%0 Journal Article
%T Paprika Pigments Attenuate Obesity-Induced Inflammation in 3T3-L1 Adipocytes
%A Hayato Maeda
%A Shuuichi Saito
%A Nozomi Nakamura
%A Takashi Maoka
%J ISRN Inflammation
%D 2013
%R 10.1155/2013/763758
%X Obesity is related to various diseases, such as diabetes, hyperlipidemia, and hypertension. Adipocytokine, which is released from adipocyte cells, affects insulin resistance and blood lipid level disorders. Further, adipocytokine is related to chronic inflammation in obesity condition adipocyte cells. Paprika pigments (PPs) contain large amounts of capsanthin and capsorubin. These carotenoids affect the liver and improve lipid disorders of the blood. However, how these carotenoids affect adipocyte cells remains unknown. Present study examined the effects of PP on adipocytokine secretion, which is related to improvement of metabolic syndrome. In addition, suppressive effects of PP on chronic inflammation in adipocyte cells were analyzed using 3T3-L1 adipocyte cells and macrophage cell coculture experiments. PP promoted 3T3-L1 adipocyte cells differentiation upregulated adiponectin mRNA expression and secretion. Further, coculture of adipocyte and macrophage cells treated with PP showed suppressed interleukin-6 (IL-6), tumor necrosis factor-¦Á (TNF-¦Á), monocyte chemotactic protein-1 (MCP-1), and resistin mRNA expression, similarly to treatment with troglitazone, which is a PPAR¦Ã ligand medicine. Conclusion. These results suggest that PP ameliorates chronic inflammation in adipocytes caused by obesity. PP adjusts adipocytokine secretion and might, therefore, affect antimetabolic syndrome diseases. 1. Introduction Obesity has increased rapidly in recent years. It is currently regarded as a major risk factor for type 2 diabetes, hypertension, and dyslipidemia [1, 2]. The cluster of these three diseases is called metabolic syndrome, of which the incidence is a worldwide problem [3, 4]. Recent reports have described that obesity is characterized by low-grade chronic inflammation. Inflammation suggests a mechanism by which obesity engenders insulin resistance [5, 6]. Adipocytes are recognized as an important endocrine cell that secretes biologically active mediators called adipocytokines [4, 7]. They affect insulin sensitivity, glucose and lipid metabolism in muscle, liver, and adipose tissue and induce metabolic syndrome. TNF-¦Á and resistin, adipocytokines, are known to be elevated in obesity. They play important roles in the development of insulin resistance and type 2 diabetes [8, 9]. MCP-1 induces the infiltration of macrophages into adipose tissue. Moreover, it enhances inflammation causing insulin resistance [10]. These adipocytokines, which are secreted actively from hypertrophy adipocytes in conditions of obesity, exacerbate blood glucose homeostasis in
%U http://www.hindawi.com/journals/isrn.inflammation/2013/763758/