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. Author manuscript; available in PMC: 2010 Feb 1.

Published in final edited form as: Brain Behav Immun. 2008 Sep 27;23(2):169–175. doi: 10.1016/j.bbi.2008.09.011

Fig. 2 — A, C57BL/6J and db/db mice were exposed to normoxia or hypoxia as indicated and social withdrawal was measured prior to hypoxia (−2 h) and at 0, 2, 6, 10 and 22 h after return of animals to normoxia. Results are expressed as percentages of the baseline measurement, means ± SEM; n = 5/treatment group; *p < 0.05, main effect of hypoxia vs normoxia, #p < 0.05, phenotype effect of C57BL/6J vs db/db. B/C, Db/db mice were treated as in A and IL-1RA was measured in WAT (B) and serum (C) by ELISA. D/E, Db/db mice were treated as in A and leptin measured in WAT (D) and serum (E) by ELISA. Results are expressed as means ± SEM; n = 4/time point; *p < 0.05 versus −2.

Fig. 2 — A, C57BL/6J and db/db mice were exposed to normoxia or hypoxia as indicated and social withdrawal was measured prior to hypoxia (−2 h) and at 0, 2, 6, 10 and 22 h after return of animals to normoxia. Results are expressed as percentages of the baseline measurement, means ± SEM; n = 5/treatment group; *p < 0.05, main effect of hypoxia vs normoxia, #p < 0.05, phenotype effect of C57BL/6J vs db/db. B/C, Db/db mice were treated as in A and IL-1RA was measured in WAT (B) and serum (C) by ELISA. D/E, Db/db mice were treated as in A and leptin measured in WAT (D) and serum (E) by ELISA. Results are expressed as means ± SEM; n = 4/time point; *p < 0.05 versus −2.