Corticotropin-releasing hormone (CRH) transgenic mice display hyperphagia with increased Agouti-related protein mRNA in the hypothalamic arcuate nucleus
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- Nakayama Shuichi
- Department of Endocrinology, Metabolism and Nephrology, Kochi Medical School, Kochi University, Nankoku, Japan
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- Nishiyama Mitsuru
- Department of Endocrinology, Metabolism and Nephrology, Kochi Medical School, Kochi University, Nankoku, Japan
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- Iwasaki Yasumasa
- Department of Endocrinology, Metabolism and Nephrology, Kochi Medical School, Kochi University, Nankoku, Japan
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- Shinahara Masayuki
- Department of Endocrinology, Metabolism and Nephrology, Kochi Medical School, Kochi University, Nankoku, Japan
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- Okada Yasushi
- Department of Laboratory Animal Science, Kochi Medical School, Kochi University, Nankoku, Japan
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- Tsuda Masayuki
- Department of Laboratory Animal Science, Kochi Medical School, Kochi University, Nankoku, Japan
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- Okazaki Mizuho
- Department of Endocrinology, Metabolism and Nephrology, Kochi Medical School, Kochi University, Nankoku, Japan
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- Tsugita Makoto
- Department of Endocrinology, Metabolism and Nephrology, Kochi Medical School, Kochi University, Nankoku, Japan
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- Taguchi Takafumi
- Department of Endocrinology, Metabolism and Nephrology, Kochi Medical School, Kochi University, Nankoku, Japan
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- Makino Shinya
- Department of Endocrinology, Metabolism and Nephrology, Kochi Medical School, Kochi University, Nankoku, Japan
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- Stenzel-Poore Mary P
- Department of Molecular Microbiology and Immunology, Oregon Health Science University, Portland, USA
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- Hashimoto Kozo
- Department of Endocrinology, Metabolism and Nephrology, Kochi Medical School, Kochi University, Nankoku, Japan
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- Terada Yoshio
- Department of Endocrinology, Metabolism and Nephrology, Kochi Medical School, Kochi University, Nankoku, Japan
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Although glucocorticoid-induced hyperphagia is observed in the patients with glucocorticoid treatment or Cushing’s syndrome, its molecular mechanism is not clear. We thus explored the expression of neuropeptide mRNAs in the hypothalamus related to appetite regulation in CRH over-expressing transgenic mice (CRH-Tg), a model of Cushing’s syndrome. We measured food intake, body weight (including body fat weight) and plasma corticosterone levels in CRH-Tg and their wild-type littermates (WT) at 6 and 14 weeks old. We also examined neuropeptide Y (NPY), proopiomelanocortin (POMC) and Agouti-related protein (AgRP) mRNAs in the arcuate nucleus (ARC) using in situ hybridization. Circulating corticosterone levels in CRH-Tg were markedly elevated at both 6 and 14 weeks old. Body fat weight in CRH-Tg was significantly increased at 14 weeks old, which is considered as an effect of chronic glucocorticoid excess. At both 6 and 14 weeks old, CRH-Tg mice showed significant hyperphagia compared with WT (14w old: WT 3.9±0.1, CRH-Tg 5.1±0.7 g/day, p<0.05). Unexpectedly, NPY mRNA levels in CRH-Tg were significantly decreased at 14 weeks old (WT: 1571.5±111.2, CRH-Tg: 949.1±139.3 dpm/mg, p<0.05), and there were no differences in POMC mRNA levels between CRH-Tg and WT. On the other hand, AgRP mRNA levels in CRH-Tg were significantly increased compared with WT at both ages (14w old: WT 365.6±88.6, CRH-Tg 660.1±87.2 dpm/ mg, p<0.05). These results suggest that glucocorticoid-induced hyperphagia is associated with increased hypothalamic AgRP. Our results also indicate that hypothalamic NPY does not have an essential role in the increased food intake during glucocorticoid excess.
収録刊行物
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- Endocrine Journal
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Endocrine Journal 58 (4), 279-286, 2011
一般社団法人 日本内分泌学会
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詳細情報 詳細情報について
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- CRID
- 1390001206298470656
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- NII論文ID
- 10029588270
- 130004443684
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- NII書誌ID
- AA10901436
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- ISSN
- 13484540
- 09188959
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- 本文言語コード
- en
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- データソース種別
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- JaLC
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