Plasma Semicarbazide-Sensitive Amine Oxidase Activity is Elevated in Diabetes Mellitus and Correlates with Glycosylated Haemoglobin

1995 ◽  
Vol 88 (6) ◽  
pp. 675-679 ◽  
Author(s):  
Frans Boomsma ◽  
Frans H. M. Derkx ◽  
Anton H. van den Meiracker ◽  
Arie J. man in't Veld ◽  
Maarten A. D. H. Schalekamp

1. Semicarbazide-sensitive amine oxidase is a common name for a group of heterogeneous amine oxidases which are present in various mammalian tissues, especially in vascular smooth muscle cells, cartilage and adipose tissue, but also in plasma. 2. Plasma semicarbazide-sensitive amine oxidase activity was elevated in a group of 104 patients with insulin-dependent diabetes mellitus compared with normal control subjects (555 ± 172 versus 352 ± 102 m-units/l, P < 0.0005). 3. Plasma semicarbazide-sensitive amine oxidase activity was higher in subgroups with either retinopathy or nephropathy or both [583 ± 116 (n = 34), 581 ± 229 (n = 10) and. 646 ± 249 m-units/l (n = 19), respectively] than in the subgroup without overt complications [486 ± 129 m-units/l (n = 41), P < 0.005]. 4. Plasma semicarbazide-sensitive amine oxidase activity was positively correlated with plasma glycosylated haemoglobin (r = 0.40; P < 0.0001) and with log urinary albumin excretion (r = 0.26; P < 0.025). 5. The possibility that semicarbazide-sensitive amine oxidase, by its conversion of endogenous amines like methylamine and aminoacetone into cytotoxic aldehydes, plays a role in the development of microvascular complications in diabetes mellitus, needs further investigation.

1995 ◽  
Vol 23 (6) ◽  
pp. 467-472 ◽  
Author(s):  
S Okada ◽  
K Ishii ◽  
H Hamada ◽  
K Ichiki ◽  
S Tanokuchi ◽  
...  

The possibility that glycosylated haemoglobin levels and/or blood pressure might correlate with cardiac sympathetic neuropathy and/or diabetic somatic neuropathy was investigated in patients with non-insulin-dependent diabetes mellitus. Sympathetic nerve function was quantified by analysis of [123I]metaiodobenzylguanidine accumulation in the cardiac muscle. Somatic nerve function was assessed by measuring the motor nerve conduction velocities of the peroneal and tibial nerves, and the sensory nerve conduction velocity of the sural nerve. None of the parameters of cardiac sympathetic neuropathy or diabetic somatic neuropathy showed any correlation with blood pressure, nor was there any evidence of a correlation between cardiac sympathetic neuropathy and glycosylated haemoglobin levels; there was, however, a significant correlation between diabetic somatic neuropathy (as indicated by tibial nerve conduction velocity) and glycosylated haemoglobin levels. The results are consistent with the view that different mechanisms are involved in the two types of neuropathies.


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