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  • 1990-1994  (2)
  • Experimental diabetic neuropathy  (1)
  • Key words Diabetes mellitus, complications, brain, cerebral dysfunction, cognitive dysfunction, pathogenesis, cerebral blood flow, hypoglycaemia, hyperglycaemia, review.  (1)
Material
Years
  • 1990-1994  (2)
Year
Keywords
  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Diabetologia 37 (1994), S. 643-650 
    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
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  • 2
    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
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