Effects of Ethanol on the Induction of Uncoupling Protein-1 (UCP1) mRNA in the Mouse Brown Adipose Tissue
Expression of uncoupling protein-1 (UCP1) is increased by cold acclimation and overfeeding, and reduced in fasting and genetic obesity. It is known that the mitochondrial UCP1 in the brown adipose tissue (BAT) is an important key molecule for non-shivering thermogenesis. On the other hand, ethanol (...
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Published in: | The Tohoku Journal of Experimental Medicine Vol. 204; no. 1; pp. 45 - 51 |
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Abstract | Expression of uncoupling protein-1 (UCP1) is increased by cold acclimation and overfeeding, and reduced in fasting and genetic obesity. It is known that the mitochondrial UCP1 in the brown adipose tissue (BAT) is an important key molecule for non-shivering thermogenesis. On the other hand, ethanol (EtOH) alters thermoregulation in humans and laboratory animals. However, the relationship between EtOH intake and UCP1 expression is not yet clear. Accordingly, the present study employed the technique of real-time quantitative polymerase-chain reaction (PCR) to investigate the effects of EtOH (0.5 or 2.0 g/kg) on the expression of UCP1 mRNA in the mouse BAT. Control mice were injected with the same volume of physiological saline intraperitoneally (IP). IP injection of EtOH (0.5 g/kg) caused a decrease and an increase of the expression of BAT UCP1 mRNA at 1 and 4 hours, respectively. Treatment with EtOH (2.0 g/kg) caused an increases of the expression of BAT UCP1 mRNA at both 2 and 4 hours. BAT UCP1 mRNA levels in both groups increased at 4 hours after EtOH administration. The levels of UCP1 mRNA returned to the control levels by 8 hours after EtOH administration. The expression of BAT UCP1 mRNA was upregulated following EtOH administration, although a lower dose of EtOH initially reduced the expression of UCP1 mRNA in BAT. These findings suggest that EtOH-induced UCP1 mRNA expression in BAT reflects an alteration of the set point of thermogenesis. |
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AbstractList | Expression of uncoupling protein-1 (UCP1) is increased by cold acclimation and overfeeding, and reduced in fasting and genetic obesity. It is known that the mitochondrial UCP1 in the brown adipose tissue (BAT) is an important key molecule for non-shivering thermogenesis. On the other hand, ethanol (EtOH) alters thermoregulation in humans and laboratory animals. However, the relationship between EtOH intake and UCP1 expression is not yet clear. Accordingly, the present study employed the technique of real-time quantitative polymerase-chain reaction (PCR) to investigate the effects of EtOH (0.5 or 2.0 g/kg) on the expression of UCP1 mRNA in the mouse BAT. Control mice were injected with the same volume of physiological saline intraperitoneally (IP). IP injection of EtOH (0.5 g/kg) caused a decrease and an increase of the expression of BAT UCP1 mRNA at 1 and 4 hours, respectively. Treatment with EtOH (2.0 g/kg) caused an increases of the expression of BAT UCP1 mRNA at both 2 and 4 hours. BAT UCP1 mRNA levels in both groups increased at 4 hours after EtOH administration. The levels of UCP1 mRNA returned to the control levels by 8 hours after EtOH administration. The expression of BAT UCP1 mRNA was upregulated following EtOH administration, although a lower dose of EtOH initially reduced the expression of UCP1 mRNA in BAT. These findings suggest that EtOH-induced UCP1 mRNA expression in BAT reflects an alteration of the set point of thermogenesis. |
Author | Yokoyama, Chihiro Komura, Setsuo Yoshimoto, Kanji Yoshida, Toshihide Kogure, Akinori Fukuda, Fumihiko Yasuhara, Masahiro Uchiyama, Yuki Nishimura, Akira Misumi, Yuki Wakabayashi, Yasuo Hioki, Chizuko Satomi, Yoshiko Hori, Masafumi |
Author_xml | – sequence: 1 fullname: Yoshimoto, Kanji organization: Department of Legal Medicine, Kyoto Prefectural University of Medicine – sequence: 2 fullname: Yasuhara, Masahiro organization: Department of Legal Medicine, Kyoto Prefectural University of Medicine – sequence: 3 fullname: Komura, Setsuo organization: Department of Legal Medicine, Kyoto Prefectural University of Medicine – sequence: 4 fullname: Misumi, Yuki organization: Department of Legal Medicine, Kyoto Prefectural University of Medicine – sequence: 5 fullname: Uchiyama, Yuki organization: Department of Legal Medicine, Kyoto Prefectural University of Medicine – sequence: 6 fullname: Kogure, Akinori organization: Department of Endocrinology, Diabetes and Metabolism, Kyoto Prefectural University of Medicine – sequence: 7 fullname: Hioki, Chizuko organization: Department of Endocrinology, Diabetes and Metabolism, Kyoto Prefectural University of Medicine – sequence: 8 fullname: Wakabayashi, Yasuo organization: Department of Biochemistry, Kyoto Prefectural University of Medicine – sequence: 9 fullname: Satomi, Yoshiko organization: Department of Biochemistry, Kyoto Prefectural University of Medicine – sequence: 10 fullname: Nishimura, Akira organization: Department of Pediatrics, Kyoto Prefectural University of Medicine – sequence: 11 fullname: Fukuda, Fumihiko organization: Department of Legal Medicine, Kyoto Prefectural University of Medicine – sequence: 12 fullname: Hori, Masafumi organization: Department of Legal Medicine, Kyoto Prefectural University of Medicine – sequence: 13 fullname: Yokoyama, Chihiro organization: Department of Psychiatry, Kyoto Prefectural University of Medicine – sequence: 14 fullname: Yoshida, Toshihide organization: Department of Endocrinology, Diabetes and Metabolism, Kyoto Prefectural University of Medicine |
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Cites_doi | 10.1016/S0006-2952(02)01167-X 10.1046/j.1440-1681.2002.03675.x 10.1152/physrev.1984.64.1.1 10.1016/S0014-5793(97)00755-2 10.1016/0163-7258(83)90018-9 10.1016/0091-3057(88)90272-9 10.1007/978-3-642-74078-7_4 10.1177/002215540205000103 10.1016/0741-8329(93)90006-A 10.1507/endocrj1954.38.397 10.1152/physrev.00015.2003 10.1016/S0893-133X(00)00221-9 10.1016/S0009-9120(98)00092-7 10.1152/ajpregu.00678.2003 10.1016/S0021-9258(18)66957-1 10.1620/tjem.201.11 10.1016/0163-7827(89)90009-X 10.1159/000137443 10.1016/0091-3057(89)90506-6 10.1016/0741-8329(92)90004-T 10.1016/S0741-8329(97)00136-5 10.1016/0300-9432(76)90059-5 |
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Snippet | Expression of uncoupling protein-1 (UCP1) is increased by cold acclimation and overfeeding, and reduced in fasting and genetic obesity. It is known that the... |
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SubjectTerms | Adipose Tissue, Brown - drug effects Adipose Tissue, Brown - physiology Animals brown adipose tissue Carrier Proteins - genetics Carrier Proteins - metabolism ethanol Ethanol - administration & dosage Ethanol - pharmacology Gene Expression Regulation - drug effects Humans Ion Channels Male Membrane Proteins - genetics Membrane Proteins - metabolism Mice Mitochondrial Proteins mouse RNA, Messenger - metabolism Thermogenesis - physiology Time Factors uncoupling protein Uncoupling Protein 1 |
Title | Effects of Ethanol on the Induction of Uncoupling Protein-1 (UCP1) mRNA in the Mouse Brown Adipose Tissue |
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