Salsalate Improves Glycemia and Inflammatory Parameters in Obese Young Adults

  1. Amy Fleischman, MD, MMSC123,
  2. Steven E. Shoelson, MD, PHD12,
  3. Raquel Bernier, BS12 and
  4. Allison B. Goldfine, MD12
  1. 1Harvard Medical School, Boston, Massachusetts
  2. 2Joslin Diabetes Center, Boston, Massachusetts
  3. 3Children's Hospital Boston, Boston, Massachusetts
  1. Address correspondence and reprint requests to Allison B. Goldfine, MD, Joslin Diabetes Center, One Joslin Place, Boston, MA 02215. E-mail: allison.goldfine{at}joslin.harvard.edu

Abstract

OBJECTIVE—Sedentary lifestyle and a western diet promote subacute-chronic inflammation, obesity, and subsequently dysglycemia. The aim of the current study was to evaluate the efficacy of the anti-inflammatory drug salsalate to improve glycemia by reducing systemic inflammation in obese adults at risk for the development of type 2 diabetes.

RESEARCH DESIGN AND METHODS—In a double-masked, placebo controlled trial, we evaluated 20 obese nondiabetic adults at baseline and after 1 month of salsalate or placebo.

RESULTS—Compared with placebo, salsalate reduced fasting glucose 13% (P < 0.002), glycemic response after an oral glucose challenge 20% (P < 0.004), and glycated albumin 17% (P < 0.0003). Although insulin levels were unchanged, fasting and oral glucose tolerance test C-peptide levels decreased in the salsalate-treated subjects compared with placebo (P < 0.03), consistent with improved insulin sensitivity and a known effect of salicylates to inhibit insulin clearance. Adiponectin increased 57% after salsalate compared with placebo (P < 0.003). Additionally, within the group of salsalate-treated subjects, circulating levels of C-reactive protein were reduced by 34% (P < 0.05).

CONCLUSIONS—This proof-of-principle study demonstrates that salsalate reduces glycemia and may improve inflammatory cardiovascular risk indexes in overweight individuals. These data support the hypothesis that subacute-chronic inflammation contributes to the pathogenesis of obesity-related dysglycemia and that targeting inflammation may provide a therapeutic route for diabetes prevention.

Footnotes

  • Published ahead of print at http://care.diabetesjournals.org on 24 October 2007. DOI: 10.2337/dc07-1338. Clinical trial reg. no. NCT00258115, clinicaltrials.gov.

    The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked “advertisement” in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

    • Accepted October 18, 2007.
    • Received September 5, 2007.
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  1. Diabetes Care vol. 31 no. 2 289-294
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