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Kim, Minji,Furuzono, Tomoya,Yamakuni, Kanae,Li, Yongjia,Kim, Young-Il,Takahashi, Haruya,Ohue-Kitano, Ryuji,Jheng, Huei-Fen,Takahashi, Nobuyuki,Kano, Yuriko,Yu, Rina,Kishino, Shigenobu,Ogawa, Jun,Uchid The Federation of American Societies for Experimen 2017 The FASEB Journal Vol.31 No.11
<P>Gutmicrobiota can regulate the host energymetabolism; however, the underlying mechanisms that could involve gut microbiota-derived compounds remain to be understood. Therefore, in this study, we investigated the effects ofKetoA [10-oxo-12(Z)-octadecenoic acid]-a linoleic acidmetaboliteproduced by gut lactic acid bacteria-on whole-body energy metabolism and found that dietary intake of KetoA could enhance energy expenditure in mice, thereby protecting mice from diet-induced obesity. By using Ca2+ imaging and whole-cell patch-clamp methods, KetoA was noted to potently activate transient receptor potential vanilloid 1 (TRPV1) and enhance noradrenalin turnover in adipose tissues. In addition, KetoA up-regulated genes that are related to brown adipocyte functions, including uncoupling protein 1 (UCP1) inwhite adipose tissue (WAT), whichwas later diminished in the presence of a b-adrenoreceptor blocker. By using obese and diabetic model KK-Ay mice, we further show that KetoA intake ameliorated obesity-associatedmetabolic disorders. In the absence of any observedKetoA-induced antiobesity effect or UCP1 up-regulation in TRPV1-deficient mice, we prove that the antiobesity effect of KetoAwas caused by TRPV1 activation-mediated browning inWAT. KetoA produced in the gut could therefore be involved in the regulation of host energy metabolism.-Kim, M., Furuzono, T., Yamakuni, K., Li, Y., Kim, Y.-I., Takahashi, H., Ohue-Kitano, R., Jheng, H.-F., Takahashi, N., Kano, Y., Yu, R., Kishino, S., Ogawa, J., Uchida, K., Yamazaki, J., Tominaga, M., Kawada, T., Goto, T. 10-oxo-12(Z)-octadecenoic acid, a linoleic acid metabolite produced by gut lactic acid bacteria, enhances energy metabolism by activation of TRPV1.</P>
Over-expression of PPARα in obese mice adipose tissue improves insulin sensitivity
Takahashi, Haruya,Sanada, Kohei,Nagai, Hiroyuki,Li, Yongjia,Aoki, Yumeko,Ara, Takeshi,Seno, Shigeto,Matsuda, Hideo,Yu, Rina,Kawada, Teruo,Goto, Tsuyoshi Elsevier 2017 Biochemical and biophysical research communication Vol. No.
<P><B>Abstract</B></P> <P>Peroxisome proliferator-activated receptor α (PPARα) is important in the regulation of lipid metabolism and expressed at high levels in the liver. Although PPARα is also expressed in adipose tissue, little is known about the relationship between its activation and the regulation of glucose metabolism. In this study, we developed adipose tissue specific PPARα over-expression (OE) mice. Metabolomics and insulin tolerance tests showed that OE induces branched-chain amino acid (BCAA) profile and improvement of insulin sensitivity. Furthermore, LC-MS and PCR analyses revealed that OE changes free fatty acid (FFA) profile and reduces obesity-induced inflammation. These findings suggested that PPARα activation in adipose tissue contributes to the improvement of glucose metabolism disorders via the enhancement of BCAA and FFA metabolism.</P>
[New insights into the pathogenesis of neuromyelitis optica]
Misu, Tatsuro,Takahashi, Toshiyuki,Nishiyama, Shuhei,Takano, Rina,Nakashima, Ichiro,Fujihara, Kazuo,Itoyama, Yasuto 醫學書院 2010 Brain and nerve Vol.62 No.9
<P>Recently, the disease-specific antibody was found in the sera from neuromyelitis optica (NMO) patients, and its target was identified as aquaporin-4 (AQP4), mainly expressed in astroglial foot processes. In our immunohistochemical studies, loss of AQP4 and glial fibrillary acidic protein (GFAP) was evident in about 90% of NMO lesions, especially in perivascular areas of acute inflammatory lesions where immunoglobulins and complements were deposited. In contrast, myelin basic protein (MBP)-stained myelinated fibers were relatively preserved in those lesions, which probably suggested the secondary damage of myelin sheaths following astrocytic damage. Recently, there are developing evidences of the effect of AQP4 antibody in vitro or in vivo. In HEK293 cells transfected with AQP4, AQP4 antibody could bind to the membrane AQP4, and induced the degradation and endocytosis of AQP4 in complement-dependent manner. In vitro experiments by primary cultured astrocytes, AQP4 antibody had cytotoxic effects with complement, and also could impair the astrocytic function such as the maintenance of the blood brain barrier or glutamate homeostasis. In vivo study, the lesions lacking AQP4 and GFAP was appeared by passive-transferred Lewis rats with human purified IgG from NMO patients. Furthermore, in cerebrospinal fluid (CSF) biomarker study, astrocytic damage reflected by marked increase of CSF-GFAP, far severe than demyelination (CSF-MBP), was evident in NMO but not in classical multiple sclerosis (MS). These evidences suggested the pathogenic role of AQP4 antibody with astrocytopathy in NMO. Now it is indispensable to check the AQP4 antibody,and is important to reconsider the role of astrocyte in demyelinating disorders.</P>
Yuichi Tomiki,Jun Aoki,Shunsuke Motegi,Rina Takahashi,Toshiaki Hagiwara,Yu Okazawa,Kosuke Mizukoshi,Masaya Kawai,Shinya Munakata,Shun Ishiyama,Kiichi Sugimoto,Kazuhiro Sakamoto 대한소화기내시경학회 2019 Clinical Endoscopy Vol.52 No.6
Background/Aims: Sclerotherapy with aluminum potassium sulfate and tannic acid (ALTA) has a potent effect on internalhemorrhoids. In this retrospective study, we compared the effects of endoscopic ALTA therapy and standard ALTA therapy. Methods: We investigated patients who underwent treatment for internal hemorrhoids at our institution between 2014 and 2016. Theywere divided into a standard ALTA group (n=33, treated using proctoscopy) and an endoscopic ALTA group (n=48). We compared theclinical findings between the 2 groups. Results: There were no intergroup differences in background factors. The mean ALTA dose was 21.9±7.2 mL and 17.8±3.4 mL inthe standard and endoscopic ALTA groups, respectively (p<0.01). Adverse events occurred in 4 patients (12.1%) from the standardALTA group and 6 patients (12.5%) from the endoscopic ALTA group. In both groups, the patients reported good satisfaction withthe therapeutic effect at 1 month after the procedure. Hemorrhoids recurred in 2 patients (6.3%) from the standard ALTA group and 4patients (8.3%) from the endoscopic ALTA group. Conclusions: Endoscopic ALTA sclerotherapy is equivalent to standard ALTA therapy in terms of efficacy, adverse events, andrecurrence. Therefore, it is a useful non-surgical option for patients with internal hemorrhoids who prefer a less invasive treatment.
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>
Dehydroabietic acid, a diterpene, improves diabetes and hyperlipidemia in obese diabetic KK-Ay mice.
Kang, Min-Sook,Hirai, Shizuka,Goto, Tsuyoshi,Kuroyanagi, Kayo,Kim, Young-Il,Ohyama, Kana,Uemura, Taku,Lee, Joo-Young,Sakamoto, Tomoya,Ezaki, Yoichiro,Yu, Rina,Takahashi, Nobuyuki,Kawada, Teruo Published for International Union of Biochemistry 2009 Biofactors Vol.35 No.5
<P>Terpenoids, which are contained in a large number of dietary and herbal plants, have many biological effects. In this study, the effects of dehydroabietic acid (DAA), a diterpene, on glucose and lipid metabolism were examined using obese diabetic KK-Ay mice. We showed here that DAA treatment decreased not only plasma glucose and insulin levels but also plasma triglyceride (TG) and hepatic TG levels. To examine the mechanism underlying the effects of DAA, the production of inflammatory cytokines was measured. It was shown that the DAA treatment suppressed the production of monocyte chemoattractant protein-1 (MCP-1) and tumor necrosis factor-alpha (TNFalpha) (proinflammatory cytokines) and increased that of adiponectin (an anti-inflammatory cytokine). As a result of the changes in the production of inflammatory cytokines caused by the DAA treatment, the accumulation of macrophages in adipose tissues was reduced. These results indicate that treatment with DAA improves the levels of plasma glucose, plasma insulin, plasma TG, and hepatic TG through the decrease in the macrophage infiltration into adipose tissues, suggesting that DAA is a useful food-derived compound for treating obesity-related diseases.</P>