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Goto, Tsuyoshi,Hirata, Mariko,Aoki, Yumeko,Iwase, Mari,Takahashi, Haruya,Kim, Minji,Li, Yongjia,Jheng, Huei-Fen,Nomura, Wataru,Takahashi, Nobuyuki,Kim, Chu-Sook,Yu, Rina,Seno, Shigeto,Matsuda, Hideo,A American Society for Biochemistry and Molecular Bi 2017 The Journal of biological chemistry Vol.292 No.22
<P>Obesity causes excess fat accumulation in white adipose tissues (WAT) and also in other insulin-responsive organs such as the skeletal muscle, increasing the risk for insulin resistance, which can lead to obesity-related metabolic disorders. Peroxisome proliferator-activated receptor-alpha (PPAR alpha) is a master regulator of fatty acid oxidation whose activator is known to improve hyperlipidemia. However, the molecular mechanisms underlying PPAR alpha activator-mediated reduction in adiposity and improvement of metabolic disorders are largely unknown. In this study we investigated the effects of PPAR alpha agonist (fenofibrate) on glucose metabolism dysfunction in obese mice. Fenofibrate treatment reduced adiposity and attenuated obesity-induced dysfunctions of glucose metabolism in obese mice fed a high-fat diet. However, fenofibrate treatment did not improve glucose metabolism in lipodystrophic A-Zip/F1 mice, suggesting that adipose tissue is important for the fenofibrate-mediated amelioration of glucose metabolism, although skeletal muscle actions could not be completely excluded. Moreover, we investigated the role of the hepatokine fibroblast growth factor 21 (FGF21), which regulates energy metabolism in adipose tissue. In WAT of WT mice, but not of FGF21-deficient mice, fenofibrate enhanced the expression of genes related to brown adipocyte functions, such as Ucp1, Pgc1a, and Cpt1b. Fenofibrate increased energy expenditure and attenuated obesity, whole body insulin resistance, and adipocyte dysfunctions in WAT in high-fat-diet-fed WT mice but not in FGF21-defi-the fenofibrate-mediated improvement of whole body glucose metabolism in obese mice via the amelioration of WAT dysfunctions.</P>
Nguyen Thi Trang,Takuya Hirai,Tsukasa Yamamoto,Mari Matsuda,Naoko Okumura,Nguyen Thi Huong Giang,Nguyen Thi Lan,Ryoji Yamaguchi 대한수의학회 2014 JOURNAL OF VETERINARY SCIENCE Vol.15 No.3
The objectives of the present study were to evaluate theanatomic localization of porcine reproductive andrespiratory syndrome virus (PRRSV) in naturally infectedpigs and to determine whether oral fluid could be used todetect the virus in infected animals. Two sows, seven2-month-old grower pigs, and 70 6-month-old gilts wereincluded in this study. PRRSV in sera and oral fluid wereidentified by nested reverse transcription PCR (nRT-PCR)while lung, tonsil, and tissue associated with oral cavity weresubjected to nRT-PCR, immunohistochemistry, and in situhybridization. In sows, PRRSV was identified in oral fluidand tonsils. PRRSV was also detected in oral fluid, tonsils,salivary glands, oral mucosa, and lungs of all seven growerpigs. However, viremia was observed in only two growerpigs. Double staining revealed that PRRSV was distributedin macrophages within and adjacent to the tonsillar cryptepithelium. In gilts, the North American type PRRSV fieldstrain was detected 3 to 8 weeks after introducing theseanimals onto the farm. These results confirm previousfindings that PRRSV primarily replicates in tonsils and isthen shed into oral fluid. Therefore, oral fluid sampling maybe effective for the surveillance of PRRSV in breeding herds.