Abstract

ObjectiveTo evaluate the effect of insulin sensitizer on inflammatory cytokines and oxidative stress in patients with newly diagnosed type 2 diabetes mellitus (T2DM).MethodsAfter intensive insulin therapy, patients with newly diagnosed T2DM were continuously treated with either insulin sensitizer or insulin for 48 weeks, and then their inflammatory cytokine and oxidative stress levels were measured.ResultsTumor necrosis factor alpha (TNF-α), interleukin (IL)-6, hypersensitive C reactive protein (hs-CRP), malondialdehyde (MDA), and 8-iso-prostaglandin F2α (8-iso-PGF2α) levels of the rosiglitazone (RSG) group and the rosiglitazone combined with metformin (RSG + metformin) group were significantly reduced after the treatments (P < 0.05). Hs-CRP, MDA, and 8-iso-PGF2α levels of the metformin group were significantly reduced after the treatments (P < 0.05). Superoxide dismutase (SOD) and total antioxidant capacity (TAC) were significantly increased after the treatments in all three groups (P < 0.05 and P < 0.01).ConclusionEarly application of insulin sensitizers improved inflammation and oxidative stress in patients with newly diagnosed T2DM.

Highlights

  • Patients with type 2 diabetes mellitus (T2DM) are at increased risk of cardiovascular diseases and associated clinical complications

  • Basic clinical conditions In this study, bodyweight, body mass index (BMI), fasting blood glucose, and 2-h postprandial blood glucose in the RSG group were significantly higher after the 48-week treatment

  • In the metformin group, fasting and 2-h postprandial blood glucose of the T2DM patients were significantly higher after the 48-week treatment (P < 0.05, P < 0.01); whereas bodyweight, BMI, ­HbA1c, insulin resistance index of homeostasis model assessment (HOMA-IR), triglyceride, and gamma-glutamyl transferase (γ-GT) were significantly lower after the 48-week treatment (P < 0.05, P < 0.01)

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Summary

Results

Basic clinical conditions In this study, bodyweight, BMI, fasting blood glucose, and 2-h postprandial blood glucose in the RSG group were significantly higher after the 48-week treatment (P < 0.05, P < 0.01); whereas ­HbA1c, HOMA-IR, and γ-GT were significantly lower (P < 0.05, P < 0.01). In the metformin group, fasting and 2-h postprandial blood glucose of the T2DM patients were significantly higher after the 48-week treatment (P < 0.05, P < 0.01); whereas bodyweight, BMI, ­HbA1c, HOMA-IR, triglyceride, and γ-GT were significantly lower after the 48-week treatment (P < 0.05, P < 0.01). In the RSG + metformin group, fasting and 2-h postprandial blood glucose of the T2DM patients were significantly higher after the 48-week treatment (P < 0.05, P < 0.01); whereas ­HbA1c, HOMA-IR, triglyceride, and γ-GT were significantly lower (P < 0.05, P < 0.01). In the RSG + metformin group, TNFα, IL-6, hsCRP, MDA, and 8-iso-PGF2α were significantly reduced after the 48-week treatment (P < 0.05); while SOD and TAC significantly increased (P < 0.05, P < 0.01). There was no significant change in TNFα, IL-6, hs-CRP, and IL-1β after the 48-week insulin aspart treatment (P > 0.05) (Table 2)

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