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. 2019 May 13;116(22):10937–10942. doi: 10.1073/pnas.1901655116

Fig. 7.

Fig. 7.

FPLC analysis of plasma cholesterols and schematic diagram of mechanisms underlying the mirabegron-accelerated atherosclerotic plaque growth and instability. (A and B) Plasma cholesterol and triglyceride levels of the mirabegron- and vehicle-treated ApoE−/− mice (n = 6 animals per group). Values from fractions 5–10 were used for calculation of VLDL/IDL, whereas fractions 11–19 and fractions 20–30 represent LDL and HDL, respectively. (C) Mirabegron induces browning of WAT and activation of BAT, which undergo thermogenesis by the UCP1-dependent lipolysis. FFA promotes biosynthesis of VLDL remnants to facilitate the atherosclerotic plaque growth and instability. Accelerated plaque growth and instability increase the cardiovascular and cerebrovascular events.