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. 2015 Aug 21;156(11):4047–4058. doi: 10.1210/en.2015-1184

Figure 2.

Figure 2.

FcϵR1 deficiency increased obesity but improved glucose tolerance in mice. A, Body weight gain of male WT and Fcer1a−/− mice on a HFD. B, DEXA determined food intake and whole-body lean and fat masses after mice consumed a HFD for 17 weeks. Glucose and insulin tolerance test (C) and glucose-induced insulin release (D) from male WT and Fcer1a−/− mice after 17 weeks of a HFD were performed. E, Insulin production from islets treated with and without different doses of glucose and IgE. Insulin secretion is expressed as a percentage of the islet insulin content (n = 4). F, The mRNA expression levels of FcϵR1a in the islets treated with different doses of IgE (n = 4). Bone marrow-derived macrophages were used as a positive control. Plasma IgE and insulin levels (G), WAT extract IgE (H), and plasma serum amyloid A (SAA), IL-6, and MCP-1 levels (I) from male WT and Fcer1a−/− mice after 17 weeks of a HFD are shown. The number of mice per group is indicated in parentheses.