 9) according to sex, age and calorie intake. They underwent an intravenous glucose tolerance test and a euglycaemic hyperinsulinaemic clamp with infusion of [6,6-2H2]-glucose combined with indirect calorimetry. To estimate net gluconeogenesis the usual diet was enriched by deuterated water or U-[13C6]-glucose and breath and plasma were sampled.¶Results. Glucose-stimulated insulin secretion was increased in the high protein group (516 ± 45 pmol/l vs 305 ± 32, p = 0.012) due to reduced glucose threshold of the endocrine beta cells (4.2 ± 0.5 mmol/l vs 4.9 ± 0.3, p = 0.031). Endogeneous glucose output was increased by 12 % (p = 0.009) at 40 pmol/l plasma insulin in the high protein group, but not at higher insulin concentration whereas overall glucose disposal was reduced. Fasting plasma glucagon was 34 % increased in the high protein group (p = 0.038). Fractional gluconeogenesis was increased by 40 % in subjects receiving a high protein diet as determined by both methods.¶Conclusion/interpretation. High protein diet is accompanied by increased stimulation of glucagon and insulin within the endocrine pancreas, high glycogen turnover and stimulation of gluconeogenesis. [Diabetologia (2000) 43: 1257–1265]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250051521
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  • 6
    Electronic Resource
    Electronic Resource
    Antibodies to the Mr 64,000 (64K) protein in islet cell antibody positive non-diabetic individuals indicate high risk for impaired Beta-cell function (1992)
    Springer
    Diabetologia 35 (1992), S. 550-554 
    Details
    ISSN: 1432-0428
    Keywords: Population study ; 64K antibodies ; islet cell antibodies ; complement-fixing islet cell antibodies ; insulin autoantibodies ; HLA
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary A prospective study of a normal childhood population identified 44 islet cell antibody positive individuals. These subjects were typed for HLA DR and DQ alleles and investigated for the presence of antibodies to the Mr 64,000 (64K) islet cell antigen, complement-fixing islet cell antibodies and radiobinding insulin autoantibodies to determine their potency in detecting subjects with impaired Beta-cell function. At initial testing 64K antibodies were found in six of 44 islet cell antibody positive subjects (13.6%). The same sera were also positive for complement-fixing islet cell antibodies and five of them had insulin autoantibodies. During the follow-up at 18 months, islet cell antibodies remained detectable in 50% of the subjects studied. In all six cases who were originally positive, 64K antibodies were persistently detectable, whereas complement-fixing islet cell antibodies became negative in two of six and insulin autoantibodies in one of five individuals. HLA DR4 (p 〈 0.005) and absence of asparic acid (Asp) at position 57 of the HLA DQ β chain (p 〈 0.05) were significantly increased in subjects with 64K antibodies compared with control subjects. Of 40 individuals tested in the intravenous glucose tolerance test, three had a first phase insulin response below the first percentile of normal control subjects. Two children developed Type 1 (insulin-dependent) diabetes mellitus after 18 and 26 months, respectively. Each of these subjects was non-Asp homozygous and had persistent islet cell and 64K antibodies. We conclude that 64K antibodies, complement-fixing islet cell antibodies and insulin autoantibodies represent sensitive serological markers in assessing high risk for a progression to Type 1 diabetes in islet cell antibody positive non-diabetic individuals.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00400483
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  • 7
    Electronic Resource
    Electronic Resource
    Effects of ganglioside (Cronassial) treatment on MHC Ia antigen expression and allograft survival of pancreatic islets in diabetic rats (1990)
    Springer
    Diabetologia 33 (1990), S. 112-114 
    Details
    ISSN: 1432-0428
    Keywords: Gangliosides ; islet transplantation ; immunosuppression ; immunomodulation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Streptozotocin-diabetic BdII rats were treated daily with 20 mg/kg body weight gangliosides for ten days beginning two days before transplantation. This treatment did not prolong allograft survival of untreated Lewis islets. Culture treatment of isolated Lewis islets with gangliosides (100 μg/ml in RPMI 1640) for one day resulted in a significant reduction of MHC Ia antigen positive cells but not of class I antigens within the islets. Tranplantation of the ganglioside pretreated islets into non-immunosuppressed BdII recipients prolonged allograft survival to 12 days only in one of five animals.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00401049
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  • 8
    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
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  • 9
    Electronic Resource
    Electronic Resource
    Transduction of non-dividing adult human pancreatic beta cells by an integrating lentiviral vector (1998)
    Springer
    Diabetologia 41 (1998), S. 736-739 
    Details
    ISSN: 1432-0428
    Keywords: Keywords Lentiviral vector ; retrovirus ; human islet beta-cell ; gene transfer ; transplantation.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Pancreatic islet cells are terminally differentiated endocrine cells and are refractory to stable infection by retroviral vectors, which require the breakdown of the nuclear membrane during cell division in order to insert the transgene into the host cell genome. Thus, attempts to render beta-cell allografts less immunogenic have had to rely on stable transfection of surrogate cells. Similarly, this problem has precluded the development of conditionally immortalized human beta cells for clinical allotransplantation. In this report, we demonstrate that adult human islet beta cells can be transduced by a new three-plasmid integrating lentiviral vector with an efficiency of 62 ± 1.8 % at a multiplicity of infection (MOI) of 2.5 in vitro. This work makes genetic engineering of adult human pancreatic beta cells possible for the first time, allowing strategies to render beta-cell allografts non-immunogenic to be optimized and to creating conditionally immortalized human beta cells for clinical transplantation. [Diabetalogia (1998) 41: 736–739]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250050977
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  • 10
    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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