研究者データベース

岡松 優子(オカマツ ユウコ)
獣医学研究院 獣医学部門 基礎獣医科学分野
准教授

基本情報

所属

  • 獣医学研究院 獣医学部門 基礎獣医科学分野

職名

  • 准教授

学位

  • 博士(獣医学)(北海道大学)

ホームページURL

J-Global ID

研究キーワード

  • メタボリックシンドローム   細胞増殖   体温調節   褐色脂肪   脂肪細胞   肥満   代謝   

研究分野

  • ライフサイエンス / 代謝、内分泌学
  • ライフサイエンス / 生理学
  • ライフサイエンス / 獣医学
  • ライフサイエンス / 獣医学
  • ライフサイエンス / 獣医学

職歴

  • 2018年11月 - 現在 北海道大学 大学院獣医学研究院 生化学教室 准教授
  • 2015年09月 - 2018年10月 北海道大学 大学院獣医学研究院 生化学教室 講師
  • 2008年06月 - 2015年08月 北海道大学 大学院獣医学研究科 生化学教室 助教
  • 2008年04月 - 2008年05月 日本学術振興会 特別研究員 (PD)
  • 2007年04月 - 2008年03月 日本学術振興会 特別研究員 (DC2)

学歴

  • 2004年04月 - 2008年03月   北海道大学   獣医学研究科
  •         - 2008年   北海道大学
  • 1998年04月 - 2004年03月   北海道大学   獣医学部
  •         - 2004年   北海道大学

所属学協会

  • 日本獣医学会   日本肥満学会   

研究活動情報

論文

  • Association of circulating exosomal miR-122 levels with BAT activity in healthy humans.
    Okamatsu-Ogura Y, Matsushita M, Bariuan JV, Nagaya K, Tsubota A, Saito M
    Sci Rep 9 1 13243  2019年 [査読有り][通常論文]
  • Role of brown adipose tissue in body temperature control during the early postnatal period in Syrian hamsters and mice.
    Tsubota A, Okamatsu-Ogura Y, Bariuan JV, Mae J, Matsuoka S, Nio-Kobayashi J, Kimura K
    J Vet Med Sci 81 6 799 - 807 2019年 [査読有り][通常論文]
  • Impaired adrenergic agonist-dependent beige adipocyte induction in obese mice.
    Shin W, Okamatsu-Ogura Y, Matsuoka S, Tsubota A, Kimura K
    J Vet Med Sci 81 6 799 - 807 2019年 [査読有り][通常論文]
  • Effect of ambient temperature on the proliferation of brown adipocyte progenitors and endothelial cells during postnatal BAT development in Syrian hamsters.
    Nagaya K, Okamatsu-Ogura Y, Nio-Kobayashi J, Nakagiri S, Tsubota A, Kimura K
    J Physiol Sci 69 23 - 30 2019年 [査読有り][通常論文]
  • Yuko Okamatsu-Ogura, Junko Nio-Kobayashi, Kazuki Nagaya, Ayumi Tsubota, Kazuhiro Kimura
    Journal of Applied Physiology 124 1 99 - 108 2018年01月01日 [査読有り][通常論文]
     
    To investigate the postnatal development of brown adipose tissue (BAT) in Syrian hamsters, we histologically examined interscapular fat tissue from 5-16-day-old pups, focusing on how brown adipocytes arise. Interscapular fat of 5-day-old hamsters mainly consisted of white adipocytes containing large unilocular lipid droplets, as observed in typical white adipose tissue (WAT). On day 7, clusters of small, proliferative nonadipocytes with a strong immunoreactivity for Ki67 appeared near the edge of the interscapular fat tissue. The area of the Ki67-positive regions expanded to ~50% of the total tissue area by day 10.The interscapular fat showed the typical BAT feature by day 16. A brown adipocyte-specific marker, uncoupling protein-1, was clearly detected on day 10 and thereafter, while not detected on day 7. During conversion of interscapular fat from WAT to BAT, unilocular adipocytes completely and rapidly disappeared without obvious apoptosis. Dual immunofluorescence staining for Ki67 and monocarboxylate transporter 1 (MCT1), another selective marker for brown adipocytes, revealed that most of the proliferating cells were of the brown adipocyte lineage. Electron microscopic examination showed that some of the white adipocytes contained small lipid droplets in addition to the large droplet and expressed MCT1 as do progenitor and mature brown adipocytes, implying a direct conversion from white to brown adipocytes. These results suggest that BAT of Syrian hamsters develops postnatally through two different pathways: The proliferation and differentiation of brown adipocyte progenitors and the conversion of unilocular adipocytes to multilocular brown adipocytes.
  • Role of macrophages in depot-dependent browning of white adipose tissue.
    Machida K, Okamatsu-Ogura Y, Shin W, Matsuoka S, Tsubota A, Kimura K
    J Physiol Sci 68 5 601 - 608 2018年 [査読有り][通常論文]
  • Woongchul Shin, Yuko Okamatsu-Ogura, Ken Machida, Ayumi Tsubota, Junko Nio-Kobayashi, Kazuhiro Kimura
    OBESITY 25 2 417 - 423 2017年02月 [査読有り][通常論文]
     
    Objective: There are two types of thermogenic adipocytes expressing uncoupling protein ( UCP)-1: the brown adipocyte activated by adrenergic stimulation and the beige adipocyte that appears within the white adipose tissue ( WAT) in response to chronic adrenergic stimulation. This study examined age-related changes in responses of both types of adipocytes to adrenergic stimulation in mice. Methods: Aged ( age 20 months) and young ( 4 months) mice were injected daily with either saline or beta 3-adrenergic receptor agonist CL316,243 ( CL; 0.1 mg/kg, once a day) for 1 week. Results: The body and WAT weight tended to be higher in aged mice. CL treatment increased UCP-1 protein amounts in both brown adipose tissue and inguinal WAT, suggesting activation of brown and beige adipocytes. However, induction of beige adipocytes was impaired in aged mice, whereas brown adipocyte activation was comparable to young mice. The number of platelet-derived growth factor receptor alpha-expressing progenitor cells, which were reported to differentiate into beige adipocytes, significantly decreased in inguinal WAT of aged mice compared with that of young mice. Conclusions: Inductive ability of beige adipocytes in WAT declines with aging in mice. It may be partly because of a decreased number of progenitor cells associated with aging.
  • Cell-cycle arrest in mature adipocytes impairs BAT development but not WAT browning, and reduces adaptive thermogenesis in mice.
    Okamatsu-Ogura Y, Fukano K, Tsubota A, Nio-Kobayashi J, Nakamura K, Morimatsu M, Sakaue H, Saito M, Kimura K
    Sci Rep 7 1 6648  2017年 [査読有り][通常論文]
  • Keigo Fukano, Yuko Okamatsu-Ogura, Ayumi Tsubota, Junko Nio-Kobayashi, Kazuhiro Kimura
    PLoS One 11 11 e0166579  2016年11月 [査読有り][通常論文]
     
    Hyperplasia of brown adipose tissue (BAT) is a fundamental mechanism for adaptation to survive in the cold environment in rodents. To determine which cell types comprising BAT contribute to tissue hyperplasia, immunohistochemical analysis using a proliferative marker Ki67 was performed on the BAT from 6-week-old C57BLJ6J mice housed at 23 degrees C (control) or 10 degrees C (cold) for 5 days. Interestingly, in the control group, the cell proliferative marker Ki67 was detected in the nuclei of uncoupling protein 1-positive mature brown adipocytes (7.2% +/- 0.4% of brown adipocyte), as well as in the non-adipocyte stromal-vascular (SV) cells (19.6% +/- 2.3% of SV cells), which include preadiopocytes. The percentage of Ki67-positive brown adipocytes increased to 25.6% +/- 1.8% at Day 1 after cold exposure and was significantly higher than the non-cold acclimated control until Day 5 (21.8%+/- 1.7%). On the other hand, the percentage of Ki67-positive SV cells gradually increased by a cold exposure and peaked to 42.1%+/- 8.3% at Day 5. Injection of a beta 3-adrenergic receptor (beta 3-AR) agonist for continuous 5 days increased the number of Ki67-positive brown adipocytes even at Day 1 but not that of SV cells. In addition, the beta 3-AR antagonist, but not beta 1-AR antagonist, attenuated the cold exposure-induced increase in the number of Ki67-positive brown adipocytes. These results suggest that mature brown adipocytes proliferate immediately after cold exposure in a beta 3-AR-mediated pathway. Thus, proliferation of mature brown adipocytes as well as preadipocytes in SV cells may contribute to cold exposure-induced BAT hyperplasia.
  • Yuko Okamatsu-Ogura, Ayumi Tsubota, Kana Ohygma, Yoshihito Nogusa, Masayuki Saito, Kazuhiro Kimura
    JOURNAL OF FUNCTIONAL FOODS 19 1 - 9 2015年12月 [査読有り][通常論文]
     
    Capsinoids are less pungent capsaicin analogues that increase whole body energy expenditure and hence reduce fat. Several studies have suggested that capsinoids activate brown adipose tissue (BAT), a major site of adaptive thermogenesis, but the actual contribution of BAT and uncoupling protein 1 (UCP1), a thermogenic protein expressed in BAT, to the fat-reducing effect of capsinoids has not yet been determined. Here, we investigated the effect of capsinoids on high-fat diet (HFD)-induced obesity using wild-type (WT) and UCP1-deficient (KO) mice. Capsinoids feeding potently suppressed HFD-induced increase in body weight, adiposity, and fatty liver development in WT mice. In contrast, such effects of capsinoids were completely abolished in UCP1-KO mice. Moreover, capsinoids significantly increased UCP1 protein expression in BAT without its apparent induction in white adipose tissue (WAT) in WT mice. These results indicate that capsinoids suppress diet-induced obesity of mice through the UCP1 function in BAT but not in WAT. (C) 2015 Elsevier Ltd. All rights reserved.
  • Yuta Sakurai, Yuko Okamatsu-Ogura, Masayuki Saito, Kazuhiro Kimura, Ryo Nakao, Aiko Ohnuma, Mari Kobayashi
    MARINE MAMMAL SCIENCE 31 2 818 - 827 2015年04月 [査読有り][通常論文]
  • Masaaki K. Sato, Masaya Toda, Naoki Inomata, Hisataka Maruyama, Yuko Okamatsu-Ogura, Fumihito Arai, Takahito Ono, Akihiko Ishijima, Yuichi Inoue
    Biophysical Journal 106 11 2458 - 2464 2014年06月03日 [査読有り][通常論文]
     
    Mammalian cells must produce heat to maintain body temperature and support other biological activities. Methods to measure a cell's thermogenic ability by inserting a thermometer into the cell or measuring the rate of oxygen consumption in a closed vessel can disturb its natural state. Here, we developed a noninvasive system for measuring a cell's heat production with a bimaterial microcantilever. This method is suitable for investigating the heat-generating properties of cells in their native state, because changes in cell temperature can be measured from the bending of the microcantilever, without damaging the cell and restricting its supply of dissolved oxygen. Thus, we were able to measure increases in cell temperature of <1 K in a small number of murine brown adipocytes (n = 4-7 cells) stimulated with norepinephrine, and observed a slow increase in temperature over several hours. This long-term heat production suggests that, in addition to converting fatty acids into heat energy, brown adipocytes may also adjust protein expression to raise their own temperature, to generate more heat. We expect this bimaterial microcantilever system to prove useful for determining a cell's state by measuring thermal characteristics. © 2014 Biophysical Society.
  • Teramura Y, Terao A, Okada Y, Tomida J, Okamatsu-Ogura Y, Kimura K
    Jpn J Vet Res 62 3 117 - 127 2014年 [査読有り][通常論文]
  • Yuko Okamatsu-Ogura, Keigo Fukano, Ayumi Tsubota, Akihiro Uozumi, Akira Terao, Kazuhiro Kimura, Masayuki Saito
    PLOS ONE 8 12 e84229  2013年12月 [査読有り][通常論文]
     
    Chronic adrenergic activation leads to the emergence of beige adipocytes in some depots of white adipose tissue in mice. Despite their morphological similarities to brown adipocytes and their expression of uncoupling protein 1 (UCP1), a thermogenic protein exclusively expressed in brown adipocytes, the beige adipocytes have a gene expression pattern distinct from that of brown adipocytes. However, it is unclear whether the thermogenic function of beige adipocytes is different from that of classical brown adipocytes existing in brown adipose tissue. To examine the thermogenic ability of UCP1 expressed in beige and brown adipocytes, the adipocytes were isolated from the fat depots of C57BL/6J mice housed at 24 degrees C (control group) or 10 degrees C (cold-acclimated group) for 3 weeks. Morphological and gene expression analyses revealed that the adipocytes isolated from brown adipose tissue of both the control and cold-acclimated groups consisted mainly of brown adipocytes. These brown adipocytes contained large amounts of UCP1 and increased their oxygen consumption when stimulated with norepinephirine. Adipocytes isolated from the perigonadal white adipose tissues of both groups and the inguinal white adipose tissue of the control group were white adipocytes that showed no increase in oxygen consumption after norepinephrine stimulation. Adipocytes isolated from the inguinal white adipose tissue of the cold-acclimated group were a mixture of white and beige adipocytes, which expressed UCP1 and increased their oxygen consumption in response to norepinephrine. The UCP1 content and thermogenic ability of beige adipocytes estimated on the basis of their abundance in the cell mixture were similar to those of brown adipocytes. These results revealed that the inducible beige adipocytes have potent thermogenic ability comparable to classical brown adipocytes.
  • Tsutomu Sasaki, Mayumi Shimpuku, Tomoya Kitazumi, Haruna Hiraga, Yuko Nakagawa, Hiroshi Shibata, Yuko Okamatsu-Ogura, Osamu Kikuchi, Hye-Jin Kim, Yuki Fujita, Jun Maruyama, Vina Yanti Susanti, Hiromi Yokota-Hashimoto, Masaki Kobayashi, Masayuki Saito, Tadahiro Kitamura
    Endocrine Journal 60 10 1117 - 1129 2013年 [査読有り][通常論文]
     
    Miglitol is an alpha-glucosidase inhibitor that improves post-prandial hyperglycemia, and it is the only drug in its class that enters the bloodstream. Anecdotally, miglitol lowers patient body weight more effectively than other alphaglucosidase inhibitors, but the precise mechanism has not been addressed. Therefore, we analyzed the anti-obesity effects of miglitol in mice and in the HB2 brown adipocyte cell line. Miglitol prevented diet-induced obesity by stimulating energy expenditure without affecting food intake in mice. Long-term miglitol treatment dose-dependently prevented dietinduced obesity and induced mitochondrial gene expression in brown adipose tissue. The anti-obesity effect was independent of preventing carbohydrate digestion in the gastrointestinal tract. Miglitol effectively stimulated energy expenditure in mice fed a high-fat high-monocarbohydrate diet, and intraperitoneal injection of miglitol was sufficient to stimulate energy expenditure in mice. Acarbose, which is a non-absorbable alpha glucosidase inhibitor, also prevented diet-induced obesity, but through a different mechanism: it did not stimulate energy expenditure, but caused indigestion, leading to less energy absorption. Miglitol promoted adrenergic signaling in brown adipocytes in vitro. These data indicate that circulating miglitol stimulates brown adipose tissue and increases energy expenditure, thereby preventing diet-induced obesity. Further optimizing miglitol's effect on brown adipose tissue could lead to a novel anti-obesity drug. © The Japan Endocrine Society.
  • Kohei Shimada, Yuta Ohno, Yuko Okamatsu-Ogura, Masahiro Suzuki, Akihiro Kamikawa, Akira Terao, Kazuhiro Kimura
    PEPTIDES 34 2 336 - 342 2012年04月 [査読有り][通常論文]
     
    The thermogenic function of brown adipose tissue (BAT) is increased by norepinephrine (NE) released from sympathetic nerve endings, but the roles of NPY released along with NE are poorly elucidated. Here, we examined effect of NPY on basal and NE-enhanced thermogenesis in isolated brown adipocytes that express Y1 and Y5 receptor mRNA. Treatment of cells with NPY did not influence the basal and NE-enhanced rates of oxygen consumption and cAMP accumulation. Treatment with NPY also failed to induce ERK (Thr202/Tyr204) phosphorylation in the brown adipocytes. In contrast, treatment with NPY increased ERK phosphorylation in cultured stromal vascular cells from the BAT that express Y1 receptor mRNA. In the latter treatment with NPY also increased STAT3 (Ser727) phosphorylation. These results suggest that NPY mainly acts on stromal vascular cells in BAT and plays roles in the regulation of their gene transcription through ERK and STAT3 pathways, while NPY does not affect the thermogenic function of brown adipocytes. (C) 2012 Elsevier Inc. All rights reserved.
  • Yuko Okamatsu-Ogura, Junko Nio-Kobayashi, Toshihiko Iwanaga, Akira Terao, Kazuhiro Kimura, Masayuki Saito
    EXPERIMENTAL BIOLOGY AND MEDICINE 236 11 1274 - 1281 2011年11月 [査読有り][通常論文]
     
    Leptin reduces body fat by decreasing food intake and increasing energy expenditure. Uncoupling protein (UCP) 1, a key molecule for brown adipose tissue (BAT) thermogenesis, was reported to contribute to the stimulatory effect of leptin on energy expenditure. To clarify whether UCP1 is also involved in the anorexigenic effect of leptin, in this study we examined the effect of leptin on food intake using wild-type (WT) and UCP1-deficient (UCP1-KO) mice. Repeated injection of leptin decreased food intake more markedly in WT mice than in UCP1-KO mice, while a single injection of leptin showed similar effects in the two groups of mice. As chronic leptin stimulation induces UCP1 expression in BAT and ectopically in white adipose tissue (WAT), we mimicked the UCP1 induction by repeated injection of CL316,243 (CL), a highly specific beta 3-adrenoceptor agonist, and measured food intake in response to a single injection of leptin. Two-week treatment with CL enhanced the anorexigenic effect of leptin in WT mice, but not in UCP1-KO mice. Three-day treatment with CL in WT mice also enhanced the anorexigenic effect of leptin and leptin-induced phosphorylation of signal transducer and activator of transcription 3 (STAT3) in the arcuate nucleus of the hypothalamus, without any notable change in adiposity. These results indicate that UCP1 enhances leptin action at the hypothalamus level, suggesting UCP1 contributes to the control of energy balance not only through the regulation of energy expenditure but also through appetite control by modulating leptin action.
  • Takeshi Yoneshiro, Sayuri Aita, Mami Matsushita, Yuko Okamatsu-Ogura, Toshimitsu Kameya, Yuko Kawai, Masao Miyagawa, Masayuki Tsujisaki, Masayuki Saito
    OBESITY 19 9 1755 - 1760 2011年09月 [査読有り][通常論文]
     
    Brown adipose tissue (BAT) can be identified by (18)F-fluorodeoxyglucose (FDG)-positron emission tomography (PET) combined with X-ray computed tomography (CT) in adult humans. The objective of this study was to clarify the relationship between BAT and adiposity in healthy adult humans, particularly to test the idea that decreased BAT activity may be associated with body fat accumulation with age. One hundred and sixty-two healthy volunteers aged 20-73 years (103 males and 59 females) underwent FDG-PET/CT after 2-h cold exposure at 19 degrees C with light clothing. Cold-activated BAT was detected in 41% of the subjects (BAT-positive). Compared with the BAT-negative group, the BAT-positive group was younger (P < 0.01) and showed a lower BMI (P < 0.01), body fat content (P < 0.01), and abdominal fat (P < 0.01). The incidence of cold-activated BAT decreased with age (P < 0.01), being more than 50% in the twenties, but less than 10% in the fifties and sixties. The adiposity-related parameters showed some sex differences, but increased with age in the BAT-negative group (P < 0.01), while they remained unchanged from the twenties to forties in the BAT-positive group, in both sexes. These results suggest that decreased BAT activity may be associated with accumulation of body fat with age.
  • Takashi Sawada, Hideaki Miyoshi, Kohei Shimada, Akira Suzuki, Yuko Okamatsu-Ogura, James W. Perfield, Takuma Kondo, So Nagai, Chikara Shimizu, Narihito Yoshioka, Andrew S. Greenberg, Kazuhiro Kimura, Takao Koike
    PLOS ONE 5 11 e14006  2010年11月 [査読有り][通常論文]
     
    Background: Perilipin A (PeriA) exclusively locates on adipocyte lipid droplets and is essential for lipid storage and lipolysis. Previously, we reported that adipocyte specific overexpression of PeriA caused resistance to diet-induced obesity and resulted in improved insulin sensitivity. In order to better understand the biological basis for this observed phenotype, we performed additional studies in this transgenic mouse model. Methodology and Principal Findings: When compared to control animals, whole body energy expenditure was increased in the transgenic mice. Subsequently, we performed DNA microarray analysis and real-time PCR on white adipose tissue. Consistent with the metabolic chamber data, we observed increased expression of genes associated with fatty acid beta-oxidation and heat production, and a decrease in the genes associated with lipid synthesis. Gene expression of Pgc1a, a regulator of fatty acid oxidation and Ucp1, a brown adipocyte specific protein, was increased in the white adipose tissue of the transgenic mice. This observation was subsequently verified by both Western blotting and histological examination. Expression of RIP140, a regulator of white adipocyte differentiation, and the lipid droplet protein FSP27 was decreased in the transgenic mice. Importantly, FSP27 has been shown to control gene expression of these crucial metabolic regulators. Overexpression of PeriA in 3T3-L1 adipocytes also reduced FSP27 expression and diminished lipid droplet size. Conclusions: These findings demonstrate that overexpression of PeriA in white adipocytes reduces lipid droplet size by decreasing FSP27 expression and thereby inducing a brown adipose tissue-like phenotype. Our data suggest that modulation of lipid droplet proteins in white adipocytes is a potential therapeutic strategy for the treatment of obesity and its related disorders.
  • Masayuki Saito, Yuko Okamatsu-Ogura, Mami Matsushita, Kumiko Watanabe, Takeshi Yoneshiro, Junko Nio-Kobayashi, Toshihiko Iwanaga, Masao Miyagawa, Toshimitsu Kameya, Kunihiro Nakada, Yuko Kawai, Masayuki Tsujisaki
    DIABETES 58 7 1526 - 1531 2009年07月 [査読有り][通常論文]
     
    OBJECTIVE-The significant roles of brown adipose tissue (BAT) in the regulation of energy expenditure and adiposity are established in small rodents but have been controversial in humans. The objective is to examine the prevalence of metabolically active BAT in healthy adult humans and to clarify the effects of cold exposure and adiposity. RESEARCH DESIGN AND METHODS-In vivo 2-[(18)F]fluoro-2-deoxyglucose (FDG) uptake into adipose tissue was measured in 56 healthy volunteers (31 male and 25 female subjects) aged 23-65 years by positron emission tomography (PET) combined with X-ray computed tomography (CT). RESULTS-When exposed to cold (19 C) for 2 h, 17 of 32 younger subjects (aged 23-35 years) and 2 of 24 elderly subjects (aged 38-65 years) showed a substantial FDG uptake into adipose tissue of the supraclavicular and paraspinal regions, whereas they showed no detectable uptake when kept warm (27 C). Histological examinations confirmed the presence of brown adipocytes in these regions. The cold-activated FDG uptake was increased in winter compared with summer (P < 0.001) and was inversely related to BMI (P < 0.001) and total (P < 0.01) and visceral (P < 0.001) fat areas estimated from CT image at the umbilical level. CONCLUSIONS-Our findings, being against the conventional view, indicate the high incidence of metabolically active BAT in adult humans and suggest a role in the control of body temperature and adiposity. Diabetes 58:1526-1531, 2009
  • Akihiro Kamikawa, Osamu Ichii, Daisuke Yamaji, Takeshi Imao, Chihairu Suzuki, Yuko Okamatsu-Ogura, Akira Terao, Yasuhiro Kon, Kazuhiro Kimura
    DEVELOPMENTAL DYNAMICS 238 5 1092 - 1099 2009年05月 [査読有り][通常論文]
     
    Mammary glands develop postnatally in response to the hypothalamic-pituitary-gonadal axis. Obesity-induced changes in the local environment, however, retard mammary gland development during late pregnancy and lactation. To clarify the effects of obesity on fundamental duct development, we compared the mammary glands of nulliparous nonpregnant obese mice fed a high-fat diet with those of lean mice fed a normal diet. Obese mice had enlarged mammary glands, reflecting fat pad size, whereas the ducts in obese mice showed a less dense distribution with less frequent branching. Additionally, the ducts were surrounded by thick collagen layers, and were incompletely lined with myoepithelium. Because leptin receptors were localized in the epithelium region and leptin that was highly expressed in the obese glands suppressed mammary epithelial cell proliferation in vitro, the present results suggest that obesity disrupts mammary ductal development, possibly by remodeling the mammary microenvironment and promoting the expression of such paracrine factors as leptin. Developmental Dynamics 238:1092-1099, 2009. (C) 2009 Wiley-Liss, Inc.
  • Yuko Okamatsu-Ogura, Akihiro Uozumi, Chitoku Toda, Kazuhiro Kimura, Hitoshi Yamashita, Masayuki Saito
    OBESITY RESEARCH & CLINICAL PRACTICE 1 4 233 - 241 2007年12月 [査読有り][通常論文]
     
    Leptin is proposed to reduce body fat by increasing energy expenditure, in addition to decreasing food intake, through the activation of brown adipose tissue (BAT) thermogenesis. To confirm this, we investigated the effects of leptin on whole body energy expenditure, BAT functions and adiposity in wild-type (WT) mice, and compared with those in mice deficient in uncoupling protein 1 (UCP1), a key molecule for BAT thermogenesis. Chronic hyperleptinemia induced by adenovirus gene transfer reduced food intake in both WT and UCP1-KO mice. WT mice with hyperleptinemia, compared to pair-fed controls, showed increased oxygen consumption, elevated UCP1 expression in BAT, ectopic UCP1 induction in white adipose tissue (WAT), and reduced body fat content. These effects of chronic hyperleptinemia were not observed in UCP1-KO mice. It was concluded that the fat-reducing effect of leptin is due to not only decreased food intake, but also increased UCP1-dependent energy expenditure. (c) 2007 Asian Oceanian Association for the Study of Obesity. Published by Elsevier Ltd. All rights reserved.
  • Mohamed Soliman, Kazuhiro Kimura, Mohamed Ahmed, Daisuke Yamaji, Yukiko Matsushita, Yuko Okamatsu-Ogura, Kennedy Makondo, Masayuki Saito
    DOMESTIC ANIMAL ENDOCRINOLOGY 33 4 400 - 409 2007年11月 [査読有り][通常論文]
     
    Leptin is an adipose tissue-derived cytokine plays key roles in the regulation of food intake and energy expenditure. However, regulatory mechanisms of leptin gene expression are not fully elucidated in ruminants that utilize short-chain fatty acids (SCFA), known as volatile fatty acids, as principal energy sources. In this study, we determined effects of SCFA and long-chain fatty acids (LCFA) on leptin expression in bovine adipocytes. Bovine stromal vascular cells isolated from subcutaneous adipose tissue of Holstein cows were cultured to confluence and treated sequentially with dexamethasone and isobutylmethylxanthine for 2 days and insulin and troglitazone for 12 days to achieve full differentiation to adipocytes. The cells started to accumulate lipids 4 days after the onset of treatment, with increased mRNA expression of leptin, as well as aP2, adiponectin, and PPAR-gamma. Removal of fetal calf serum and reduction of glucose in the culture medium of differentiated adipocytes decreased leptin mRNA expression. Subsequent addition of acetate, butyrate, or propionate dose-dependently restored and rather increased leptin expression, while addition of LCFA suppressed it. The stimulatory effect of acetate was abolished by prior treatment of the cells with pertussis toxin and by addition of LCFA. Furthermore, cows fasted for 48 h and fed thereafter, elaborate reduced and increased plasma leptin levels, respectively. Thus. these results suggest that plasma leptin levels in cows are inversely controlled at the transcription level by VFA and LCFA, and that the effects of SCFA possibly act through a G protein-coupled receptor for SCFA. (c) 2006 Elsevier Inc. All rights reserved.
  • Okamatsu-Ogura Y, Kitao N, Kimura K, Saito M
    Am J Physiol Endocrinol Metab 292 4 E1135 - E1139 2007年04月 [査読有り][通常論文]
     
    Brown fat UCP1 is not involved in the febrile and thermogenic responses to IL-1 beta in mice. Am J Physiol Endocrinol Metab 292: E1135-E1139, 2007. First published December 12, 2006; doi:10.1152/ajpendo.00425.2006. - The activity of brown adipose tissue (BAT), a site of nonshivering metabolic thermogenesis, has been reported to increase after interleukin (IL)-1 beta/lipopolysaccharide injection. To clarify the possible contribution of BAT thermogenesis to whole body febrile response, we investigated febrile and thermogenic response to IL-1 beta using mice deficient in uncoupling protein-1 (UCP1), a key molecule for BAT thermogenesis. In wild-type (WT) mice, IL-1 beta injection (5 mu g/kg ip) increased body temperature (+1.82 degrees C at 20 min), decreased physical activity (-37% at 1 h), and produced a slight and insignificant rise (+15% at 1 h) in oxygen consumption (V-O2). V-O2 dependent on metabolic thermogenesis (Delta V-O2 thermogenesis) calculated by correcting the effect of physical activity was increased after IL-1 beta injection (726 +/- 200 ml center dot h(-1)center dot kg(-1) at 1 h). Almost the same responses were observed in UCP1-deficient mice, showing 638 +/- 87 ml center dot h(-1)center dot kg(-1) of Delta V-O2 (thermogenesis) at 1 h. In contrast, CL316,243, a selective activator of BAT thermogenesis, increased body temperature, decreased physical activity, and produced a significant rise in V-O2 in WT mice, showing 1,229 +/- 35 ml center dot h(-1)center dot kg(-1) of Delta V-O2 thermogenesis at 1 h. These changes were not observed in UCP1-deficient mice. These results, conflicting with a previously proposed idea of a role of BAT in fever, suggest a minor contribution of BAT thermogenesis to IL-1 beta-induced fever. In support of this, we found no effect of IL-1 beta on triglyceride content and UCP1 mRNA level in BAT, in contrast with apparent effects of CL316,243.
  • Kitao N, Yahata T, Matsumoto T, Okamatsu-Ogura Y, Omachi A, Kimura K, Saito M
    J Vet Med Sci 69 1065 - 1068 2007年 [査読有り][通常論文]
  • Okamatsu-Ogura Y, Uozumi A, Kitao N, Kimura K, Saito M
    Obes Res Clin Prac 1 1 61 - 67 2007年01月 [査読有り][通常論文]
     
    beta 3-adrenergic receptor (beta 3-AR) agonist, a drug that reduces body fat, stimulates lipomobilization from white adipose tissue (WAT) and thermogenesis in brown adipose tissue (BAT). To test the day-night difference in the effects of beta 3-AR agonist, in the present study, we examined the responses of lipomobitization and energy expenditure to CL316,243 (CL) during the daytime at 10:00 and nighttime at 22:00 in mice kept in a 12 h light-dark cycle with lights on from 07:00. CL injection increased plasma free fatty acid to the same extent at 10:00 and 22:00. In contrast, CL injection increased total oxygen consumption more markedly at 10:00 than 22:00. Physical activity was suppressed by CL injection especially at 22:00. Correcting total oxygen consumption by the suppressive effect on physical activity, oxygen consumption dependent on BAT thermogenesis was estimated. This revealed that the effect of CL on BAT thermogenesis was not different between 10:00 and 22:00. Thus, we concluded that there is no day-night difference in the CL effects on lipomobilization from WAT and thermogenesis in BAT. The stronger effect of CL on total energy expenditure in the daytime was largely due to a more suppressive effect on physical activity in the nighttime. (C) 2006 Asian Oceanian Association for the Study of Obesity. Published by Elsevier Ltd. All rights reserved.
  • Inokuma K, Okamatsu-Ogura Y, Omachi A, Matsushita Y, Kimura K, Yamashita H, Saito M
    Am J Physiol Endocrinol Metab 290 5 E1014 - E1021 2006年05月 [査読有り][通常論文]
     
    Mitochondrial uncoupling protein-1 ( UCP1) has been thought to be a key molecule for thermogenesis during cold exposure and spontaneous hyperphagia and thereby in the autonomic regulation of energy expenditure and adiposity. However, UCP1 knockout ( KO) mice were reported to be cold intolerant but unexpectedly did not get obese even after hyperphagia, implying that UCP1 may not be involved in the regulation of adiposity. Treatment of obese animals with beta(3)-adrenergic agonists is known to increase lipid mobilization, induce UCP1, and, finally, reduce body fat content. To obtain direct evidence for the role of UCP1 in the anti-obesity effect of beta(3)-adrenergic stimulation, in the present study, UCP1-KO and wild-type ( WT) mice were fed on cafeteria diets for 8 wk and then given a beta(3)-adrenergic agonist, CL-316,243 ( CL), or saline for 2 wk. A single injection of CL increased whole body oxygen consumption and brown fat temperature in WT mice but not in KO mice, and it elicited almost the same plasma free fatty acid response in WT and KO mice. WT and KO mice increased similarly their body and white fat pad weights on cafeteria diets compared with those on laboratory chow. Daily treatment with CL resulted in a marked reduction of white fat pad weight and the size of adipocytes in WT mice, but not in KO mice. Compared with WT mice, KO mice expressed increased levels of UCP2 in brown fat but decreased levels in white fat and comparable levels of UCP3. It was concluded that the anti-obesity effect of beta(3)-adrenergic stimulation is largely attributable to UCP1, but less to UCP2 and UCP3, and thereby to UCP1-dependent degradation of fatty acids released from white adipose tissue.
  • K Inokuma, Y Ogura-Kamatsu, C Toda, K Kimura, H Yamashita, M Saito
    DIABETES 54 5 1385 - 1391 2005年05月 [査読有り][通常論文]
     
    Sympathetic stimulation activates glucose utilization in parallel with fatty acid oxidation and thermogenesis in brown adipose tissue (BAT) through the beta-adrenergic receptors. To clarify the roles of the principal thermogenic molecule mitochondrial uncoupling protein 1 (UCP1) in the sympathetically stimulated glucose utilization, we investigated the uptake of 2-deoxyglucose (2-DG) into BAT and some other tissues of UCP1-knockout (KO) mice in vivo. In wild-type (WT) mice, administration of norepinephrine (NE) accelerated the disappearance of plasma 2-DG and increased 2-DG uptake into BAT and heart without any rise of plasma insulin level. In UCP1-KO mice, the stimulatory effect of NE on 2-DG uptake into BAT, but not into heart, disappeared completely. Insulin administration increased 2-DG uptake into BAT and also heart similarly in WT and UCP1-KO mice. NE also increased the activity of AMP-activated protein kinase (AMP kinase) in BAT of WT but not UCP1-KO mice. Our results, together with reports that the activation of AMP kinase increases glucose transport in myocytes, suggest that the sympathetically stimulated glucose utilization in BAT is due to the serial activation of UCP1 and AMP kinase.

書籍

  • ここまでわかった燃える褐色脂肪の不思議
    岡松 優子 (担当:分担執筆範囲:いろいろな動物の褐色脂肪組織とその役割)
    有限会社ナップ 2013年
  • 体と温度の辞典
    岡松優子, 斉藤昌之 (担当:分担執筆範囲:熱産生機構2 褐色脂肪組織)
    朝倉書店 2010年
  • 肥満と脂肪エネルギー代謝
    岡松優子, 斉藤昌之 (担当:分担執筆範囲:褐色脂肪と肥満・メタボリックシンドローム:実験動物からヒトへ)
    建帛社 2008年
  • 糖尿病カレントライブラリー7 脂肪細胞と脂肪組織
    岡松優子, 斉藤昌之, 辻崎正幸 (担当:分担執筆範囲:白色脂肪と褐色脂肪の代謝特性)
    文光堂 2007年
  • 別冊医学の歩み『糖尿病・代謝症候群ムstate of arts 2004-2006』
    小倉優子, 猪熊健一 (担当:分担執筆範囲:エネルギー消費における脱共役蛋白質UCP1の役割)
    医歯薬出版 2004年

講演・口頭発表等

  • 肥満対策のターゲットとしての褐色脂肪組織:実験動物を用いた検討  [招待講演]
    岡松 優子
    第157回日本獣医学会 2014年09月 シンポジウム・ワークショップパネル(指名)
  • 食品成分カプシノイドの抗肥満作用  [招待講演]
    岡松 優子
    第34回日本肥満学会 2013年10月 シンポジウム・ワークショップパネル(指名)
  • 褐色脂肪細胞の増殖とその病態生理学的意義  [招待講演]
    岡松 優子
    第18回アディポサイエンス・シンポジウム 2013年08月 シンポジウム・ワークショップパネル(指名)
  • 褐色脂肪細胞の増殖と意義  [招待講演]
    岡松 優子
    第33回日本肥満学会 2012年10月 シンポジウム・ワークショップパネル(指名)
  • Roles of UCP1 in the regulation of energy metabolism  [招待講演]
    岡松 優子
    Brown Adipose Tissue 2011 Update 2011年03月 シンポジウム・ワークショップパネル(指名)
  • Protective roles of brown adipose tissue against age-related development of obesity  [招待講演]
    岡松 優子
    14th International Congress of Endocrinology Official Satellite Symposium 2010年03月 シンポジウム・ワークショップパネル(指名)

その他活動・業績

  • 褐色脂肪細胞の増殖とその生理的意義
    岡松優子, 深野圭吾 医学のあゆみ 250 (9) 822 -826 2014年 [査読無し][招待有り]
  • 褐色/ベージュ脂肪細胞の発生機構と生理的役割
    岡松優子, 木村和弘 バイオインダストリー 30 (11) 4 -10 2013年 [査読無し][招待有り]
  • UCP1の機能と比較生物学
    岡松 優子 The Lipid 25 (1) 29 -35 2013年 [査読無し][招待有り]
  • 褐色脂肪細胞によるエネルギー代謝制御におけるPGC-1 の役割
    岡松優子, 木村和弘 内分泌・糖尿病科 29 (2) 109 -116 2009年 [査読無し][招待有り]
  • レプチンの体脂肪減少効果にUCP1は貢献しているのか?
    岡松優子, 斉藤昌之 肥満研究 12 73 -75 2006年 [査読無し][招待有り]
  • 褐色脂肪細胞の起源と分化制御
    岡松優子, 斉藤昌之 The Lipid 17 65 -71 2006年 [査読無し][招待有り]
  • 褐色脂肪の機能と分化機構
    岡松優子, 斉藤昌之 細胞 38 14 -18 2006年 [査読無し][招待有り]
  • 褐色脂肪によるエネルギー代謝の調節
    岡松優子, 斉藤昌之 Clinical Neuroscience 24 914 -916 2006年 [査読無し][招待有り]
  • 褐色脂肪と白色脂肪:エネルギー代謝における役割
    岡松優子, 大町麻子, 斉藤昌之 分子細胞治療 5 28 -34 2006年 [査読無し][招待有り]

受賞

  • 2019年11月 日本肥満学会 学術奨励賞
     
    受賞者: 岡松 優子
  • 2008年03月 北海道大学 大塚賞
     
    受賞者: 岡松 優子
  • 2005年10月 日本肥満学会 若手研究奨励賞
     
    受賞者: 岡松 優子
  • 2004年08月 アディポサイエンス研究会シンポジウム 若手優秀ポスター賞
     
    受賞者: 岡松 優子

共同研究・競争的資金等の研究課題

  • 体温制御システム構築の細胞分子基盤:ハムスターの恒温性獲得機構をモデルとして
    日本学術振興会:科学研究費助成事業(科学研究費補助金) 基盤(C)
    研究期間 : 2017年 -2019年 
    代表者 : 岡松 優子
  • 母乳の質がもたらす乳児期の脂肪組織リモデリングと成長後のメタボリックシンドロームの発症しやすさとの関わりの解明
    森永奉仕会:研究奨励
    研究期間 : 2019年 
    代表者 : 岡松 優子
  • 冬眠動物における体温制御システム構築の分子基盤:発熱細胞プロジェニターの同定と局所環境の役割
    内藤記念科学振興財団:内藤記念女性研究者研究助成
    研究期間 : 2015年 -2017年 
    代表者 : 岡松 優子
  • 乳幼児期のベージュ脂肪細胞の誘導と消失に母乳の摂取が与える影響の解明
    糧食研究会:一般公募研究
    研究期間 : 2017年 
    代表者 : 岡松 優子
  • 生体のエネルギー消費能力を増大させる褐色脂肪由来アディポカインの同定
    日本学術振興会:科学研究費助成事業(科学研究費補助金) 若手研究(B)
    研究期間 : 2014年 -2016年 
    代表者 : 岡松 優子
  • 冬眠動物の体温を制御する熱産生脂肪細胞の発生・誘導機構の解明
    秋山記念生命科学振興財団:奨励助成
    研究期間 : 2014年 
    代表者 : 岡松 優子
  • アザラシはどのように脂肪を蓄えるのか —皮下脂肪の重度蓄積と内臓脂肪の欠損の謎に迫る—
    栗林育英学術財団:研究助成
    研究期間 : 2012年 -2013年 
    代表者 : 岡松 優子
  • 乳腺組織形成における脂肪細胞分泌因子レプチンの役割
    森永奉仕会:研究奨励
    研究期間 : 2012年 
    代表者 : 岡松 優子
  • 食品成分を利用した肥満対策法の開発に向けた褐色脂肪増加機構の解析
    ノーステック財団:フードイノベーション創造支援事業 研究シーズ発掘補助金
    研究期間 : 2012年 
    代表者 : 岡松 優子
  • 白色脂肪の褐色化機構の解明:新規肥満治療法の開発に向けた基礎研究
    日本学術振興会:科学研究費助成事業(科学研究費補助金) 若手研究(B)
    研究期間 : 2009年 -2010年 
    代表者 : 岡松 優子
  • 褐色脂肪の増殖及び機能におけるp27Kip1の役割
    秋山記念生命科学振興財団:奨励助成
    研究期間 : 2009年 
    代表者 : 岡松 優子
  • エネルギー消費組織:褐色脂肪の増殖・機能分化機構の解明
    北海道大学:公募型プロジェクト研究等支援経費(若手研究者自立支援)
    研究期間 : 2009年 
    代表者 : 岡松 優子
  • 白色脂肪の褐色化 -太りにくい体質の獲得に向けて-
    日本学術振興会:科学研究費助成事業(科学研究費補助金) (特別研究員奨励費)
    研究期間 : 2007年 -2008年 
    代表者 : 岡松 優子
  • レプチンの作用におけるUCP1の役割
    伊藤医薬学術交流財団:海外研究交流助成
    研究期間 : 2006年 
    代表者 : 岡松 優子

教育活動情報

主要な担当授業

  • 獣医科学基礎科目B 生命科学特論Ⅰ:実験の原理
    開講年度 : 2018年
    課程区分 : 博士後期課程
    開講学部 : 獣医学研究科
  • 生物学Ⅱ
    開講年度 : 2018年
    課程区分 : 学士課程
    開講学部 : 全学教育
    キーワード : 生物の多様性,系統,進化,生物の形態,生命活動の多様性
  • 獣医科学基礎科目 生命科学特論
    開講年度 : 2018年
    課程区分 : 博士後期課程
    開講学部 : 獣医学院
  • 生化学実習
    開講年度 : 2018年
    課程区分 : 学士課程
    開講学部 : 獣医学部
    キーワード : 溶液とpH、蛋白質の定量、糖質の定量、脂質の定量、核酸の定量、酵素反応速度
  • 先端獣医科学科目 先端生命科学特論Ⅲ
    開講年度 : 2018年
    課程区分 : 博士後期課程
    開講学部 : 獣医学院
  • 代謝生化学
    開講年度 : 2018年
    課程区分 : 学士課程
    開講学部 : 獣医学部
    キーワード : 酵素学、糖質・脂質・アミノ酸代謝,臓器相関,比較生化学
  • アドバンスト演習
    開講年度 : 2018年
    課程区分 : 学士課程
    開講学部 : 獣医学部


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