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

Hyeong Jin Kim, Eun Seok Kang, Dae Jung Kim, So Hun Kim, Chul Woo Ahn, Bong Soo Cha, Moonsuk Nam, Choon Hee Chung, Kwan Woo Lee, Chung Mo Nam, Hyun Chul Lee

Research output: Contribution to journalArticle

55 Citations (Scopus)

Abstract

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 β-cell function in patients treated with rosiglitazone plus glimepiride. Design and patients: 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. Measurements: Markers of insulin sensitivity and β-cell function were determined by the quantitative insulin sensitivity check index (QUICKI) and the homeostasis model assessment of β-cell function (HOMA-β), respectively. Plasma concentrations of adiponectin were measured by radioimmunoassay. Plasma concentrations of resistin, tumour necrosis factor-α (TNF-α), interleukin-6 (IL-6) and interleukin-18 (IL-18) were measured using ELISA. Results: Improvements in fasting insulin level, QUICKI and HOMA-β 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-α, 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-β 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-β in type 2 diabetes mellitus.

Original languageEnglish
Pages (from-to)282-289
Number of pages8
JournalClinical Endocrinology
Volume66
Issue number2
DOIs
Publication statusPublished - 2007 Feb 1

Fingerprint

rosiglitazone
Interleukin-18
glimepiride
Adipokines
Metformin
Type 2 Diabetes Mellitus
Homeostasis
Insulin Resistance
Resistin
Adiponectin
Interleukin-6
Tumor Necrosis Factor-alpha
C-Reactive Protein
Radioimmunoassay
Fasting

All Science Journal Classification (ASJC) codes

  • Endocrinology, Diabetes and Metabolism
  • Endocrinology

Cite this

Kim, Hyeong Jin ; Kang, Eun Seok ; Kim, Dae Jung ; Kim, So Hun ; Ahn, Chul Woo ; Cha, Bong Soo ; Nam, Moonsuk ; Chung, Choon Hee ; Lee, Kwan Woo ; Nam, Chung Mo ; Lee, Hyun Chul. / 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. In: Clinical Endocrinology. 2007 ; Vol. 66, No. 2. pp. 282-289.
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abstract = "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 β-cell function in patients treated with rosiglitazone plus glimepiride. Design and patients: 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. Measurements: Markers of insulin sensitivity and β-cell function were determined by the quantitative insulin sensitivity check index (QUICKI) and the homeostasis model assessment of β-cell function (HOMA-β), respectively. Plasma concentrations of adiponectin were measured by radioimmunoassay. Plasma concentrations of resistin, tumour necrosis factor-α (TNF-α), interleukin-6 (IL-6) and interleukin-18 (IL-18) were measured using ELISA. Results: Improvements in fasting insulin level, QUICKI and HOMA-β 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-α, 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-β 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-β in type 2 diabetes mellitus.",
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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. / Kim, Hyeong Jin; Kang, Eun Seok; Kim, Dae Jung; Kim, So Hun; Ahn, Chul Woo; Cha, Bong Soo; Nam, Moonsuk; Chung, Choon Hee; Lee, Kwan Woo; Nam, Chung Mo; Lee, Hyun Chul.

In: Clinical Endocrinology, Vol. 66, No. 2, 01.02.2007, p. 282-289.

Research output: Contribution to journalArticle

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T1 - Effects of rosiglitazone and metformin on inflammatory markers and adipokines

T2 - Decrease in interleukin-18 is an independent factor for the improvement of homeostasis model assessment-beta in type 2 diabetes mellitus

AU - Kim, Hyeong Jin

AU - Kang, Eun Seok

AU - Kim, Dae Jung

AU - Kim, So Hun

AU - Ahn, Chul Woo

AU - Cha, Bong Soo

AU - Nam, Moonsuk

AU - Chung, Choon Hee

AU - Lee, Kwan Woo

AU - Nam, Chung Mo

AU - Lee, Hyun Chul

PY - 2007/2/1

Y1 - 2007/2/1

N2 - 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 β-cell function in patients treated with rosiglitazone plus glimepiride. Design and patients: 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. Measurements: Markers of insulin sensitivity and β-cell function were determined by the quantitative insulin sensitivity check index (QUICKI) and the homeostasis model assessment of β-cell function (HOMA-β), respectively. Plasma concentrations of adiponectin were measured by radioimmunoassay. Plasma concentrations of resistin, tumour necrosis factor-α (TNF-α), interleukin-6 (IL-6) and interleukin-18 (IL-18) were measured using ELISA. Results: Improvements in fasting insulin level, QUICKI and HOMA-β 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-α, 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-β 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-β in type 2 diabetes mellitus.

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