Teruki Miyake1, Teru Kumagi1,2, Masashi Hirooka1, Shinya Furukawa3, Osamu Yoshida1, Mitsuhito Koizumi1,4, Shin Yamamoto1, Takao Watanabe1, Yasunori Yamamoto1, Yoshio Tokumoto1, Eiji Takeshita1, Masanori Abe1, Kohichiro Kitai4, Bunzo Matsuura1, Yoichi Hiasa5. 1. Department of Gastroenterology and Metabology, Ehime University Graduate School of Medicine, Shitsukawa, Toon, Ehime, 791-0295, Japan. 2. Department of Community Medicine, Ehime University Graduate School of Medicine, Shitsukawa, Toon, Ehime, Japan. 3. Department of Public Health, Ehime University Graduate School of Medicine, Shitsukawa, Toon, Ehime, Japan. 4. Ehime General Health Care Association, Misake, Matsuyama, Ehime, Japan. 5. Department of Gastroenterology and Metabology, Ehime University Graduate School of Medicine, Shitsukawa, Toon, Ehime, 791-0295, Japan. hiasa@m.ehime-u.ac.jp.
Abstract
BACKGROUND: Fatty liver disease is associated with glucose intolerance and hepatic insulin resistance. However, there are distinct etiologies for alcoholic versus non-alcoholic fatty liver disease (NAFLD), and it is unknown whether alcohol consumption influences the onset of glucose intolerance in fatty liver disease patients. Therefore, we investigated the relationship between fatty liver disease and the onset of impaired fasting glucose (IFG) with respect to alcohol consumption. METHODS: The records of 6804 Japanese subjects were reviewed to identify those meeting the criteria for IFG. Male and female subjects were classified into five and four groups, respectively, based on average alcohol consumption (g/week). IFG onset was defined as fasting plasma glucose levels ≥110 mg/dl. RESULTS: In the non-drinker, >0-70 g/week, >70-140 g/week, >140-210 g/week (men only), and >210 g/week (men only) or >140 g/week (women only) groups, 7.3, 6.7, 6.4, 9, and 6.4 % of men and 2, 1.7, 3.1, and 3.2 % of women, respectively, developed IFG. Fatty liver was positively associated with the onset of IFG in men of the >0-70 g/week group (adjusted hazard ratio [aHR], 2.808; 95 % confidence interval [CI] 1.605-5.049, p < 0.001) and women of the >70-140 g/week group (aHR, 4.193; 95 % CI, 1.036-14.584, p = 0.045) after adjusting for previously reported IFG risk factors. No associations were observed in the other groups. CONCLUSIONS: A small amount of alcohol consumption is a significant risk factor for the onset of IFG in NAFLD patients; onset risk differs according to the amount of alcohol consumption.
BACKGROUND:Fatty liver disease is associated with glucose intolerance and hepatic insulin resistance. However, there are distinct etiologies for alcoholic versus non-alcoholic fatty liver disease (NAFLD), and it is unknown whether alcohol consumption influences the onset of glucose intolerance in fatty liver diseasepatients. Therefore, we investigated the relationship between fatty liver disease and the onset of impaired fasting glucose (IFG) with respect to alcohol consumption. METHODS: The records of 6804 Japanese subjects were reviewed to identify those meeting the criteria for IFG. Male and female subjects were classified into five and four groups, respectively, based on average alcohol consumption (g/week). IFG onset was defined as fasting plasma glucose levels ≥110 mg/dl. RESULTS: In the non-drinker, >0-70 g/week, >70-140 g/week, >140-210 g/week (men only), and >210 g/week (men only) or >140 g/week (women only) groups, 7.3, 6.7, 6.4, 9, and 6.4 % of men and 2, 1.7, 3.1, and 3.2 % of women, respectively, developed IFG. Fatty liver was positively associated with the onset of IFG in men of the >0-70 g/week group (adjusted hazard ratio [aHR], 2.808; 95 % confidence interval [CI] 1.605-5.049, p < 0.001) and women of the >70-140 g/week group (aHR, 4.193; 95 % CI, 1.036-14.584, p = 0.045) after adjusting for previously reported IFG risk factors. No associations were observed in the other groups. CONCLUSIONS: A small amount of alcohol consumption is a significant risk factor for the onset of IFG in NAFLD patients; onset risk differs according to the amount of alcohol consumption.
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