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  • Insulin treatment  (1)
  • Key words Diabetic retinopathy  (1)
  • 1
    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
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  • 2
    ISSN: 1432-5233
    Keywords: Diabetic cardiomyophaty ; Cardiac metabolism ; Cardiac performance ; Insulin treatment ; Islet transplantation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The aim of the present experimental study in the rat heart was to assess cardiac performance and metabolism in mild diabetes of 2 months' duration (postprandial blood sugar levels of 307±101 mg/dl and nearly normal fasting blood glucose of 102±40 mg/dl) using the working rat heart model at physiological workload with a perfusion time of 60 min. We also compared the effect of two forms of therapy for diabetes, islet transplantation and insulin therapy (s.c.), after 2 months. A 36% reduction in glucose utilization is metabolically characteristic for the diabetic heart, mainly caused by a 55% reduced glucose uptake (P〈0.001), but also by a nearly twofold increased lactate and pyruvate production (P〈0.001). This reduced carbohydrate metabolism is accompanied by a 37% reduction of oxygen uptake (P〈0.001) as well as a significant reduction in myocardial ATP and CP levels (P〈0.001), resulting in a significantly reduced cardiac output (P〈0.001). Moreover, the balance of energy reveals that the diabetic heart obtains 46% of its energy requirements for 1 h from endogenous glycogen, whereas the control heart obtains 91% of its energy needs (i.e. preferentially) from exogenous glucose (only 9% from endogenous glycogen). Both investigated therapeutic interventions led to a complete reversibility of the hemodynamic and metabolic alterations, indicating that the cause of diabetic cardiomyopathy in this model of mild and short-term diabetes is due to a defect in cardiac carbohydrate metabolism, which is correctable by insulin administration.
    Type of Medium: Electronic Resource
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