Effects of rosiglitazone and metformin on inflammatory markers and adipokines: decrease in interleukin-18 is an independent factor for the improvement of homeostasis model assessment-beta in type 2 diabetes mellitus.
OBJECTIVE
We examined the individual pharmacological effects of the addition of rosiglitazone and metformin to glimepiride on inflammatory markers and adipokines in patients with type 2 diabetes mellitus. We analysed the relationships between these variables, the measurements of insulin sensitivity and beta-cell function in patients treated with rosiglitazone plus glimepiride.


METHODS
One hundred twenty (120) patients with type 2 diabetes mellitus were randomized and treated with glimepiride plus rosiglitazone or glimepiride plus metformin for 12 weeks. The plasma concentrations of the inflammatory markers and adipokines were measured at baseline and after 12 weeks.


METHODS
Markers of insulin sensitivity and beta-cell function were determined by the quantitative insulin sensitivity check index (QUICKI) and the homeostasis model assessment of beta-cell function (HOMA-beta), respectively. Plasma concentrations of adiponectin were measured by radioimmunoassay. Plasma concentrations of resistin, tumour necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6) and interleukin-18 (IL-18) were measured using ELISA.


RESULTS
Improvements in fasting insulin level, QUICKI and HOMA-beta were noted in the rosiglitazone-treated group. Only the QUICKI value improved in the metformin-treated group. Adiponectin concentrations significantly increased in the rosiglitazone-treated group after 12 weeks. Significant decreases in resistin, C-reactive protein, TNF-alpha, IL-6 and IL-18 were seen in the rosiglitazone-treated patients but not in the metformin-treated patients. The independent risk factor for the HOMA-beta change according to stepwise multivariate regression analysis was a change in IL-18.


CONCLUSIONS
Rosiglitazone, but not metformin, improved the plasma concentrations of inflammatory markers and adipokines in patients with type 2 diabetes mellitus. A decrease in IL-18 is an independent factor for the improvement of HOMA-beta in type 2 diabetes mellitus.
Kim
Hyeong Jin
HJ
Division of Endocrinology, Department of Internal Medicine, Kwandong University College of Medicine, Myongji Hospital, Koyang, Korea.
Kang
Eun Seok
ES
Kim
Dae Jung
DJ
Kim
So Hun
SH
Ahn
Chul Woo
CW
Cha
Bong Soo
BS
Nam
Moonsuk
M
Chung
Choon Hee
CH
Lee
Kwan Woo
KW
Nam
Chung Mo
CM
Lee
Hyun Chul
HC
D052242:Adiponectin / Q000097:blood; D000704:Analysis of Variance; D015415:Biomarkers / Q000097:blood; D001786:Blood Glucose / Q000032:analysis; D002097:C-Reactive Protein / Q000032:analysis; D003924:Diabetes Mellitus, Type 2 / Q000097:blood / Q000188:drug therapy* / Q000276:immunology; D004334:Drug Administration Schedule; D006706:Homeostasis; D006801:Humans; D007004:Hypoglycemic Agents / Q000627:therapeutic use*; D007328:Insulin / Q000097:blood; D007333:Insulin Resistance; D020382:Interleukin-18 / Q000097:blood*; D015850:Interleukin-6 / Q000097:blood; D008687:Metformin / Q000627:therapeutic use*; D015999:Multivariate Analysis; D052243:Resistin / Q000097:blood; D000077154:Rosiglitazone; D013453:Sulfonylurea Compounds / Q000627:therapeutic use*; D045162:Thiazolidinediones / Q000627:therapeutic use*; D013997:Time Factors; D014409:Tumor Necrosis Factor-alpha / Q000097:blood
D052242:Adiponectin; D015415:Biomarkers; D001786:Blood Glucose; D007004:Hypoglycemic Agents; D007328:Insulin; D020382:Interleukin-18; D015850:Interleukin-6; D052243:Resistin; D013453:Sulfonylurea Compounds; D045162:Thiazolidinediones; D014409:Tumor Necrosis Factor-alpha; D000077154:Rosiglitazone; C057619:glimepiride; D002097:C-Reactive Protein; D008687:Metformin