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Endotoxin increases plasma leptin and ghrelin levels in dogs*

Yilmaz, Zeki PhD, DMV; Ilcol, Yesim Ozarda MD; Ulus, Ismail H. MD

doi: 10.1097/01.CCM.0B013E3181611F5AA
Laboratory Investigations

Objective: Evaluations of plasma leptin and ghrelin levels and their relations with circulating levels of proinflammatory mediators, stress hormones, and biochemical markers of hepatorenal injury during experimental endotoxemia in dogs.

Setting: Uludag University.

Design: Placebo-controlled animal study.

Animals: Adult mongrel dogs (n = 16).

Interventions: Intravenous injection of endotoxin (1 mg/kg) and blood sample withdrawal before and at 0.5–48 hrs posttreatment.

Measurements and Main Results: Mean baseline plasma leptin and ghrelin levels were 2.4 ± 0.1 ng/mL and 867 ± 58 pg/mL, respectively. Plasma leptin and ghrelin increased significantly by 16% (p < .05) and 72% (p < .001) at 0.5 hr, and they remained elevated by 33–41% (p < .001) and 59–74% (p < .001) at 48 hrs after administration of endotoxin, respectively. There was positive correlation (r = .844; p < .001) between plasma leptin and ghrelin levels in endotoxin-treated dogs. Endotoxemia was associated with several-fold elevations in circulating levels of stress hormones, proinflammatory mediators, and hepatorenal injury markers. Plasma leptin and ghrelin levels in endotoxin-treated dogs were correlated with serum nitric oxide (r = .955 and r = .890; p < .001), procalcitonin (r = .825 and r = .716; p < .001), cortisol (r = .823 and r = .786; p < .001), and hepatorenal injury markers (r = .580 to .745 and r = .393 to .574; p < .05 to .01).

Conclusions: Circulating leptin and ghrelin levels increase during endotoxemia, and these increases are associated with elevated levels of proinflammatory mediators, stress hormones, and serum biochemical markers for hepatorenal dysfunction.

From the Departments of Internal Medicine (ZY), Biochemistry (YOI), and Pharmacology and Clinical Pharmacology (IHU), Uludag University, Bursa, Turkey.

The authors have not disclosed any potential conflicts of interest.

Supported, in part, by the Research Fund of Uludag University, Bursa, Turkey.

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© 2008 by the Society of Critical Care Medicine and Lippincott Williams & Wilkins