Fig. 3

Immunoglobulin A (IgA) deficiency, specifically in intestinal B cells, increases insulin resistance in high fat diet (HFD)-fed mice. a Weight gain (n = 21 WT, 16 IgA^−/− HFD; 4 distinct cohorts) and b organ weights (n = 5 WT, 5 IgA^−/−) of IgA^−/− mice fed HFD compared to wild-type (WT) littermate controls over 14 weeks of diet. c Fasting glucose (left), fasting insulin (right) (n = 4 WT, 4 IgA^−/−), d glucose tolerance test (GTT) (left) also represented by area under the curve (AUC) (right), and e insulin tolerance test (ITT) (left) also represented by AUC (right) in IgA^−/− mice fed HFD (n = 12 WT, 12–13 IgA^−/−, 3 distinct cohorts). f Weight gain (left) (n = 5 WT, 8 IgA^−/− NCD), fasting glucose (middle left), glucose tolerance also represented by AUC (middle right), and insulin tolerance and AUC (right) of IgA^−/− mice fed normal control diet (NCD) compared to WT littermate controls after 14 weeks of diet (n = 5 WT, 7 IgA^−/− NCD). g Weights (left), fasting glucose levels (left middle), blood concentrations of glucose during GTT and AUC (right middle), and ITT and AUC (right) of 12-week HFD-fed B cell-deficient muMT⁻ (B^null) mice 2 weeks post adoptive transfer of IgA^−/− or WT intestinal pan B cells, or a sham phosphate-buffered saline (PBS) control (n = 2 PBS control, 5 WT gut B cells, 6 IgA^−/− gut B cells). Data are means ± SEM. * denotes p < 0.05 and ** denotes p < 0.01