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. 2011 Sep;3(9):559–572. doi: 10.1002/emmm.201100159

Figure 3. Metabolic disturbances and increased bacterial translocation to mesenteric adipose tissue (MAT) in Myd88 knockout mice.

Figure 3

  • A. Intraperitoneal glucose tolerance test (IPGTT) (1 g/kg) in Myd88-deficient mice (Myd88−/−) and their corresponding wild-type controls (WT) fed a normal chow (NC) diet (mean ± SEM; n = 7; *p < 0.05 versus controls).
  • B,C,D,E. Body weight (B), fat mass (% of body weight; EchoMRI) (C), fasted plasma insulin (µU/ml) (D) and insulin sensitivity (glucose turnover rate in mg/kg min) (E), in Myd88−/− mice and their corresponding WT controls fed a NC diet (mean ± SEM; n = 5; data with identical superscript letters do not differ from each other with p > 0.05).
  • F. Number of GFP-E. coli cfu per g of MAT in Myd88−/− mice and their corresponding WT controls fed a NC diet, 2 h post-gavage with 109 cfu of GFP-E. coli (mean ± SEM; n = 7; data with identical superscript letters do not differ from each other with p > 0.05).
  • G. 16S rRNA DNA concentration (pg/µg total DNA; qPCR) from total bacteria in MAT of Myd88−/− mice and their corresponding WT controls fed a NC diet (mean ± SEM; n = 7; data with identical superscript letters do not differ from each other with p > 0.05).