Serum adipokine concentrations in dogs with acute pancreatitis

Abstract

Background: Limited information is available about the role of adipokines in the development and progression of acute pancreatitis (AP) in dogs.

Objectives: To determine whether the circulating concentrations of adipokines differed between healthy dogs and dogs with AP, and whether the circulating concentrations differed between AP survivors and AP nonsurvivors.

Animals: Twenty-eight healthy dogs and 25 client-owned dogs with AP.

Methods: Prospective observational cohort study of 25 client-owned dogs with newly diagnosed AP and 28 otherwise healthy dogs with similar body condition scores. The serum concentrations of leptin, adiponectin, resistin, visfatin, interleukin (IL)-1β, IL-6, IL-10, IL-18, and tumor necrosis factor (TNF)-α were measured.

Results: The serum concentrations of leptin (P = .0021), resistin (P = .0010), visfatin (P < .0001), IL-1β (P < .0001), IL-6 (P = .0002), IL-10 (P < .0001), and IL-18 (P < .0001) were significantly higher in dogs with AP than healthy dogs, whereas the adiponectin concentration (P = .0011) was significantly lower. There were significant differences in the serum concentrations of leptin (P = .028) and adiponectin (P = .046) in survivors and nonsurvivors. After the disappearance of clinical signs, the concentrations of resistin (P = .037) and IL-1β (P = .027) decreased significantly, whereas the serum concentrations of leptin (P > .999), adiponectin (P = .11), visfatin (P = .83), IL-6 (P = .82), IL-10 (P = .82), IL-18 (P = .56), and TNF-α (P = .94) did not differ significantly.

Conclusion and clinical importance: This study showed that dysregulation of adipokines might be involved in the pathogenesis of AP. In addition, leptin and adiponectin are likely to be associated with mortality rate in AP.

Keywords: Adiponectin; Canine; Cytokine; Leptin; Resistin; Visfatin.

Figure 1

Comparison of the circulating concentrations of (A) leptin, (B) adiponectin, (C) resistin, and (D) visfatin in dogs with acute pancreatitis (n = 25) and healthy dogs (n = 28). The horizontal bars indicate the medians and ranges. *P < .05 (Mann‐Whitney U‐test).

Figure 2

Comparison of the circulating concentrations of (A) interleukin (IL)‐1β, (B) IL‐6, (C) IL‐10, (D) IL‐18, and (E) tumor necrosis factor (TNF)‐α in dogs with acute pancreatitis (n = 25) and healthy dogs (n = 28). The horizontal bars indicate the medians and ranges. *P < .05 (Mann‐Whitney U‐test).

Figure 3

Differences in the circulating concentrations of (A) leptin, (B) adiponectin, (C) resistin, and (D) visfatin in the survivors (n = 12) and nonsurvivors (n = 13) among the dogs with acute pancreatitis. The horizontal bars indicate the medians and ranges. *P < .05 (Mann‐Whitney U‐test).

Figure 4

Differences in the circulating concentrations of (A) interleukin (IL)‐1β, (B) IL‐6, (C) IL‐10, (D) IL‐18, and (E) tumor necrosis factor (TNF)‐α in the survivors (n = 12) and nonsurvivors (n = 13) among the dogs with acute pancreatitis. The horizontal bars indicate the medians and ranges.

Figure 5

Differences in the circulating concentrations of (A) leptin, (B) adiponectin, (C) resistin, and (D) visfatin before and after treatment in the dogs with acute pancreatitis (n = 10). The horizontal bars indicate the medians and ranges. *P < .05 (Wilcoxon matched‐pairs signed rank test).

Figure 6

Differences in the circulating concentrations of (A) interleukin (IL)‐1β, (B) IL‐6, (C) IL‐10, (D) IL‐18, and (E) tumor necrosis factor (TNF)‐α before and after treatment in dogs with acute pancreatitis (n = 10). The horizontal bars indicate the medians and ranges. *P < .05 (Wilcoxon matched‐pairs signed rank test).