Response to Comment on: Turban et al. Optimal Elevation of β-Cell 11β-Hydroxysteroid Dehydrogenase Type 1 Is a Compensatory Mechanism That Prevents High-Fat Diet–Induced β-Cell Failure. Diabetes 2012;61:642–652

  1. Nicholas M. Morton1
  1. From the 1Molecular Metabolism Group, University of Edinburgh/British Heart Foundation Centre for Cardiovascular Science, Queen’s Medical Research Institute, University of Edinburgh, Edinburgh, U.K.; and the
  2. 2Endocrinology Unit, University of Edinburgh/British Heart Foundation Centre for Cardiovascular Science, Queen’s Medical Research Institute, University of Edinburgh, Edinburgh, U.K
  1. Corresponding author: Nicholas M. Morton, nik.morton{at}ed.ac.uk.

We thank the editor for allowing us to clarify an aspect of our recent article (1) in response to Liu et al. (2). We and others (3) found that KsJ mice resist excessive weight gain on a high-fat (HF) diet. There are well-known strain differences in this response. Nevertheless, epididymal fat pad mass and fed plasma nonesterified fatty acid levels were increased by HF in both genotypes (Table 1 in ref. 1). We did not claim obesity or diabetes. We agree that β-cell dysfunction was subclinical by basic measures …

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