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Jacquelyn A. Reed, Deborah J. Clegg, Kathleen Blake Smith, Emeline G. Tolod-Richer, Emily K. Matter, Lara S. Picard, Randy J. Seeley
Published in Volume 115, Issue 11
J Clin Invest. 2005; 115(11):3035–3044 doi:10.1172/JCI25681
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Figure 1

i3vt injection of rat GM-CSF in rats. (A) Rats received a single injection of 0.03, 0.06, or 0.6 μg recombinant rat GM-CSF, or vehicle (Veh) alone. Twenty-four-hour food intake was significantly decreased in rats receiving 0.6 μg GM-CSF. (B) Change in body weight at 24 hours after injection was significantly greater in rats receiving 0.6 μg GM-CSF. (C) Rats were injected with 0.6 μg GM-CSF or vehicle. GM-CSF treatment significantly suppressed food intake at 4 hours, compared with vehicle treatment. (D) Rats were injected with 0.6 μg rat GM-CSF or recombinant human GM-CSF (hGM). While 24-hour food intake was suppressed with rat GM-CSF, human GM-CSF–treated rats did not differ from vehicle-treated rats. (E) Rats were injected with 0.6 μg GM-CSF or vehicle, followed by a 24-hour fast (day 1). Weight loss at 24 hours after injection was greater in rats injected with GM-CSF compared with vehicle. (F) When food was returned, anorexia persisted for an additional 24 hours (day 2). For all rat studies, n = 7–9; error bars show mean ± SEM. Twenty-four-hour food intake (G) and body weight (H) were decreased in mice receiving 1 μg mouse GM-CSF, compared with those receiving vehicle. n = 5–6; mean ± SEM. *P < 0.05.