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

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          Abstract

          Background

          The concentrations of circulating adipokines in dogs with myxomatous mitral valve disease ( MMVD) have not been investigated in detail.

          Objectives

          To 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.

          Animals

          In 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.

          Methods

          Prospective 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.

          Results

          In 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 Importance

          Circulating concentrations of leptin and adiponectin might be altered in dogs with MMVD.

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          Most cited references56

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          Adipose tissue, adipokines, and inflammation.

          White adipose tissue is no longer considered an inert tissue mainly devoted to energy storage but is emerging as an active participant in regulating physiologic and pathologic processes, including immunity and inflammation. Macrophages are components of adipose tissue and actively participate in its activities. Furthermore, cross-talk between lymphocytes and adipocytes can lead to immune regulation. Adipose tissue produces and releases a variety of proinflammatory and anti-inflammatory factors, including the adipokines leptin, adiponectin, resistin, and visfatin, as well as cytokines and chemokines, such as TNF-alpha, IL-6, monocyte chemoattractant protein 1, and others. Proinflammatory molecules produced by adipose tissue have been implicated as active participants in the development of insulin resistance and the increased risk of cardiovascular disease associated with obesity. In contrast, reduced leptin levels might predispose to increased susceptibility to infection caused by reduced T-cell responses in malnourished individuals. Altered adipokine levels have been observed in a variety of inflammatory conditions, although their pathogenic role has not been completely clarified.
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            Leptin signaling, adiposity, and energy balance.

            A chronic minor imbalance between energy intake and energy expenditure may lead to obesity. Both lean and obese subjects eventually reach energy balance and their body weight regulation implies that the adipose tissue mass is "sensed", leading to appropriate responses of energy intake and energy expenditure. The cloning of the ob gene and the identification of its encoded protein, leptin, have provided a system signaling the amount of adipose energy stores to the brain. Leptin, a hormone secreted by fat cells, acts in rodents via hypothalamic receptors to inhibit feeding and increase thermogenesis. A feedback regulatory loop with three distinct steps has been identified: (1) a sensor (leptin production by adipose cells) monitors the size of the adipose tissue mass; (2) hypothalamic centers receive and integrate the intensity of the leptin signal through leptin receptors (LRb); (3) effector systems, including the sympathetic nervous system, control the two main determinants of energy balance-energy intake and energy expenditure. While this feedback regulatory loop is well established in rodents, there are many unsolved questions about its applicability to body weight regulation in humans. The rate of leptin production is related to adiposity, but a large portion of the interindividual variability in plasma leptin concentration is independent of body fatness. Gender is an important factor determining plasma leptin, with women having markedly higher leptin concentrations than men for any given degree of fat mass. The ob mRNA expression is also upregulated by glucocorticoids, whereas stimulation of the sympathetic nervous system results in its inhibition. Furthermore, leptin is not a satiety factor in humans because changes in food intake do not induce short-term increases in plasma leptin levels. After its binding to LRb in the hypothalamus, leptin stimulates a specific signaling cascade that results in the inhibition of several orexigenic neuropeptides, while stimulating several anorexigenic peptides. The orexigenic neuropeptides that are downregulated by leptin are NPY (neuropeptide Y), MCH (melanin-concentrating hormone), orexins, and AGRP (agouti-related peptide). The anorexigenic neuropeptides that are upregulated by leptin are alpha-MSH (alpha-melanocyte-stimulating hormone), which acts on MC4R (melanocortin-4 receptor); CART (cocaine and amphetamine-regulated transcript); and CRH (corticotropin-releasing-hormone). Obese humans have high plasma leptin concentrations related to the size of adipose tissue, but this elevated leptin signal does not induce the expected responses (i.e., a reduction in food intake and an increase in energy expenditure). This suggests that obese humans are resistant to the effects of endogenous leptin. This resistance is also shown by the lack of effect of exogenous leptin administration to induce weight loss in obese patients. The mechanisms that may account for leptin resistance in human obesity include a limitation of the blood-brain-barrier transport system for leptin and an inhibition of the leptin signaling pathways in leptin-responsive hypothalamic neurons. During periods of energy deficit, the fall in leptin plasma levels exceeds the rate at which fat stores are decreased. Reduction of the leptin signal induces several neuroendocrine responses that tend to limit weight loss, such as hunger, food-seeking behavior, and suppression of plasma thyroid hormone levels. Conversely, it is unlikely that leptin has evolved to prevent obesity when plenty of palatable foods are available because the elevated plasma leptin levels resulting from the increased adipose tissue mass do not prevent the development of obesity. In conclusion, in humans, the leptin signaling system appears to be mainly involved in maintenance of adequate energy stores for survival during periods of energy deficit. Its role in the etiology of human obesity is only demonstrated in the very rare situations of absence of the leptin signal (mutations of the leptin gene or of the leptin receptor gene), which produces an internal perception of starvation and results in a chronic stimulation of excessive food intake.
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              Recommendations for standards in transthoracic two-dimensional echocardiography in the dog and cat. Echocardiography Committee of the Specialty of Cardiology, American College of Veterinary Internal Medicine.

              Recommendations are presented for standardized imaging planes and display conventions for two-dimensional echocardiography in the dog and cat. Three transducer locations ("windows") provide access to consistent imaging planes: the right parasternal location, the left caudal (apical) parasternal location, and the left cranial parasternal location. Recommendations for image display orientations are very similar to those for comparable human cardiac images, with the heart base or cranial aspect of the heart displayed to the examiner's right on the video display. From the right parasternal location, standard views include a long-axis four-chamber view and a long-axis left ventricular outflow view, and short-axis views at the levels of the left ventricular apex, papillary muscles, chordae tendineae, mitral valve, aortic valve, and pulmonary arteries. From the left caudal (apical) location, standard views include long-axis two-chamber and four-chamber views. From the left cranial parasternal location, standard views include a long-axis view of the left ventricular outflow tract and ascending aorta (with variations to image the right atrium and tricuspid valve, and the pulmonary valve and pulmonary artery), and a short-axis view of the aortic root encircled by the right heart. These images are presented by means of idealized line drawings. Adoption of these standards should facilitate consistent performance, recording, teaching, and communicating results of studies obtained by two-dimensional echocardiography.
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                Author and article information

                Contributors
                jhkang@chungbuk.ac.kr
                Journal
                J Vet Intern Med
                J. Vet. Intern. Med
                10.1111/(ISSN)1939-1676
                JVIM
                Journal of Veterinary Internal Medicine
                John Wiley and Sons Inc. (Hoboken )
                0891-6640
                1939-1676
                30 August 2016
                Sep-Oct 2016
                : 30
                : 5 ( doiID: 10.1111/jvim.2016.30.issue-5 )
                : 1589-1600
                Affiliations
                [ 1 ] Laboratory of Veterinary Internal Medicine College of Veterinary MedicineChunghuk National University Cheongju ChungbukKorea
                [ 2 ] Laboratory of Veterinary Biochemistry and Molecular Biology College of Veterinary MedicineChunghuk National University Cheongju ChungbukKorea
                Author notes
                [*] [* ]Corresponding author: J.‐H. Kang, DVM, MS, PhD, Associate Professor, College of Veterinary Medicine, Chungbuk National University, Cheongju, Chungbuk 362‐763, Korea; e‐mail: jhkang@ 123456chungbuk.ac.kr
                Article
                JVIM14570
                10.1111/jvim.14570
                5032864
                27573621
                fe069fce-7e10-43b2-bf38-f34bbed916fc
                Copyright © 2016 The Authors. Journal of Veterinary Internal Medicine published by Wiley Periodicals, Inc. on behalf of the American College of Veterinary Internal Medicine .

                This is an open access article under the terms of the Creative Commons Attribution‐NonCommercial License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.

                History
                : 02 July 2015
                : 23 May 2016
                : 02 August 2016
                Page count
                Figures: 5, Tables: 4, Pages: 12, Words: 8494
                Funding
                Funded by: Basic Science Research Program
                Funded by: National Research Foundation of Korea (NRF)
                Funded by: Ministry of Science, ICT and Future Planning
                Award ID: 2013R1A1A1011113
                Categories
                Standard Article
                SMALL ANIMAL
                Standard Articles
                Cardiology
                Custom metadata
                2.0
                jvim14570
                September/October 2016
                Converter:WILEY_ML3GV2_TO_NLMPMC version:4.9.4 mode:remove_FC converted:26.09.2016

                Veterinary medicine
                adipokine,canine,cardiology,heart failure,valvular disease
                Veterinary medicine
                adipokine, canine, cardiology, heart failure, valvular disease

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