OBJECTIVE: To evaluate the effect of salsalate as an antiinflammatory agent on insulin resistance and glycemic control in persons with prediabetes. METHODS: In this double-blind, placebo-controlled clinical trial, 66 persons who had prediabetes on the basis of the American Diabetes Association criteria were enrolled. They were randomly assigned to receive salsalate (3 g daily) or placebo for 12 weeks. Fasting plasma glucose (FPG) and insulin, glucose 2 hours after oral administration of 75 g of glucose, hemoglobinA1c, lipid profile, homeostasis model assessment of insulin resistance (HOMA-IR), and homeostasis model assessment of beta-cell function were determined before and after treatment. RESULTS:Salsalate treatment reduced the FPG level from 5.86 ± 0.07 mmol/L to 5.20 ± 0.11 mmol/L and HOMA-IR from 4.2 ± 0.9 to 3.8 ± 0.3 (P = .01 for both changes). Homeostasis model assessment of beta-cell function increased in the salsalate-treatment group from 139.8 ± 11.0 to 189.4 ± 24.6 (P = .01). At the end of the study, FPG, HOMA-IR, and insulin levels were significantly different between salsalate and placebo groups (5.20 ± 0.11 mmol/L versus 5.53 ± 0.10 mmol/L, 3.8 ± 0.3 versus 4.4 ± 0.9, and 16.1 ± 1.9 μIU/mL versus 18.2 ± 2 μIU/mL, respectively; P<.05 for all). There were no persistent complications after salsalate therapy. CONCLUSION: Treatment with salsalate can reduce insulin resistance and the FPG level in subjects with prediabetes. Determination of the long-term safety and efficacy of the use of salsalate necessitates further investigation.
RCT Entities:
OBJECTIVE: To evaluate the effect of salsalate as an antiinflammatory agent on insulin resistance and glycemic control in persons with prediabetes. METHODS: In this double-blind, placebo-controlled clinical trial, 66 persons who had prediabetes on the basis of the American Diabetes Association criteria were enrolled. They were randomly assigned to receive salsalate (3 g daily) or placebo for 12 weeks. Fasting plasma glucose (FPG) and insulin, glucose 2 hours after oral administration of 75 g of glucose, hemoglobin A1c, lipid profile, homeostasis model assessment of insulin resistance (HOMA-IR), and homeostasis model assessment of beta-cell function were determined before and after treatment. RESULTS:Salsalate treatment reduced the FPG level from 5.86 ± 0.07 mmol/L to 5.20 ± 0.11 mmol/L and HOMA-IR from 4.2 ± 0.9 to 3.8 ± 0.3 (P = .01 for both changes). Homeostasis model assessment of beta-cell function increased in the salsalate-treatment group from 139.8 ± 11.0 to 189.4 ± 24.6 (P = .01). At the end of the study, FPG, HOMA-IR, and insulin levels were significantly different between salsalate and placebo groups (5.20 ± 0.11 mmol/L versus 5.53 ± 0.10 mmol/L, 3.8 ± 0.3 versus 4.4 ± 0.9, and 16.1 ± 1.9 μIU/mL versus 18.2 ± 2 μIU/mL, respectively; P<.05 for all). There were no persistent complications after salsalate therapy. CONCLUSION: Treatment with salsalate can reduce insulin resistance and the FPG level in subjects with prediabetes. Determination of the long-term safety and efficacy of the use of salsalate necessitates further investigation.
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