Leptin Expression in Dogs with Cardiac Disease and Congestive Heart Failure

Kang

Jeung

et al. 2016

BackgroundThe concentrations of circulating adipokines in dogs with myxomatous mitral valve disease (MMVD) have not been investigated in detail.ObjectivesTo determine whether serum concentrations of adipokines differ between healthy dogs and dogs with MMVD and whether circulating concentrations depend on the severity of heart failure resulting from MMVD.AnimalsIn the preliminary study, 30 healthy dogs and 17 client‐owned dogs with MMVD, and in the subsequent study, 30 healthy dogs and 46 client‐owned dogs with MMVD.MethodsProspective case‐controlled observational study. In the preliminary study, serum concentrations of leptin, adiponectin, resistin, visfatin, interleukin (IL)‐1β, IL‐6, IL‐10, IL‐18, and tumor necrosis factor‐α were measured. In the subsequent study, MMVD dogs were divided into three groups according to the International Small Animal Cardiac Health Council (ISACHC) classification, and serum concentrations of leptin and adiponectin were measured.ResultsIn the preliminary study, serum leptin and adiponectin concentrations differed significantly between dogs with MMVD and healthy dogs. Serum leptin (P = .0013) concentrations were significantly higher in dogs with MMVD than in healthy dogs, whereas adiponectin (P = .0009) concentrations were significantly lower in dogs with MMVD. However, we observed no significant differences in the other variables. In the subsequent study, dogs classified as ISACHC class 3 had higher serum concentrations of leptin (P = .0022) than healthy dogs but ISACHC class 1 or 2 dogs did not. Serum adiponectin concentrations were significantly lower in ISACHC class 1 (P < .0001) dogs than in healthy dogs, whereas adiponectin concentrations in ISACHC class 3 dogs were significantly higher than in ISACHC class 1 dogs (P = .0081).Conclusions and Clinical ImportanceCirculating concentrations of leptin and adiponectin might be altered in dogs with MMVD.

Section: Discussionsupporting

confidence: 89%

mentioning

confidence: 99%

Serum Concentrations of Leptin and Adiponectin in Dogs with Myxomatous Mitral Valve Disease

Kang

Jeung

et al. 2016

“…The primer sequences for each gene used in real‐time PCR are shown in Table . These primers of leptin and the leptin receptor were reported previously. The identity of amplified PCR products was confirmed by DNA cloning and sequencing with Sanger's method.…”

Section: Methodsmentioning

confidence: 83%

Increased Leptin and Leptin Receptor Expression in Dogs With Gallbladder Mucocele

Lee

Kweon

2016

BackgroundLeptin and its receptor play a role in several disease processes such as pancreatitis and heart disease. However, their association with gallbladder mucocele (GBM) in dogs has not been reported.Hypothesis/ObjectivesTo evaluate differences in the expression of leptin and leptin receptor between dogs with and without GBM.AnimalsTwenty‐five healthy dogs, including 9 laboratory beagle dogs, and 22 client‐owned dogs with GBM.MethodsSerum leptin concentration was determined in blood samples of all dogs by ELISA. Canine gallbladder samples were collected from 9 dogs with GBM that underwent surgery for therapeutic purposes and from 9 healthy laboratory beagle dogs as a normal control group. Samples were analyzed for leptin and leptin receptor mRNA by real‐time polymerase chain reaction.ResultsSerum leptin concentration was significantly higher in dogs with GBM than in healthy dogs (medians of 7.03 and 2.18 ng/mL, respectively; P < .001). Patients with GBM that had undergone surgery had significantly higher serum leptin concentrations than those that had not (medians of 12.2 and 4.09 ng/mL, respectively; P = .001). However, no difference in serum leptin concentration was found between dogs with GBM with or without endocrinopathies. The mRNA expression levels of leptin and its receptor were significantly increased in the gallbladder tissues of dogs with GBM.Conclusions and Clinical ImportanceDysregulation of leptin might be involved in the pathophysiology of GBM, and leptin concentrations might be associated with GBM severity.

“…Adipocytes are the main site of leptin synthesis and the main contributor to the serum leptin levels, but other tissue sites have been identified that can produce leptin. In dogs, leptin, leptin receptors, or both were recently detected in the stomach, mammary tissue, myocardium, corpus luteum, and even oral melanoma, but not in the pancreas, although it remains to be determined whether these findings were dependent on the experimental methods employed. However, it has been shown that leptin and its receptors are present in the pancreas in humans and laboratory animals, and it has been suggested that leptin may also play roles in the modulation of pancreatic function, as well as being involved in pancreatitis .…”

Section: Discussionmentioning

confidence: 99%

Serum Adipokine Concentrations in Dogs with Acute Pancreatitis

Paek

Kang

et al. 2014

BackgroundLimited information is available about the role of adipokines in the development and progression of acute pancreatitis (AP) in dogs.ObjectivesTo 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.AnimalsTwenty‐eight healthy dogs and 25 client‐owned dogs with AP.MethodsProspective 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.ResultsThe 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 ImportanceThis 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.