
Serum Adipokine Concentrations in Dogs with Acute Pancreatitis
Author(s) -
Paek J.,
Kang J.H.,
Kim H.S.,
Lee I.,
Seo K.W.,
Yang M.P.
Publication year - 2014
Publication title -
journal of veterinary internal medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.356
H-Index - 103
eISSN - 1939-1676
pISSN - 0891-6640
DOI - 10.1111/jvim.12437
Subject(s) - adipokine , resistin , medicine , adiponectin , leptin , endocrinology , acute pancreatitis , pathogenesis , interleukin 6 , obesity , insulin resistance , cytokine
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 .