Chang Won Won1, Kyung Mook Choi2, Eun Roh3, Soon Young Hwang4, Hye Jin Yoo3, Sei Hyun Baik3, Jin-Hee Lee5, Sang Joon Son6, Hyeon Ju Kim7, Yong Soon Park8, Sam-Gyu Lee9, Be Long Cho10, Hak Chul Jang11, Bong Jo Kim12, Miji Kim13. 1. Department of Family Medicine, College of Medicine, Kyung Hee University, Seoul, Republic of Korea. chunwon62@naver.com. 2. Division of Endocrinology and Metabolism, Department of Internal Medicine, Korea University College of Medicine, Seoul, Republic of Korea. medica7@gmail.com. 3. Division of Endocrinology and Metabolism, Department of Internal Medicine, Korea University College of Medicine, Seoul, Republic of Korea. 4. Department of Biostatistics, Korea University College of Medicine, Seoul, Republic of Korea. 5. Catholic Institute of U-Healthcare, The Catholic University of Korea, Seoul, Republic of Korea. 6. Department of Psychiatry, Ajou University School of Medicine, Suwon, Republic of Korea. 7. Department of Family Medicine, Jeju National University School of Medicine, Jeju, Republic of Korea. 8. Department of Family Medicine, Hallym University Chuncheon Sacred Heart Hospital, Chuncheon, Republic of Korea. 9. Department of Physical & Rehabilitation Medicine, Chonnam National University Medical School, Gwangju, Republic of Korea. 10. Department of Family Medicine, Center for Health Promotion and Optimal Aging, Seoul National University College of Medicine, Seoul, Republic of Korea. 11. Department of Internal Medicine, Seoul National University Bundang Hospital, Seongnam, Republic of Korea. 12. Department of Psychiatry, Gyeongsang National University College of Medicine, Jinju, Republic of Korea. 13. East-West Medical Research Institute, Kyung Hee University, Seoul, Republic of Korea.
Abstract
BACKGROUND AND AIMS: Despite the association between sarcopenia and non-alcoholic fatty liver disease (NAFLD), no study has evaluated the predictive role of NAFLD in sarcopenia. We investigated impact of NAFLD on the risk of low muscle mass (LMM) and low muscle strength (LMS) in a nationwide multicenter study. METHODS: A total of 1595 community-dwelling people aged 70-84 years were followed for 2 years in the Korean Frailty and Aging Cohort Study. Muscle mass was estimated by dividing appendicular skeletal muscle mass (ASM) by body mass index (BMI). Muscle strength was measured as handgrip strength (HGS) divided by BMI. The sex-specific lowest quintiles of ASM/BMI and HGS/BMI of the study population were used as cutoffs for LMM and LMS, respectively. The risk of LMM and LMS were assessed according to hepatic steatosis index (HSI) and fatty liver index (FLI) quartiles. RESULTS: As HSI quartiles increased, the LMM risk increased gradually, after adjusting for age, sex, lifestyle factors, comorbidities, and several causative factors (insulin resistance, inflammation, and vitamin D) (Q4 vs. Q1 OR [95% CI] 3.46 [2.23-5.35]). The increased risk of LMS was even higher according to HSI quartiles (Q4 vs. Q1 5.81 [3.67-9.21]). Multivariate analyses based on FLI showed similar results. People with NAFLD (HSI > 36) were at higher risk of developing LMM and LMS compared to those without (1.65 [1.19-2.31] and 2.29 [1.61-3.26], respectively). CONCLUSIONS: The presence of NAFLD may predict future risk of LMM and LMS, with greater impact on LMS than on LMM.
BACKGROUND AND AIMS: Despite the association between sarcopenia and non-alcoholic fatty liver disease (NAFLD), no study has evaluated the predictive role of NAFLD in sarcopenia. We investigated impact of NAFLD on the risk of low muscle mass (LMM) and low muscle strength (LMS) in a nationwide multicenter study. METHODS: A total of 1595 community-dwelling people aged 70-84 years were followed for 2 years in the Korean Frailty and Aging Cohort Study. Muscle mass was estimated by dividing appendicular skeletal muscle mass (ASM) by body mass index (BMI). Muscle strength was measured as handgrip strength (HGS) divided by BMI. The sex-specific lowest quintiles of ASM/BMI and HGS/BMI of the study population were used as cutoffs for LMM and LMS, respectively. The risk of LMM and LMS were assessed according to hepatic steatosis index (HSI) and fatty liver index (FLI) quartiles. RESULTS: As HSI quartiles increased, the LMM risk increased gradually, after adjusting for age, sex, lifestyle factors, comorbidities, and several causative factors (insulin resistance, inflammation, and vitamin D) (Q4 vs. Q1 OR [95% CI] 3.46 [2.23-5.35]). The increased risk of LMS was even higher according to HSI quartiles (Q4 vs. Q1 5.81 [3.67-9.21]). Multivariate analyses based on FLI showed similar results. People with NAFLD (HSI > 36) were at higher risk of developing LMM and LMS compared to those without (1.65 [1.19-2.31] and 2.29 [1.61-3.26], respectively). CONCLUSIONS: The presence of NAFLD may predict future risk of LMM and LMS, with greater impact on LMS than on LMM.