Concentration of the complement activation product, acylation-stimulating protein, is related to C-reactive protein in patients with type 2 diabetes.
Type 2 diabetes is characterized by increased acute phase serum proteins. We wanted to study how these proteins are related to complement activation in type 2 diabetes and how improvement of glycemic control affects them or complement activation. A total of 29 type 2 diabetic patients (age, 55.2 +/- 1.8 years, glycosylated hemoglobin [HbA(1c)] 8.9% +/- 0.2%, body mass index [BMI] 30.9 +/- 0.8 kg/m(2), duration 5.9 +/- 1.3 years) participated in the study. They were previously treated either with diet alone or in combination with 1 oral antihyperglycemic medication. After a period of at least 4 weeks run-in on diet only, the patients were randomized to pioglitazone, glibenclamide, or placebo. Blood samples were taken before the treatments and at the end of the 6-month therapy. Basal C-reactive protein (CRP) level was related to acylation-stimulating protein (ASP) concentration (r =.55, P <.01), and many acute phase serum protein concentrations were associated with each other. The treatment reduced HbA(1c) level in the pioglitazone (from 9.1 +/- 0.3% to 8.0 +/- 0.5%, P <.05) and glibenclamide (from 8.9 % +/- 0.3% to 7.7% +/- 0.2%, P <.05) groups. Glibenclamide treatment was associated with a reduction in alpha-1-antitrypsin (P <.05), ceruloplasmin (P <.01), and complement C3 protein (C3) (P <.05). Although ASP did not change significantly in any of the treatment subgroups, in the whole patient population, the change in HbA(1c) during the treatments correlated positively with the change in ASP, (r =.43, P <.05). The changes in many acute phase serum proteins and ASP were related to each other. In conclusion, (1) inflammatory factors and complement activation are associated in patients with type 2 diabetes, and (2) changes in hyperglycemia are related to changes in the concentration of the complement activation product, ASP.
Ebeling
P
P
Department of Medicine, Helsinki University Central Hospital, Helsinki, Finland.
Teppo
A M
AM
Koistinen
H A
HA
Koivisto
V A
VA
D000209:Acute-Phase Proteins / Q000032:analysis; D001786:Blood Glucose / Q000032:analysis; D001798:Blood Proteins / Q000032:analysis*; D002097:C-Reactive Protein / Q000032:analysis*; D003167:Complement Activation / Q000502:physiology*; D003176:Complement C3 / Q000032:analysis; D015926:Complement C3a / Q000031:analogs & derivatives*; D003924:Diabetes Mellitus, Type 2 / Q000097:blood* / Q000188:drug therapy; D004311:Double-Blind Method; D005260:Female; D005905:Glyburide / Q000627:therapeutic use; D006442:Glycated Hemoglobin / Q000032:analysis; D006801:Humans; D007004:Hypoglycemic Agents / Q000627:therapeutic use; D008297:Male; D008875:Middle Aged; D009994:Osmolar Concentration; D000077205:Pioglitazone; D013844:Thiazoles / Q000627:therapeutic use; D045162:Thiazolidinediones
D000209:Acute-Phase Proteins; D001786:Blood Glucose; D001798:Blood Proteins; D002097:C-Reactive Protein; D003176:Complement C3; D015926:Complement C3a; D005905:Glyburide; D006442:Glycated Hemoglobin; D007004:Hypoglycemic Agents; D000077205:Pioglitazone; D013844:Thiazoles; D045162:Thiazolidinediones; C044541:complement C3a, des-Arg-(77)-