title: [Serum stefin A in patients with type 2 diabetes].
abstract: Stefin A is the low-molecular, intracellular inhibitor of the human lysosomal cysteine proteinases, cathepsins B, H and L. The concentration of this inhibitor in plasma and in other biological fluids shows not only local expression and secretion but also immunity of the whole organism. The aim of our study was to examine if concentration of stefin A in plasma of patients with diabetes type 2 is different than in healthy subjects, depends on vascular complications, body mass index, glycaemic control and whether exists the relationship between activities of cathepsin B (CB) as well as N-acetyl-beta-D-glucosaminidase (NAG). In plasma of 62 diabetic patients and 14 control subjects, concentration of stefin A (using ELISA test) and activities of CB and NAG (using fluorescence methods) were investigated. Concentration of stefin A (4.95 micrograms/l) in comparison to control (2.80 micrograms/l) increased statistically significantly (p < 0.05). The highest increase of stefin A was discovered in patients with macrovascular complication (7.70 micrograms/l) and was significantly different (p < 0.01) in comparison with control group and patients with microangiopathy as well as both types of complications (micro- and macroangiopathy). Significantly higher concentration of stefin A was noted in patients with overweight and obesity (5.50 micrograms/l and 6.05 micrograms/l). No influence of glycaemic short and long term control on concentration of this inhibitor was observed. In patients divided into subgroups according to increasing plasma NAG activity, increase of stefin A was noted successively from subgroup K2 to K4 (NAG from 8.80 U/l to above 12.82 U/l). The results indicate contribution of stefin A in pathogenesis of vascular complications in patients with diabetes type 2 and its relationship with obesity.
authors.affiliation: Katedra i Zakład Biochemii Farmaceutycznej we Wrocławiu. piwowar@bf.uni.wroc.pl
authors.forename: Agnieszka
authors.initials: A
authors.lastname: Piwowar
authors.forename: Izabela
authors.initials: I
authors.lastname: Fus
authors.forename: Maria
authors.initials: M
authors.lastname: Kanapik-Kordecka
authors.forename: Maria
authors.initials: M
authors.lastname: Warwas
mesh_terms: D000118:Acetylglucosaminidase / Q000097:blood; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D001786:Blood Glucose / Q000378:metabolism; D015992:Body Mass Index; D016022:Case-Control Studies; D002401:Cathepsin B / Q000097:blood; D055312:Cystatin A; D015891:Cystatins / Q000097:blood*; D015853:Cysteine Proteinase Inhibitors / Q000097:blood; D003924:Diabetes Mellitus, Type 2 / Q000097:blood* / Q000201:enzymology; D003925:Diabetic Angiopathies / Q000097:blood; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D009765:Obesity / Q000097:blood / Q000150:complications*; D012307:Risk Factors; D013997:Time Factors
chemical_list: D001786:Blood Glucose; D055312:Cystatin A; D015891:Cystatins; D015853:Cysteine Proteinase Inhibitors; C026407:CSTA protein, human; D000118:Acetylglucosaminidase; D002401:Cathepsin B