reported [18]. We observed similar body weights to WT mice, but dramatically decreased fat mass and commensurate increases in lean mass (Figure S2A–C), in addition we observed hyperglycemia (Figure S2D), and mild/sporadic glucose intolerance (Figure S2E–F). Additionally, Tg mice were severely insulin resistant (Figure S2G–H). Food intake was mildly increased in Tg mice compared to WT mice (Figure S2I). Tg mice exhibited hepatomegaly, and dramatically reduced WAT depot weights (Figure S2J). Triglycerides levels were lower, with little change in cholesterol levels (Figure S2K–L) in Tg mice. Taken together these mice present a similar model of lipodystrophy to that produced by Shimomura et al [18]. In contrast to the former model of lipodystrophy, we observed reduced triglycerides in Tg mice compared to WT mice. This could possibly be related to the difference in genetic background of the mice. Simomura et al. bred their mice on a B6/SJL background whereas here we breed to FVB mice. We found that WT FVB levels of plasma triglycerides are massively increased compared to WT mice of the original lipodystrophy mice (∼400 mg/dL vs. 74–123 mg/dL (Figure S1K and [18]). Futhermore we found that WT insulin levels are considerably higher than typical B6 values. It has
