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Sato, Koichi ; Shimizu, Hiroyuki ; 佐藤, 浩一 ; 清水, 寛之
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Departmental Bulletin Paper
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Oh-I, Shinsuke ; Shimizu, Hiroyuki ; Satoh, Tetsurou ; Okada, Shuichi ; Adachi, Sachika ; Inoue, Kinji ; Eguchi, Hiroshi ; Yamamoto, Masanori ; Imaki, Toshihiro ; Hashimoto, Koushi ; Tsuchiya, Takafumi ; Monden, Tsuyoshi ; Horiguchi, Kazuhiko ; Yamada, Masanobu ; Mori, Masatomo
概要:
application/pdf<br />Journal Article<br />The brain hypothalamus contains certain secreted molecules that are important in regulating feeding behaviour. Here we show that nesfatin, corresponding to NEFA/nucleobindin2 (NUCB2), a
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secreted protein of unknown function, is expressed in the appetite-control hypothalamic nuclei in rats. Intracerebroventricular (i.c.v.) injection of NUCB2 reduces feeding. Rat cerebrospinal fluid contains nesfatin-1, an amino-terminal fragment derived from NUCB2, and its expression is decreased in the hypothalamic paraventricular nucleus under starved conditions. I.c.v. injection of nesfatin-1 decreases food intake in a dose-dependent manner, whereas injection of an antibody neutralizing nesfatin-1 stimulates appetite. In contrast, i.c.v. injection of other possible fragments processed from NUCB2 does not promote satiety, and conversion of NUCB2 to nesfatin-1 is necessary to induce feeding suppression. Chronic i.c.v. injection of nesfatin-1 reduces body weight, whereas rats gain body weight after chronic i.c.v. injection of antisense morpholino oligonucleotide against the gene encoding NUCB2. Nesfatin-1-induced anorexia occurs in Zucker rats with a leptin receptor mutation, and an anti-nesfatin-1 antibody does not block leptin-induced anorexia. In contrast, central injection of alpha-melanocyte-stimulating hormone elevates NUCB2 gene expression in the paraventricular nucleus, and satiety by nesfatin-1 is abolished by an antagonist of the melanocortin-3/4 receptor. We identify nesfatin-1 as a satiety molecule that is associated with melanocortin signalling in the hypothalamus.
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Shimizu, Yasuo ; Dobashi, Kunio ; Horie, Takeo ; Koga, Yasuhiko ; Yoshii, Akihiro ; Utsugi, Mitsuyoshi ; Endou, Katsuaki ; Shimizu, Hiroyuki ; Shimomura, Kenjyu ; Tsuchiya, Takafumi ; Mita, Yoshinori ; Kawata, Tadayoshi ; Iizuka, Kunihiko ; Nakazawa, Tsugio ; Mori, Masatomo
概要:
application/pdf<br />Journal Article<br />Obstructive sleep apnea syndrome (OSAS) is a problem of obese patients. Leptin prevents fat deposition in adipose tissue and insulin reduces plasma glucose, but levels of these hormones are
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sometimes high in obese patients with OSAS. Thus, leptin and insulin do not function properly in OSAS, and increase resistance to leptin and insulin may cause paradoxical state, that is, leptin and insulin resistance. The present study investigates the rapid effect of nasal continuous positive airway pressure (nCPAP) ventilation on serum leptin and insulin levels in OSAS. Levels of plasma leptin and insulin at four sampling points a day decreased in OSAS patients (*p<0.05, n=10) by nCPAP. Nocturnal mean-nadir arterial oxygen desaturation (nmSaO2) correlated with plasma leptin levels in OSAS patients (*p<0.05, n=10). Nasal CPAP did not affect circulating soluble leptin receptor levels in OSAS patients. These findings indicate that leptin and insulin are related to nocturnal hypoxia in OSAS patients, and that nCPAP have a possibility of improving leptin and insulin resistance.
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