The incidence of obesity in dogs and cats is increasing in recent years. In humans, obesity has been associated with the metabolic syndrome, which consists of a cluster of disorders including, insulin resistance, type II diabetes mellitus, hyperlipidemia, hepatic steatosis, hypertension, and atherosclerosis. Although naturally-occurring metabolic syndrome has not been described in dogs or cats, some components of this syndrome occur in diseases related to obesity, either as a predisposing factor (i.e. feline hepatic lipidosis and feline diabetes mellitus), a complicating factor (i.e. canine diabetes mellitus), or a consequence (i.e. canine hypothyroidism). Decreased adiponectin concentration has been implicated in the pathogenesis of the metabolic syndrome in humans. Findings regarding leptin are less consistent and either leptin deficiency or resistance was suggested. Consumption of n3-polyunsaturated fatty acids (PUFAs) has beneficial effects on various metabolic alterations of the syndrome. The present studies aimed to determine alterations in adipokines concentrations in obesity-related diseases in dogs and cats and to determine the effect of n3PUFAs on adipokines in health and disease.In healthy dogs, circulating concentrations of docosapentaenoic acid were positively associated with concentrations of adiponectin and leptin; dietary fish oil supplementation for 30 days yielded an increase in adiponectin. In healthy cats, associations of n3PUFAs with adipokines were differential with body condition. Concentrations of eicosapentaenoic acid and docosahexaenoic acid were positively associated with adiponectin concentrations in obese cats; while in non-obese cats, concentrations of eicosapentaenoic acid were negatively associated with concentrations of adiponectin and positively associated with concentrations of leptin.In canine adipose tissue culture, eicosapentaenoic acid stimulated adiponectin secretion by mature adipocytes and inhibited inteleukin-6 secretion by stromovascular cells. In contrast, palmitic acid inhibited adiponectin secretion by mature adipocytes and stimulated inteleukin-6 secretion by stromovascular cells. In feline adipose tissue culture, arachidonic acid stimulated inteleukin-6 secretion by stromovascular cells. Therefore, the stimulatory effect of n3PUFAs on adiponectin may be direct or mediated through inhibition of IL6. Moreover, these effects may be conveyed by n3PUFAs directly or by substitution of n6PUFAs or a saturated fatty acid.Feline hepatic lipidosis was associated with hyperadiponectinemia, which is likely related to liver injury, and with hyperleptinemia, which is suggested to be specific to lipidosis. Canine hypothyroidism was associated with hyperleptinemia, which was associated thyroid hormone deficiency, and with hyperadiponectinemia, suggestive of adiponectin resistance. Diabetes mellitus was associated with hyperleptinemia in cats and hypoleptinemia in dogs, consistent with the opposite alterations in insulin secretion in these diseases. In healthy animals, docosapentaenoic acid (dogs) or eicosapentaenoic acid (obese cats) was negatively associated with concentrations of triglyceride, supporting a hypolipidemic effect n3PUFAs. A negative association between n3PUFA and triglyceride was present in cats with hepatic lipidosis, but not the other diseases studied, suggesting preservation of a hypolipidemic effect of n3PUFA in overt feline hepatic lipidosis. Eicosapentaenoic was negatively associated with insulin concentrations in obese cats, supporting an insulin-sensitizing effect.
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