Elevated serum semicarbazide-sensitive amine oxidase activity in non-insulin-dependent diabetes mellitus: Correlation with body mass index and serum triglyceride

Metabolism ◽  
1999 ◽  
Vol 48 (1) ◽  
pp. 113-117 ◽  
Author(s):  
Zsuzsa Mészáros ◽  
Tamás Szombathy ◽  
Laura Raimondi ◽  
István Karádi ◽  
László Romics ◽  
...  
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.


1996 ◽  
Vol 24 (2) ◽  
pp. 209-213 ◽  
Author(s):  
J Katoh ◽  
Y Hara ◽  
M Kmvsu ◽  
J Miyaji ◽  
K Nabutaki

Exercise testing was used to examine 19 cardiorespiratory diabetes mellitus patients, aged 32 – 68 years (body mass index, 27.8 ± 4.8 kg/m2), and 16 healthy volunteers, aged 23 – 57 years (body mass index, 22.7 ± 2.5 kg/m2). A graded cycling exercise test was done, monitoring gas exchange, ventilation and heart rate. Values were significantly higher in the non-insulin-dependent diabetes mellitus (NIDDM) patients than in the controls for fasting blood glucose ( P < 0.01), glycosylated haemoglobin ( P < 0.01), body weight ( P < 0.05) and body mass index ( P < 0.05). The exercise testing produced values that were significantly lower in the patients with NIDDM than in the controls for percentage oxygen uptake ( P < 0.05), maximum load ( P < 0.05), maximum metabolic equivalent ( P < 0.01) and maximum oxygen uptake per unit body weight ( P < 0.01). Ventilatory capacity and forced expiratory volume at 1 sec did not differ significantly in the two groups. These results suggest that general fitness is diminished due to reduced cardiorespiratory function in patients with NIDDM.


1998 ◽  
Vol 18 (5) ◽  
pp. 3059-3068 ◽  
Author(s):  
Ying-Hue Lee ◽  
Brian Sauer ◽  
Frank J. Gonzalez

ABSTRACT Mice deficient in hepatocyte nuclear factor 1 alpha (HNF-1α) were produced by use of the Cre-loxP recombination system. HNF-1α-null mice are viable but sterile and exhibit a phenotype reminiscent of both Laron-type dwarfism and non-insulin-dependent diabetes mellitus (NIDDM). In contrast to an earlier HNF-1α-null mouse line that had been produced by use of standard gene disruption methodology (M. Pontoglio, J. Barra, M. Hadchouel, A. Doyen, C. Kress, J. P. Bach, C. Babinet, and M. Yaniv, Cell 84:575–585, 1996), these mice exhibited no increased mortality and only minimal renal dysfunction during the first 6 months of development. Both dwarfism and NIDDM are most likely due to the loss of expression of insulin-like growth factor I (IGF-I) and lower levels of insulin, resulting in stunted growth and elevated serum glucose levels, respectively. These results confirm the functional significance of the HNF-1α regulatory elements that had previously been shown to reside in the promoter regions of both the IGF-I and the insulin genes.


Sign in / Sign up

Export Citation Format

Share Document