Effects of low ethanol consumption on nonalcoholic steatohepatitis in mice
Several recent clinical and epidemiological studies have suggested inhibitory effects of light-to-moderate alcohol consumption on nonalcoholic fatty liver disease (NAFLD)/nonalcoholic steatohepatitis (NASH); however, these effects have not been confirmed in experimental studies. Therefore, in this s...
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| Veröffentlicht in: | Alcohol (Fayetteville, N.Y.) N.Y.), 2020-09, Vol.87, p.51-61 |
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| creator | Takahashi, Yoshihisa Watabe, Shiori Togashi-Kumagai, Arisa Watanabe, Masato Dungubat, Erdenetsogt Kusano, Hiroyuki Kobayashi, Yasuyuki Harada, Naoki Yamaji, Ryoichi Sugimoto, Keiichiro Fukusato, Toshio |
| description | Several recent clinical and epidemiological studies have suggested inhibitory effects of light-to-moderate alcohol consumption on nonalcoholic fatty liver disease (NAFLD)/nonalcoholic steatohepatitis (NASH); however, these effects have not been confirmed in experimental studies. Therefore, in this study, we examined the effects of small amounts of ethanol consumption on a mouse model of NASH. Nine-week-old male obese mice (db/db mice) were divided into the following groups: control, high-fat, and low-ethanol groups. The control group was provided ad libitum access to a control liquid diet, the high-fat group was provided access to a high-fat liquid diet, and the low-ethanol group was provided access to the high-fat liquid diet supplemented with 0.1% (w/w) ethanol. Eight weeks later, the mice were sacrificed and serum biochemical, histopathological, and molecular analyses were performed. Serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels were significantly lower in the low-ethanol group than in the high-fat group (p = 0.033 and 0.037, respectively). Liver histopathological analysis showed that intralobular and portal inflammation was significantly milder in the low-ethanol group than in the high-fat group (p = 0.018 and 0.041, respectively). However, no significant differences were observed among the groups in serum insulin and adiponectin levels, hepatic 4-hydroxynonenal (oxidative injury marker) levels, and hepatic cytokine and receptor gene expression levels. In conclusion, the serum transaminase levels and hepatic inflammation in NASH model mice improved after administration of small amounts of ethanol. This study directly demonstrated inhibitory effects of small amounts of ethanol on NASH in mice. The mechanisms underlying these inhibitory effects remain to be elucidated.
•Effects of light alcohol consumption were evaluated in a mouse model of NASH.•Small amounts of ethanol consumption decreased serum AST and ALT levels.•Pathological analysis showed amelioration of intralobular and portal inflammation. |
| doi_str_mv | 10.1016/j.alcohol.2020.04.004 |
| format | Article |
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•Effects of light alcohol consumption were evaluated in a mouse model of NASH.•Small amounts of ethanol consumption decreased serum AST and ALT levels.•Pathological analysis showed amelioration of intralobular and portal inflammation.</description><identifier>ISSN: 0741-8329</identifier><identifier>EISSN: 1873-6823</identifier><identifier>DOI: 10.1016/j.alcohol.2020.04.004</identifier><language>eng</language><publisher>Philadelphia: Elsevier Inc</publisher><subject>4-Hydroxynonenal ; Adiponectin ; Alanine ; Alanine transaminase ; Alcohol ; Alcohol use ; animal model ; Animal models ; Antigens ; Aspartate aminotransferase ; Cloning ; Diet ; Epidemiology ; Ethanol ; Fatty liver ; Gene expression ; High fat diet ; Inflammation ; Insulin ; Laboratory animals ; Light effects ; Liver diseases ; Low fat diet ; Lymphocytes ; nonalcoholic steatohepatitis ; Nutrient deficiency ; Transaminase ; Tumor necrosis factor-TNF</subject><ispartof>Alcohol (Fayetteville, N.Y.), 2020-09, Vol.87, p.51-61</ispartof><rights>2020 Elsevier Inc.</rights><rights>2020. Elsevier Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c506t-f18fa772b6ad8e3d16ab37c12537f05b579728e6cdb7f2afe9fc5687d3c288683</citedby><cites>FETCH-LOGICAL-c506t-f18fa772b6ad8e3d16ab37c12537f05b579728e6cdb7f2afe9fc5687d3c288683</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0741832920302093$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27903,27904,65309</link.rule.ids></links><search><creatorcontrib>Takahashi, Yoshihisa</creatorcontrib><creatorcontrib>Watabe, Shiori</creatorcontrib><creatorcontrib>Togashi-Kumagai, Arisa</creatorcontrib><creatorcontrib>Watanabe, Masato</creatorcontrib><creatorcontrib>Dungubat, Erdenetsogt</creatorcontrib><creatorcontrib>Kusano, Hiroyuki</creatorcontrib><creatorcontrib>Kobayashi, Yasuyuki</creatorcontrib><creatorcontrib>Harada, Naoki</creatorcontrib><creatorcontrib>Yamaji, Ryoichi</creatorcontrib><creatorcontrib>Sugimoto, Keiichiro</creatorcontrib><creatorcontrib>Fukusato, Toshio</creatorcontrib><title>Effects of low ethanol consumption on nonalcoholic steatohepatitis in mice</title><title>Alcohol (Fayetteville, N.Y.)</title><description>Several recent clinical and epidemiological studies have suggested inhibitory effects of light-to-moderate alcohol consumption on nonalcoholic fatty liver disease (NAFLD)/nonalcoholic steatohepatitis (NASH); however, these effects have not been confirmed in experimental studies. Therefore, in this study, we examined the effects of small amounts of ethanol consumption on a mouse model of NASH. Nine-week-old male obese mice (db/db mice) were divided into the following groups: control, high-fat, and low-ethanol groups. The control group was provided ad libitum access to a control liquid diet, the high-fat group was provided access to a high-fat liquid diet, and the low-ethanol group was provided access to the high-fat liquid diet supplemented with 0.1% (w/w) ethanol. Eight weeks later, the mice were sacrificed and serum biochemical, histopathological, and molecular analyses were performed. Serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels were significantly lower in the low-ethanol group than in the high-fat group (p = 0.033 and 0.037, respectively). Liver histopathological analysis showed that intralobular and portal inflammation was significantly milder in the low-ethanol group than in the high-fat group (p = 0.018 and 0.041, respectively). However, no significant differences were observed among the groups in serum insulin and adiponectin levels, hepatic 4-hydroxynonenal (oxidative injury marker) levels, and hepatic cytokine and receptor gene expression levels. In conclusion, the serum transaminase levels and hepatic inflammation in NASH model mice improved after administration of small amounts of ethanol. This study directly demonstrated inhibitory effects of small amounts of ethanol on NASH in mice. The mechanisms underlying these inhibitory effects remain to be elucidated.
•Effects of light alcohol consumption were evaluated in a mouse model of NASH.•Small amounts of ethanol consumption decreased serum AST and ALT levels.•Pathological analysis showed amelioration of intralobular and portal inflammation.</description><subject>4-Hydroxynonenal</subject><subject>Adiponectin</subject><subject>Alanine</subject><subject>Alanine transaminase</subject><subject>Alcohol</subject><subject>Alcohol use</subject><subject>animal model</subject><subject>Animal models</subject><subject>Antigens</subject><subject>Aspartate aminotransferase</subject><subject>Cloning</subject><subject>Diet</subject><subject>Epidemiology</subject><subject>Ethanol</subject><subject>Fatty liver</subject><subject>Gene expression</subject><subject>High fat diet</subject><subject>Inflammation</subject><subject>Insulin</subject><subject>Laboratory animals</subject><subject>Light effects</subject><subject>Liver diseases</subject><subject>Low fat diet</subject><subject>Lymphocytes</subject><subject>nonalcoholic steatohepatitis</subject><subject>Nutrient deficiency</subject><subject>Transaminase</subject><subject>Tumor necrosis factor-TNF</subject><issn>0741-8329</issn><issn>1873-6823</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>8G5</sourceid><sourceid>BENPR</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNqFkE9LxDAQxYMouK5-BCHguXWStEl6ElnWfyx40XNI04RN6TY1ySp-e7vs3oWBubz3Zt4PoVsCJQHC7_tSDyZsw1BSoFBCVQJUZ2hBpGAFl5SdowWIihSS0eYSXaXUA4AQolmgt7Vz1uSEg8ND-ME2b_UYBmzCmPa7Kfsw4nnGMJ5ueINTtjqHrZ109tkn7Ee888Zeowunh2RvTnuJPp_WH6uXYvP-_Lp63BSmBp4LR6TTQtCW605a1hGuWyYMoTUTDuq2Fo2g0nLTtcJR7WzjTM2l6JihUnLJlujumDvF8LW3Kas-7OP8X1K0YjWRwKGeVfVRZWJIKVqnpuh3Ov4qAuqATfXqVEkdsCmo1Ixt9j0cfXau8O1tVMl4Oxrb-TiDUl3w_yT8AVG8eW0</recordid><startdate>20200901</startdate><enddate>20200901</enddate><creator>Takahashi, 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of low ethanol consumption on nonalcoholic steatohepatitis in mice</title><author>Takahashi, Yoshihisa ; Watabe, Shiori ; Togashi-Kumagai, Arisa ; Watanabe, Masato ; Dungubat, Erdenetsogt ; Kusano, Hiroyuki ; Kobayashi, Yasuyuki ; Harada, Naoki ; Yamaji, Ryoichi ; Sugimoto, Keiichiro ; Fukusato, Toshio</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c506t-f18fa772b6ad8e3d16ab37c12537f05b579728e6cdb7f2afe9fc5687d3c288683</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>4-Hydroxynonenal</topic><topic>Adiponectin</topic><topic>Alanine</topic><topic>Alanine transaminase</topic><topic>Alcohol</topic><topic>Alcohol use</topic><topic>animal model</topic><topic>Animal models</topic><topic>Antigens</topic><topic>Aspartate aminotransferase</topic><topic>Cloning</topic><topic>Diet</topic><topic>Epidemiology</topic><topic>Ethanol</topic><topic>Fatty liver</topic><topic>Gene 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Basic</collection><jtitle>Alcohol (Fayetteville, N.Y.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Takahashi, Yoshihisa</au><au>Watabe, Shiori</au><au>Togashi-Kumagai, Arisa</au><au>Watanabe, Masato</au><au>Dungubat, Erdenetsogt</au><au>Kusano, Hiroyuki</au><au>Kobayashi, Yasuyuki</au><au>Harada, Naoki</au><au>Yamaji, Ryoichi</au><au>Sugimoto, Keiichiro</au><au>Fukusato, Toshio</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Effects of low ethanol consumption on nonalcoholic steatohepatitis in mice</atitle><jtitle>Alcohol (Fayetteville, N.Y.)</jtitle><date>2020-09-01</date><risdate>2020</risdate><volume>87</volume><spage>51</spage><epage>61</epage><pages>51-61</pages><issn>0741-8329</issn><eissn>1873-6823</eissn><abstract>Several recent clinical and epidemiological studies have suggested inhibitory effects of light-to-moderate alcohol consumption on nonalcoholic fatty liver disease (NAFLD)/nonalcoholic steatohepatitis (NASH); however, these effects have not been confirmed in experimental studies. Therefore, in this study, we examined the effects of small amounts of ethanol consumption on a mouse model of NASH. Nine-week-old male obese mice (db/db mice) were divided into the following groups: control, high-fat, and low-ethanol groups. The control group was provided ad libitum access to a control liquid diet, the high-fat group was provided access to a high-fat liquid diet, and the low-ethanol group was provided access to the high-fat liquid diet supplemented with 0.1% (w/w) ethanol. Eight weeks later, the mice were sacrificed and serum biochemical, histopathological, and molecular analyses were performed. Serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels were significantly lower in the low-ethanol group than in the high-fat group (p = 0.033 and 0.037, respectively). Liver histopathological analysis showed that intralobular and portal inflammation was significantly milder in the low-ethanol group than in the high-fat group (p = 0.018 and 0.041, respectively). However, no significant differences were observed among the groups in serum insulin and adiponectin levels, hepatic 4-hydroxynonenal (oxidative injury marker) levels, and hepatic cytokine and receptor gene expression levels. In conclusion, the serum transaminase levels and hepatic inflammation in NASH model mice improved after administration of small amounts of ethanol. This study directly demonstrated inhibitory effects of small amounts of ethanol on NASH in mice. The mechanisms underlying these inhibitory effects remain to be elucidated.
•Effects of light alcohol consumption were evaluated in a mouse model of NASH.•Small amounts of ethanol consumption decreased serum AST and ALT levels.•Pathological analysis showed amelioration of intralobular and portal inflammation.</abstract><cop>Philadelphia</cop><pub>Elsevier Inc</pub><doi>10.1016/j.alcohol.2020.04.004</doi><tpages>11</tpages></addata></record> |
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| subjects | 4-Hydroxynonenal Adiponectin Alanine Alanine transaminase Alcohol Alcohol use animal model Animal models Antigens Aspartate aminotransferase Cloning Diet Epidemiology Ethanol Fatty liver Gene expression High fat diet Inflammation Insulin Laboratory animals Light effects Liver diseases Low fat diet Lymphocytes nonalcoholic steatohepatitis Nutrient deficiency Transaminase Tumor necrosis factor-TNF |
| title | Effects of low ethanol consumption on nonalcoholic steatohepatitis in mice |
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