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. Author manuscript; available in PMC: 2014 Sep 3.
Published in final edited form as: Cell Metab. 2013 Sep 3;18(3):431–444. doi: 10.1016/j.cmet.2013.08.004

Figure 6. Leptin administration induces glucose uptake in soleus and iBAT of insulin-deficient mice.

Figure 6

(A) Glucose level in the blood of insulin-deficient β-less mice (that do not express any types of β-adrenergic receptors) and their wild-type controls that received icv leptin (25 ng/hour) administration (STZ-β-less-icv-leptin and STZ-wild-type-icv-leptin groups, respectively). Insulin deficiency was induced by administration of STZ as shown in Figure 2. (B) Experimental design and (C) glucose level in the blood of STZ-treated FBV/NJ mice that received icv administration of leptin (25 ng/hour) followed by administrations of β-adrenergic-receptor blocker timolol (1 mg/kg BW) or placebo (0.9% saline solution). Mice were injected ip twice a day from day 7 up to day 9 and one time 2 hours before sacrifice. (D) Experimental design of assessment of basal glucose utilization. The experiment was carried out 10 days after icv administration as described in Figure 1A. (E) Glucose utilization levels in soleus muscle, gastrocnemius muscle, vastus muscle, interscapular brown adipose tissue and brain of DT-icv-leptin, DT-icv-placebo and normal mice. Values are mean ± S.E.M. (n = 4–6). Statistical analyses were done using unpaired t-test or one-way ANOVA (Tukey's Multiple Comparison Test) *P<0.05 versus DT-icv-placebo mice. See also Figure S5 and Table S1 and S2.