Abstract
The circulating concentrations of adiponectin, an antidiabetic adipokine, have been shown to be reduced in obesity, in relation to an increase in inflammation. The aim of the present work was to assess the effect of leptin replacement on adiponectin levels and expression as well as on markers of oxidative stress and inflammation in leptin-deficient ob/ob mice. Twelve-week-old male mice (n = 7–10 per group) were treated with either saline (wild type and ob/ob mice) or leptin (ob/ob mice) for 18 days. A third group of ob/ob mice was treated with saline and pair-fed to the amount of food consumed by the leptin-treated group. Leptin replacement restored values of adiponectin (P < 0.001), reduced circulating 8-isoprostane and serum amyloid A (SAA) levels (P < 0.05 for both), and significantly downregulated the increased gene expression of osteopontin (Spp1, P < 0.05), Saa3 (P < 0.05), Cd68 (P < 0.01), Il6 (P < 0.01) and NADPH oxidase (Nox1 and Nox2, P < 0.01) in the perirenal WAT and Spp1 (P < 0.05) in the liver of ob/ob mice. In cultured adipocytes from ob/ob mice, leptin increased (P < 0.05) the mRNA expression and secretion of adiponectin. We concluded that circulating concentrations of adiponectin are positively regulated by leptin and ameliorate obesity-associated oxidative stress and inflammation in mice.
Highlights
Over the last decades, changes in lifestyle have caused a progressive increase in the incidence of obesity, being one of the most prevalent metabolic disorders[1, 2]
Leptin administration significantly reduced circulating concentrations of the acute phase reactant serum amyloid A (SAA), which were dramatically increased in the ob/ob mice, to a similar extent than pair-feeding
Serum total adiponectin concentrations were negatively correlated with the circulating levels of 8-isoprostane (r = −0.37, P = 0.032; Fig. 1d) and SAA (r = −0.54, P = 0.002; Fig. 1e)
Summary
Changes in lifestyle have caused a progressive increase in the incidence of obesity, being one of the most prevalent metabolic disorders[1, 2]. Adipose tissue secretes a wide variety of biologically active molecules representing an extremely active endocrine organ[3] These secreted proteins, collectively called adipokines, such as leptin and adiponectin, are known to be involved in the pathophysiological link between increased adiposity and cardiometabolic abnormalities[3]. Its regulatory function of energy homeostasis, leptin is involved in the regulation of neuroendocrine function, haematopoiesis, angiogenesis, and reproduction, among others[5] Adiponectin is another important adipokine of 30 kDa expressed almost exclusively in adipose tissue[6]. Leptin-deficient ob/ob mice exhibit massive obesity, dyslipidemia and insulin resistance These mice have been proposed as a model of the metabolic syndrome since they exhibit many of the pathophysiologic alterations most frequently associated with obesity, including increased oxidative stress[14,15,16] and elevated systemic inflammation[14, 17]
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