SOAT1 and Insulin resistance: In contrast, BALB/c-specific upregulated expression of pathways related to JAK STAT signalling and cytokine cytokine receptor interaction (Table S4, Figure S2), which contribute to insulin resistance and steatohepatitis [29,30], suggests the presence of inflammation in HFD-fed BALB/c that does not translate into apparent liver histopathology and may be explained by reduced corticosensitivity in BALB/c [31].