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. Author manuscript; available in PMC: 2011 Dec 15.
Published in final edited form as: Biochem J. 2011 Dec 15;440(3):385–395. doi: 10.1042/BJ20102148

Figure 1. Adiponectin blocks leptin-mediated activation of Jak2.

Figure 1

A) Top Panel: Western blot of phospho-Jak2[Tyr1007/1008 and Ser523] in lysates prepared from rat HSCs. Thirty minute leptin treatment (Lep, 100ng/ml) increased Jak2 (Tyr1007/1008) phosphorylation significantly (*p < 0.05 vs. untreated) compared to untreated samples (Utx). Co-administration of leptin and adiponectin (LA) inhibited leptin-stimulated Jak2 (Tyr1007/1008) phosphorylation (#p < 0.05 vs. leptin). Adiponectin (10μg/ml) stimulated Jak2 (Ser523) phosphorylation whether administered alone or in the presence of leptin (*p < 0.05 vs. untreated). Bottom Panel: Quantitation of data presented in top panel (A). B) Top Panel: Western Blot of phospho-Jak2 (Tyr1007/1008) from liver tissue collected from Adiponectin knockout (Ad−/−) and wild-type (WT) mice. CCl4 intoxication (2 ml/kg) and CCl4+leptin co-administration both increased Jak2 phosphorylation significantly over saline-treated control mice. Jak2 phosphorylation was always greater in Ad-/- mice compared with wild-type mice, regardless of treatment (*p < 0.05 vs. WT). Bottom Panel: Quantitation of data presented in top panel (B).