ISSN:
1432-0428
Keywords:
Key words Diabetes
;
diabetic neuropathy
;
electrolytes
;
hyperglycaemia
;
nerve conduction
;
somatostatin.
Source:
Springer Online Journal Archives 1860-2000
Topics:
Medicine
Notes:
Summary Insufficient metabolic control in diabetes mellitus is associated with a reversible reduction in nerve conduction velocity, but the mechanism behind this phenomenon is unknown. To examine the effect of acute hyperglycaemia on nerve conduction eight non-diabetic men (20–49 years of age) with no signs of peripheral neuropathy were studied before and after 3 h of hyperglycaemic clamping (plasma glucose ≈ 15 mmol/l), while insulin secretion was suppressed by somatostatin [Study 1]. Nerve conduction velocity, as determined in the proximal part of the median nerve, fell by 2.8 ± 3.0 m/s (2p-value: 0.033). However, during euglycaemic clamping (plasma glucose ≈ 5 mmol/l) in five non-diabetic men (19–38 years of age) infused solely with somatostatin [Study 2], a comparable decrement in nerve conduction velocity was found (1.7 ± 1.3 m/s, 2p-value: 0.043). In both studies relative hypoinsulinaemia was present. Serum-sodium decreased significantly (143 ± 1 mmol/l vs 137 ± 1 mmol/l [Study 1] and 143 ± 1 mmol/l vs 142 ± 2 mmol/l [Study 2]), while serum-potassium increased. In conclusion, the slight but significant reduction in nerve conduction velocity observed in both studies appears to be correlated to electrolyte changes. However, an effect of hypersomatostatinaemia or the hormonal changes associated with this cannot be excluded, while short-term hyperglycaemia per se seems to be without effect on nerve conduction velocity. [Diabetologia (1994) 37: 1216–1220]
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1007/BF00399795
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