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. Author manuscript; available in PMC: 2015 Feb 1.
Published in final edited form as: J Endocrinol. 2014 Jul;222(1):27–41. doi: 10.1530/JOE-13-0455

Figure 6.

Figure 6

Top:Change in body weight and cumulative food consumption (inset) following administration of control vector into MBH and NTS (closed squares), rAAV-leptin to NTS with rAAV-control into MBH (open circles) or rAAV-leptin to NTS simultaneously with rAAV-leptin antagonist to MBH (rAAV-Leptin NTS /Antg MBH, triangles). The rAAV-vectors were administered at day 0. Delta body weight significantly diverged from controls starting at day 4 in rAAV-Leptin NTS /Antg MBH treated group (P<0.01) by one-way ANOVA and Newman-Keuls post-hoc analysis. *P< 0.005 for difference with vector treatment by one-way ANOVA; P<0.01 for difference between rAAV-leptin NTS/Antg MBH and rAAV-Control or P<0.05 for difference from Leptin NTS by Newman-Keuls post-hoc analysis. Values represent the mean ± SE of 6-7 rats per group.

Bottom: STAT3 phosphorylation in the NTS at death in the groups described in Fig. 6 top. STAT3 phosphorylation represents that stimulated by leptin gene delivery. No further exogenous leptin was administered. Data is expressed as the ratio of STAT3 Phosphorylation to G3PDH.

The value of rAAV-Control for each individual tissue is arbitrarily set to 100 with SE adjusted proportionally with remaining groups normalized to the level in rAAV-Control. Values represent the mean ± SE of 6-7 rats per group. P< 0.05 for difference with vector treatment by one-way ANOVA; *P<0.05 for difference from rAAV-Control by Newman-Keuls post-hoc analysis.