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Oxidative stress in the brain mediates thermogenic sympathetic activation to leptin
Author(s) -
Rahmouni Kamal,
Morgan Donald A,
Mark Allyn L
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.1021.6
Subject(s) - leptin , endocrinology , medicine , oxidative stress , brown adipose tissue , adipose tissue , chemistry , hindlimb , superoxide dismutase , sympathetic nervous system , obesity , blood pressure
Leptin acts in the brain to decrease appetite and body weight and increase sympathetic nerve activity (SNA). Leptin can increase oxidative stress as shown in endothelial cells and oxidative stress modulates SNA. Here, we examined whether oxidative stress mediates leptin‐induced increases in SNA by testing the effect of intracerebroventricular (ICV) treatment with a superoxide dismutase mimetic (Tempol, 5 μM) on the regional SNA response to intravenous leptin (1 mg/kg bw) in anesthetized Sprague‐Dawley rats. Leptin increased SNA to brown adipose tissue (BAT, 184±26%, n=6), kidney (181±29%, n=6) and hindlimb (170±19%, n=6). ICV Tempol alone had no effect on BAT (4±16%, n=8), renal (10±12%, n=8) and lumbar (14±8%, n=8) SNA. However, treatment with ICV Tempol blocked leptin‐induced sympathetic activation to BAT (‐10±19%, n=5, P<0.05 vs. leptin alone), but not to kidney (157±37%, n=5) or hindlimb (196±37%, n=5). In contrast, corticotrophin‐releasing factor‐induced increase in BAT SNA was not significantly altered by ICV treatment with Tempol (215±41%, n=6) as compared to vehicle (254±41, n=6). Our data demonstrate the importance of oxidative stress as a mediator of leptin‐induced activation of sympathetic activity to thermogenic brown adipose tissue.