Response to Comment on: Reyna et al. (2008) Elevated Toll-Like Receptor 4 Expression and Signaling in Muscle From Insulin-Resistant Subjects. Diabetes 57:2595–2602

  1. Sara M. Reyna1,2,
  2. Sangeeta Ghosh1,2,
  3. Ralph A. DeFronzo1,2,
  4. Christopher P. Jenkinson1,2 and
  5. Nicolas Musi1,2
  1. 1Division of Diabetes, University of Texas Health Science Center at San Antonio, San Antonio, Texas; and
  2. 2Texas Diabetes Institute, San Antonio, Texas.
  1. Corresponding author: Nicolas Musi, nicolas.musi{at}uhs-sa.com.

We thank Shapiro et al. (1) for their interest in our study (2) and their comment about the role of low-grade endotoxemia in the pathogenesis of insulin resistance in type 2 diabetic subjects. The notion that elevated levels of lipopolysaccharide (LPS) in the circulation derived from a gastrointestinal source could be responsible for the inflammatory state present in insulin-resistant subjects (3,4) is provocative and merits further investigation. Although caution is warranted when extrapolating from a small number of studies (3,4), in the future it would be useful to measure circulating LPS levels in insulin-resistant subjects and determine whether a correlation exists between the plasma LPS concentration and toll-like receptor (TLR)4 expression/signaling in tissue.

As pointed out by Shapiro et al. (1), there is some evidence (obtained mostly in inflammatory cells) indicating that pre-exposure to LPS decreases the response to subsequent …

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