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. Author manuscript; available in PMC: 2013 Sep 10.
Published in final edited form as: Cell Rep. 2013 Aug 15;4(4):681–688. doi: 10.1016/j.celrep.2013.07.019

Figure 4. The sympathoadrenal system causes increased thermogenesis in Mlk2−/− Mlk3−/− mice.

Figure 4

(A–B) WT and MLK-deficient mice were fed a chow diet (ND) or a HFD (16 wks.). The blood concentration of epinephrine and norepinephrine was measured (mean ± SE; n = 8).

(C) The body temperature of the mice was measured (mean ± SE; n = 8).

(D–H) The expression of Dio2 (D), Ucp1 (E), Ucp3 (F), Ppargc1a (G), and Lpl (H) mRNA expression in interscapular brown fat was measured by quantitative RT-PCR and was normalized to the amount of Gapdh mRNA in each sample (mean ± SE, n=8).

(I) Sections prepared from interscapular brown fat of chow-fed (ND) and HFD-fed WT and MLK-deficient mice were stained with hematoxylin and eosin. The panels presented are representative of 5 mice per group.

(J) The body temperature of WT and MLK-deficient mice was measured (mean ± SE; n = 10). The effect of treatment of the mice with solvent (Control) or the β3 adrenergic receptor antagonist SR59230A was examined.

(K–M) The expression of Ppargc1a (K), Ucp1 (L), and Ucp3 (M) mRNA expression in brown fat was measured by quantitative RT-PCR and was normalized to the amount of Gapdh mRNA in each sample (mean ± SE, n=10).

Statistically significant differences between WT and MLK-deficient mice are indicated (*, P < 0.05; **, P<0.01).