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所属 |
薬学部 医療栄養学科 |
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職名 |
助教（転出・退職） |
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連絡先 |
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外部リンク |
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学位 【 表示 ／ 非表示 】
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博士（薬学） （ 2010年03月 城西大学 ）
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修士（医療栄養学） （ 2007年03月 城西大学 ）
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学士（医療栄養学） （ 2005年03月 城西大学 ）
出身大学院 【 表示 ／ 非表示 】
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城西大学 薬学研究科 薬学専攻 博士課程 修了
- 2010年03月
国名：日本国
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城西大学 薬学研究科 医療栄養学専攻 修士課程 修了
- 2007年03月
国名：日本国
学外略歴 【 表示 ／ 非表示 】
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医療法人晴生会 介護老人保健施設 葵の園・八千代 管理栄養士
2018年04月 - 現在
国名：日本国
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医療法人晴生会 介護老人保健施設 葵の園・常総 管理栄養士
2013年11月 - 2018年03月
国名：日本国
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自治医科大学 医学部 博士研究員
2010年04月 - 2013年10月
国名：日本国
所属学協会 【 表示 ／ 非表示 】
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日本栄養改善学会
2018年04月 - 現在
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日本摂食嚥下リハビリテーション学会
2017年05月 - 現在
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日本栄養士会（茨城県栄養士会）
2013年11月 - 現在
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日本動脈硬化学会
2007年04月 - 2014年03月
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日本栄養食糧学会
2006年04月 - 2016年12月
研究経歴 【 表示 ／ 非表示 】
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六君子湯による食欲不振改善の作用機序の解明
（選択しない）
研究期間： 2010年04月 - 2013年10月
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魚油とフェノフィブラートの糖・脂質代謝制御システムに及ぼす影響
（選択しない）
研究期間： 2005年04月 - 2010年03月
論文 【 表示 ／ 非表示 】
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GLP-1 release and vagal afferent activation mediate the beneficial metabolic and chronotherapeutic effects of D-allulose. 査読あり
Iwasaki Yusaku, Sendo Mio, Dezaki Katsuya, Hira Tohru, Sato Takehiro, Nakata Masanori, Goswami Chayon, Aoki Ryohei, Arai Takeshi, Kumari Parmila, Hayakawa Masaki, Masuda Chiaki, Okada Takashi, Hara Hiroshi, Drucker Daniel J, Yamada Yuichiro, Tokuda Masaaki, Yada Toshihiko
Nat Commun 9 ( 1 ) 113 - 113 2018年01月
記述言語：英語 掲載種別：研究論文（学術雑誌）
Overeating and arrhythmic feeding promote obesity and diabetes. Glucagon-like peptide-1 receptor (GLP-1R) agonists are effective anti-obesity drugs but their use is limited by side effects. Here we show that oral administration of the non-calorie sweetener, rare sugar D-allulose (D-psicose), induces GLP-1 release, activates vagal afferent signaling, reduces food intake and promotes glucose tolerance in healthy and obese-diabetic animal models. Subchronic D-allulose administered at the light period (LP) onset ameliorates LP-specific hyperphagia, visceral obesity, and glucose intolerance. These effects are blunted by vagotomy or pharmacological GLP-1R blockade, and by genetic inactivation of GLP-1R signaling in whole body or selectively in vagal afferents. Our results identify D-allulose as prominent GLP-1 releaser that acts via vagal afferents to restrict feeding and hyperglycemia. Furthermore, when administered in a time-specific manner, chronic D-allulose corrects arrhythmic overeating, obesity and diabetes, suggesting that chronotherapeutic modulation of vagal afferent GLP-1R signaling may aid in treating metabolic disorders.
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Fish oil and fenofibrate inhibit pancreatic islet hypertrophy, and improve glucose and lipid metabolic dysfuntions with different ways in diabetic KK mice. 査読あり
Nakasatomi Maki, Kim Hyounju, Arai Takeshi, Hirako Satoshi, Shioda Seiji, Iizuka Yuzuru, Sakurai Koji, Matsumoto Akiyo
Obes Res Clin Pract 12 ( 1S1 ) 29 - 38 2018年01月
記述言語：英語 掲載種別：研究論文（学術雑誌）
We examined the effects of fish oil and fenofibrate (FF) on the pancreatic islet hypertrophy, and on the modification of glucose and lipid metabolic dysfunctions in KK mice with insulin resistance. The mice were fed one of four diets [25en% lard/safflower oil (LSO), 25en% fish oil (FO), or each of these diets plus 0.1wt% FF (LSO/FF, FO/FF)] for 9 weeks. FO group and both FF groups had significantly lower final body and adipose tissue weights than LSO group. Pancreatic islet hypertrophy was observed only in LSO group but not in the other groups with fish oil or FF. And, it is likely that fish oil has a stronger therapeutic effect on islet hypertrophy. Plasma adiponectin level was significantly higher in FO group but not in both FF groups. Expression of hepatic lipogenic enzyme genes such as fatty acid synthase (FAS) and stearoyl-CoA desaturase-1 (SCD-1) was lower in FO groups with or without FF, whereas fatty acid oxidation-related mRNAs such as acyl-CoA oxidase (AOX) and uncoupling protein-2 (UCP-2) were more abundant in FF groups with or without fish oil. Our results suggest that both fish oil and FF improve pancreatic islet hypertrophy with the amelioration of insulin resistance. Fish oil enhances insulin sensitivity by increasing plasma adiponectin; however, the beneficial effect of FF on insulin resistance seems to be independent of the plasma adiponectin level. These results mean that improvement of glucose and lipid metabolic dysfuctions in diabetic KK mice are independently approached by fish oil and FF.
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Arcuate Na+,K+-ATPase senses systemic energy states and regulates feeding behavior through glucose-inhibited neurons. 査読あり
Kurita Hideharu, Xu Kai Y, Maejima Yuko, Nakata Masanori, Dezaki Katsuya, Santoso Putra, Yang Yifei, Arai Takeshi, Gantulga Darambazar, Muroya Shinji, Lefor Alan K, Kakei Masafumi, Watanabe Eiju, Yada Toshihiko
Am J Physiol Endocrinol Metab 309 ( 4 ) E320 - E333 2015年08月
記述言語：英語 掲載種別：研究論文（学術雑誌）
Feeding is regulated by perception in the hypothalamus, particularly the first-order arcuate nucleus (ARC) neurons, of the body's energy state. However, the cellular device for converting energy states to the activity of critical neurons in ARC is less defined. We here show that Na(+),K(+)-ATPase (NKA) in ARC senses energy states to regulate feeding. Fasting-induced systemic ghrelin rise and glucose lowering reduced ATP-hydrolyzing activity of NKA and its substrate ATP level, respectively, preferentially in ARC. Lowering glucose concentration (LG), which mimics fasting, decreased intracellular NAD(P)H and increased Na(+) concentration in single ARC neurons that subsequently exhibited [Ca(2+)]i responses to LG, showing that they were glucose-inhibited (GI) neurons. Third ventricular injection of the NKA inhibitor ouabain induced c-Fos expression in agouti-related protein (AgRP) neurons in ARC and evoked neuropeptide Y (NPY)-dependent feeding. When injected focally into ARC, ouabain stimulated feeding and mRNA expressions for NPY and AgRP. Ouabain increased [Ca(2+)]i in single NPY/AgRP neurons with greater amplitude than in proopiomelanocortin neurons in ARC. Conversely, the specific NKA activator SSA412 suppressed fasting-induced feeding and LG-induced [Ca(2+)]i increases in ARC GI neurons. NPY/AgRP neurons highly expressed NKAalpha3, whose knockdown impaired feeding behavior. These results demonstrate that fasting, via ghrelin rise and LG, suppresses NKA enzyme/pump activity in ARC and thereby promotes the activation of GI neurons and NPY/AgRP-dependent feeding. This study identifies ARC NKA as a hypothalamic sensor and converter of metabolic states to key neuronal activity and feeding behaviour, providing a new target to treat hyperphagic obesity and diabetes.
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Peripheral oxytocin activates vagal afferent neurons to suppress feeding in normal and leptin-resistant mice: a route for ameliorating hyperphagia and obesity. 査読あり
Iwasaki Yusaku, Maejima Yuko, Suyama Shigetomo, Yoshida Masashi, Arai Takeshi, Katsurada Kenichi, Kumari Parmila, Nakabayashi Hajime, Kakei Masafumi, Yada Toshihiko
Am J Physiol Regul Integr Comp Physiol 308 ( 5 ) R360 - R369 2015年03月
記述言語：英語 掲載種別：研究論文（学術雑誌）
Oxytocin (Oxt), a neuropeptide produced in the hypothalamus, is implicated in regulation of feeding. Recent studies have shown that peripheral administration of Oxt suppresses feeding and, when infused subchronically, ameliorates hyperphagic obesity. However, the route through which peripheral Oxt informs the brain is obscure. This study aimed to explore whether vagal afferents mediate the sensing and anorexigenic effect of peripherally injected Oxt in mice. Intraperitoneal Oxt injection suppressed food intake and increased c-Fos expression in nucleus tractus solitarius to which vagal afferents project. The Oxt-induced feeding suppression and c-Fos expression in nucleus tractus solitarius were blunted in mice whose vagal afferent nerves were blocked by subdiaphragmatic vagotomy or capsaicin treatment. Oxt induced membrane depolarization and increases in cytosolic Ca(2+) concentration ([Ca(2+)]i) in single vagal afferent neurons. The Oxt-induced [Ca(2+)]i increases were markedly suppressed by Oxt receptor antagonist. These Oxt-responsive neurons also responded to cholecystokinin-8 and contained cocaine- and amphetamine-regulated transcript. In obese diabetic db/db mice, leptin failed to increase, but Oxt increased [Ca(2+)]i in vagal afferent neurons, and single or subchronic infusion of Oxt decreased food intake and body weight gain. These results demonstrate that peripheral Oxt injection suppresses food intake by activating vagal afferent neurons and thereby ameliorates obesity in leptin-resistant db/db mice. The peripheral Oxt-regulated vagal afferent neuron provides a novel target for treating hyperphagia and obesity.
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Paraventricular nucleus nesfatin-1 neurons are regulated by pituitary adenylate cyclase-activating polypeptide (PACAP). 査読あり
Maejima Yuko, Shimomura Kenju, Sakuma Kazuya, Yang Yifei, Arai Takeshi, Mori Masatomo, Yada Toshihiko
Neurosci Lett 551 39 - 42 2013年09月
記述言語：英語 掲載種別：研究論文（学術雑誌）
Nesfatin-1 is a neuropeptide localized in hypothalamic paraventricular nucleus (PVN). Previously, we have reported the mechanism of feeding suppression by nesfatin-1, and also reported the ability of nesfatin-1 in regulating stress response and the circadian feeding pattern. Pituitary adenylate cyclase-activating polypeptide (PACAP) is a neuropeptide also related to the stress response, feeding, and regulation of cardiovascular and autonomic nervous systems. The neurons with receptors for PACAP are distributed in PVN. However, there are no reports showing the direct effect of PACAP on nesfatin-1 neurons. In order to explore the direct effect of PACAP on PVN nesfatin-1 neuron, we have measured the cytosolic free calcium ([Ca(2+)]i) using fura-2 microfluorometry in single neurons isolated from PVN of adult rats, followed by immunocytochemical identification of nesfatin-1 neurons. PACAP at 10(-15)M to 10(-9)M increased [Ca(2+)]i in dose dependent manner. PAC1 and VPAC2 receptor agonists also increased [Ca(2+)]i. Sixteen out of 40 neurons (40%) in PVN responded to 10(-9)M PACAP, and 12 out of 16 neurons (75%) which responded to 10(-9)M PACAP were found to be nesfatin-1 neurons. In this paper we show that PACAP directly activates nesfatin-1 neurons in PVN. The data suggest that nesfatin-1 controls feeding, stress response or autonomic response under PACAP regulation.
MISC 【 表示 ／ 非表示 】
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視床下部弓状核・室傍核と摂食・精神． 招待あり
高野 英介, 荒井 健, 矢田 俊彦
分子精神医学 13 ( 1 ) 40 - 44 2013年01月
記述言語：日本語 掲載種別：記事・総説・解説・論説等（商業誌、新聞、ウェブメディア）
担当授業科目 【 表示 ／ 非表示 】
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医療栄養学概論
2018年04月 - 現在
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調理学実習Ｂ
2018年04月 - 現在
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給食経営管理演習
2018年04月 - 現在
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給食経営管理実習
2018年04月 - 現在
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臨床栄養学実習Ａ
2018年04月 - 現在