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Endogenous Interleukin-10 Protects against Hepatic Steatosis but Does Not Improve Insulin Sensitivity during High-Fat Feeding in Mice

Departments of Endocrinology and Metabolism (M.A.M.d.B., P.J.V., J.P.S.-v.d.E., J.A.R.), Molecular Cell Biology (E.K., D.M.O), and Cardiology (L.M.H.), Leiden University Medical Center, 2333 ZA Leiden, The Netherlands; Department of Pediatrics (F.K.), University Medical Center Groningen, 9700 AB Groningen, The Netherlands; and Netherlands Organization for Applied Scientific Research Quality of Life (L.M.H.), 2333 CK Leiden, The Netherlands

Address all correspondence and requests for reprints to: Marion A. M. den Boer, Leiden University Medical Center, Department of Endocrinology and Metabolism, C4-R, Albinusdreef 2, 2333 ZA, Leiden, The Netherlands. E-mail: A.M.den_Boer{at}lumc.nl.

Several studies have demonstrated an association in humans between plasma levels or production capacity of the antiinflammatory cytokine IL-10 and insulin sensitivity. The aim of our study was to investigate the protective role of endogenous IL-10 availability in the development of diet-induced insulin resistance. We compared parameters of glucose and lipid metabolism between IL-10^–/– mice and wild-type (wt) mice fed a high-fat diet for 6 wk. This diet has previously been shown to induce steatosis and insulin resistance. After 6 wk on the high-fat diet, no differences in body weight, basal metabolism (measured by indirect calorimetry), or plasma levels of glucose, triglycerides, or cholesterol were observed between IL-10^–/– and wt mice. Nonetheless, in IL-10^–/– mice, plasma free fatty acid levels were 75% increased compared with wt mice after overnight fasting (P < 0.05). In addition, hepatic triglyceride content was 54% increased in IL-10^–/– mice (P < 0.05). During a hyperinsulinemic euglycemic clamp, no differences were observed in whole-body or hepatic insulin sensitivity between both groups. We conclude that basal IL-10 production protects against hepatic steatosis but does not improve hepatic or whole-body insulin sensitivity, during high-fat feeding.

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