Spelling suggestions: "subject:"uncoupled protein 1""
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Studies on the effects and mechanism of food components on obesity-related inflammation / 肥満関連炎症における食品成分の作用とメカニズムに関する研究Li, Yongjia 24 November 2016 (has links)
京都大学 / 0048 / 新制・課程博士 / 博士(農学) / 甲第20068号 / 農博第2197号 / 新制||農||1046(附属図書館) / 学位論文||H28||N5024(農学部図書室) / 京都大学大学院農学研究科食品生物科学専攻 / (主査)教授 河田 照雄, 教授 金本 龍平, 教授 谷 史人 / 学位規則第4条第1項該当 / Doctor of Agricultural Science / Kyoto University / DGAM
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Study on the regulatory mechanism for Uncoupling protein 1 (Ucp1) expression in beige adipocytes / ベージュ脂肪細胞の脱共役タンパク質1発現調節機構に関する研究Ana, Yuliana 24 September 2019 (has links)
京都大学 / 0048 / 新制・課程博士 / 博士(農学) / 甲第22073号 / 農博第2365号 / 新制||農||1072(附属図書館) / 学位論文||R1||N5227(農学部図書室) / 京都大学大学院農学研究科食品生物科学専攻 / (主査)教授 井上 和生, 教授 保川 清, 教授 谷 史人 / 学位規則第4条第1項該当 / Doctor of Agricultural Science / Kyoto University / DFAM
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Studies on the identification and characterization of factors that regulate uncoupling protein 1 expression in beige adipocytes / ベージュ脂肪細胞における脱共役タンパク質1発現調節因子の同定と機能解析に関する研究Iwase, Mari 23 March 2020 (has links)
京都大学 / 0048 / 新制・課程博士 / 博士(農学) / 甲第22510号 / 農博第2414号 / 新制||農||1078(附属図書館) / 学位論文||R2||N5290(農学部図書室) / 京都大学大学院農学研究科食品生物科学専攻 / (主査)教授 井上 和生, 教授 佐々木 努, 准教授 後藤 剛 / 学位規則第4条第1項該当 / Doctor of Agricultural Science / Kyoto University / DGAM
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Studies on the promoting effect of food components on energy metabolism through the induction of UCP1 in adipose tissue / 食品成分による脂肪組織のUCP1を介したエネルギー代謝促進効果に関する研究Kim, Minji 23 March 2016 (has links)
京都大学 / 0048 / 新制・課程博士 / 博士(農学) / 甲第19785号 / 農博第2181号 / 新制||農||1042(附属図書館) / 学位論文||H28||N5001(農学部図書室) / 32821 / 京都大学大学院農学研究科食品生物科学専攻 / (主査)教授 河田 照雄, 教授 金本 龍平, 教授 谷 史人 / 学位規則第4条第1項該当 / Doctor of Agricultural Science / Kyoto University / DGAM
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Studies on the regulatory expression of uncoupling protein 1 in bovine skeletal muscle / ウシ骨格筋における脱共役タンパク質1発現調節に関する研究Diao, Zhicheng 25 September 2023 (has links)
京都大学 / 新制・課程博士 / 博士(農学) / 甲第24911号 / 農博第2574号 / 新制||農||1102(附属図書館) / 京都大学大学院農学研究科応用生物科学専攻 / (主査)教授 舟場 正幸, 教授 太田 毅, 教授 横井 伯英 / 学位規則第4条第1項該当 / Doctor of Agricultural Science / Kyoto University / DGAM
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Apolipoprotein A-IV Enhances Thermogenesis in Brown Adipose Tissue and Energy ExpenditureKUO, HSUAN-CHIH 10 September 2021 (has links)
No description available.
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Nardilysin in adipocytes regulates UCP1 expression and body temperature homeostasis / 脂肪細胞のナルディライジンはUCP1の発現と体温恒常性を調節するSaijo, Sayaka 23 May 2022 (has links)
京都大学 / 新制・論文博士 / 博士(医学) / 乙第13490号 / 論医博第2258号 / 新制||医||1059(附属図書館) / 京都大学大学院医学研究科医学専攻 / (主査)教授 渡邉 大, 教授 稲垣 暢也, 教授 長船 健二 / 学位規則第4条第2項該当 / Doctor of Medical Science / Kyoto University / DFAM
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Význam metabolismu tukové tkáně pro celotělovou energetickou rovnováhu / Importance of adipose tissue metabolism for whole-body energy balanceZouhar, Petr January 2015 (has links)
Adipose tissue plays a crucial role in nutrient and energy homeostasis. At the time of worldwide pandemy of obesity and consequent metabolic syndrome, a great effort is made to find new treatments with potential to preserve insulin sensitivity, or even counteract development of obesity and type 2 diabetes. There are three principal possibilities how the adipose tissue biology can contribute to this goal: 1) induction of UCP1-dependent energy dissipation in brown adipose tissue; 2) conversion of white adipose depots to brown-like tissue (i.e. "browning"); and 3) stimulation of UCP1-independent thermogenesis in white adipose tissue. This thesis is based on two published works and one article under preparation. Generaly, it is focused on three different approaches targeting the above mentioned processes in adipose tissue of laboratory mouse: 1) diet supplementation with bile acids; 2) combination treatment of ω-3 polyunsaturated fatty acids and calorie restriction; and 3) cold exposure. In the experiments with administration of bile (specifically chenodeoxycholic) acid to mice, we confirm specific induction of UCP1 in both brown and subcutaneous white adipose tissue, as well as reversion of obesity in the response to the treatment. Nevertheless, most of the acute beneficial effects are mediated by...
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The Role of Tumor and Tumor Microenvironment on Breast Cancer-Associated Adipocyte PlasticityPearce, Janina V 01 January 2019 (has links)
Cancer-associated cachexia is a condition defined by a sustained net-negative energy imbalance. Although the different types of adipose tissue – white, beige, and brown – have been implicated in contributing to cancer-associated cachexia, the mechanisms of these maladaptive changes and their impact on whole-body energy expenditure have not been fully elucidated. Using breast cancer as our model, we demonstrate white adipose tissue browning in murine and human breast cancer; furthermore, we demonstrate that this effect is extremely localized and takes place early in tumor progression. We utilized in vitro cell culture techniques and demonstrate that cancer secreted factors and cross-talk with white adipocytes decrease expression of classic white adipose tissue-related genes. We also demonstrate in murine and human culture models that cancer secreted factors reduce white adipocyte lipid droplet size, and cross-talk between cancer cells and adipocytes results in an increase in lipolysis-related gene expression. Interestingly, our results strongly suggest that in mice, neither cancer secreted factors nor cross talk with adipocytes can induce white adipose tissue browning, indicate that this process likely occurs independently of direct cancer interactions with local white adipocytes. We demonstrate that interleukin 6, a cytokine with previous implications in white adipose tissue browning, induces interleukin 6-mediated signaling; however, that signaling alone is not enough to directly induce white adipose tissue browning. We present preliminary data suggesting that immune cell population shifts within the white adipose tissue of mice with breast cancer tumors may be source of white adipose tissue browning. We show that the Virginia Commonwealth University Health System has an identifiable population of patients with cancer with what we hypothesize as maladaptive thermogenic adipose tissue activity, and discuss ongoing experiments aimed at understanding the implications of these changes on whole body energy expenditure in human patients. Lastly, in a case of autoimmune diabetes mellitus in the setting of an extra-adrenal paraganglioma, we demonstrate that the interaction between cancer and whole-body metabolism is multifaceted. Together, these experiments demonstrate that adipose tissue plasticity occurs in breast cancer (and other cancers), and that different drivers for individual changes exist within the tumor microenvironment. We predict that further exploration of the exact mechanisms and translational implications will provide useful information to lead to new therapeutic treatments for patients with cancer-associated cachexia.
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Implications du stress oxydant et du découplage mitochondrial dans les compromis entre traits d'histoire de vie / At the crossroad of metabolism and ageing : mitochondrial proximal control of oxidants and ultimate modulation of life history trade-offsStier, Antoine 24 October 2013 (has links)
L’attention scientifique s’est récemment portée sur l’identification des mécanismes proximaux sous-tendant les compromis évolutifs;tels que les compromis existant entre croissance/reproduction et longévité. La production d’espèces réactives de l’oxygène (ROS )a été suggérée comme un candidat potentiel ,de par sa liaison étroite au métabolisme énergétique (sous-produits du fonctionnement mitochondrial) et son caractère inévitable. Si la production de ROS excède le niveau des défenses antioxydantes, une situation de stress oxydant va en résulter et a été associé au vieillissement . Puisque la mitochondrie n’est pas uniquement la centrale énergétique de la cellule mais aussi le principal producteur de ROS, cette thèse s’est attachée à clarifier les relations entre métabolisme énergétique , fonctionnement mitochondrial et stress oxydant ; avec des études concernant l’impact d’activités coûteuses en énergie (croissance, reproduction, thermogénèse) sur l’équilibre de la balance oxydative. / In recent years, scientific attention has turned towards the identification of the mechanisms underlying the trade-‐offs occurring between growth rate/reproductive investment and longevity. Amongst these mechanisms, the production of reactive oxygen species (ROS) appears to be a key factor due both to its universal and inevitable nature. ROS are by-‐products of energy processing by the mitochondria. If ROS production exceeds the capacity of the various antioxidant systems, oxidative stress will occur, and the accumulation of oxidative damage over time is thought to be a potential cause of ageing. Since mitochondria are not only the powerhouse of animal cells but also the main producer of ROS, this PhD thesis aimed to clarify the relationships between mitochondrial uncoupling state (i.e. efficiency to produce ATP), energy metabolism and oxidative stress. I investigated the impact of energy-‐demanding activities such as thermogenesis, reproduction and growth on oxidative homeostasis.
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