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  • Diabetes mellitus  (2)
  • Experimental diabetic neuropathy  (1)
  • Key words Diabetes mellitus, complications, brain, cerebral dysfunction, cognitive dysfunction, pathogenesis, cerebral blood flow, hypoglycaemia, hyperglycaemia, review.  (1)
Source
Material
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Keywords
  • 1
    Electronic Resource
    Electronic Resource
    Cerebral function in diabetes mellitus (1994)
    Springer
    Diabetologia 37 (1994), S. 643-650 
    Details
    ISSN: 1432-0428
    Keywords: Diabetes mellitus ; complications ; brain ; cerebral dysfunction ; cognitive dysfunction ; pathogenesis ; cerebral blood flow ; hypoglycaemia ; hyperglycaemia ; review
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Diabetes mellitus is a common metabolic disorder associated with chronic complications such as nephropathy, angiopathy, retinopathy and peripheral neuropathy. Diabetes is not often considered to have deleterious effects on the brain. However, long-term diabetes results in a variety of subtle cerebral disorders, which occur more frequently than is commonly believed. Diabetic cerebral disorders have been demonstrated at a neurochemical, electrophysiological, structural and cognitive level; however, the pathogenesis is still not clear. Probably alterations in cerebral blood supply and metabolic derangements play a role, as they do in the pathogenesis of diabetic neuropathy. Furthermore, the brain is also affected by recurrent episodes of hypoglycaemia and poor metabolic control. We describe herein the cerebral manifestations of diabetes and discuss the putative pathogenetic mechanisms.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00417687
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
  • 2
    Electronic Resource
    Electronic Resource
    Cerebral function in diabetes mellitus (1994)
    Springer
    Diabetologia 37 (1994), S. 643-650 
    Details
    ISSN: 1432-0428
    Keywords: Key words Diabetes mellitus, complications, brain, cerebral dysfunction, cognitive dysfunction, pathogenesis, cerebral blood flow, hypoglycaemia, hyperglycaemia, review.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Diabetes mellitus is a common metabolic disorder associated with chronic complications such as nephropathy, angiopathy, retinopathy and peripheral neuropathy. Diabetes is not often considered to have deleterious effects on the brain. However, long-term diabetes results in a variety of subtle cerebral disorders, which occur more frequently than is commonly believed. Diabetic cerebral disorders have been demonstrated at a neurochemical, electrophysiological, structural and cognitive level; however, the pathogenesis is still not clear. Probably alterations in cerebral blood supply and metabolic derangements play a role, as they do in the pathogenesis of diabetic neuropathy. Furthermore, the brain is also affected by recurrent episodes of hypoglycaemia and poor metabolic control. We describe herein the cerebral manifestations of diabetes and discuss the putative pathogenetic mechanisms. [Diabetologia (1994) 37: 643–650]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00417687
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 3
    Electronic Resource
    Electronic Resource
    Potential use of glutathione for the prevention and treatment of diabetic neuropathy in the streptozotocin-induced diabetic rat (1992)
    Springer
    Diabetologia 35 (1992), S. 813-817 
    Details
    ISSN: 1432-0428
    Keywords: Diabetes mellitus ; diabetic neuropathy ; oxidative stress ; glutathione ; nerve conduction velocity ; streptozotocin rat model
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary It has been shown that parameters of oxidative stress are increased in experimental diabetic neuropathy. The glutathione redox system is one of the intracellular scavenger systems for neutralizing free oxygen radicals. In this investigation we studied the effect of glutathione-treatment on the development of diabetic neuropathy in streptozotocin-induced diabetic rats by measuring sensory and motor nerve conduction velocities. The total study period was 10 weeks. Four groups of rats were studied: Group 1 consisted of non-diabetic, age-matched control rats; Group 2, of diabetic rats treated with placebo from week 0 to 10; Group 3, of diabetic rats treated with 200 mg glutathione/kg body weight i. v. two times per week from weeks 0 to 10; and Group 4, of diabetic rats treated with placebo from weeks 0 to 4 and as Group 3 from weeks 4 to 10. The sensory and motor nerve conduction velocity of rats treated prophylactically with glutathione (Group 3) were significantly different from those of rats treated with placebo (Group 2) or with glutathione administered at a later time point (Group 4). Complete restoration of sensory and motor nerve conduction velocity was not reached. There was a significant improvement in motor nerve conduction velocity from weeks 4 to 6 (p〈0.005), but not in sensory nerve conduction velocity in the delayed treatment group (Group 4). In conclusion, treatment with glutathione, a free radical scavenger, is partially effective in the prevention of diabetic neuropathy in streptozotocin-induced diabetic rats, but is of limited value when the neuropathy is already present.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00399926
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    Paper (German National Licenses)
    Fulltext
  • 4
    Electronic Resource
    Electronic Resource
    ACTH4–9 analogue ORG 2766 can improve existing neuropathy in streptozocin-induced diabetic rats (1993)
    Springer
    Acta diabetologica 30 (1993), S. 21-24 
    Details
    ISSN: 1432-5233
    Keywords: ACTH4–9 ; Experimental diabetic neuropathy ; Neuropeptide
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The effect of treatment of an existing neuropathy in streptozocin-induced diabetic rats with the ACTH4–9 analogue ORG 2766 was examined. Four groups of rats were studied: group 1 consisted of age-matched, non-diabetic controls and groups 2, 3 and 4 of diabetic rats. Sensory and motor nerve conduction velocity (SNCV and MNCV) were measured at weeks 0, 4, 6, 8 and 10. Four weeks after the administration of streptozocin (STZ) all diabetic rats showed a significant slowing of SNCV and MNCV. Treatment was then started: group 2 was treated with placebo, group 3 with a low dos (1 μg) of ACTH4–9 subcutaneously every 48h, and group 4 with a high dos (10 μg) of ACTH4–9 subcutaneously every 48 h. The animals treated with the high peptide dosage showed a significant improvement in both SNCV and MNCV from week 6 onwards, whereas this beneficial effect was not demonstrated for the rats treated with the low dosage. This study demonstrates that the ACTH4–9 analogue ORG 2766 can ameliorate existing diabetic neuropathy in STZ-induced diabetic rats.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00572869
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
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