Ji Hye Huh1, Kwang Joon Kim2, Seung Up Kim3, Seung Hwan Han4, Kwang-Hyub Han3, Bong-Soo Cha5, Choon Hee Chung1, Byung-Wan Lee6. 1. Division of Endocrinology and Metabolism, Department of Internal Medicine, Yonsei University Wonju College of Medicine, Wonju, Republic of Korea. 2. Severance Executive Healthcare Clinic, Severance Hospital, Seoul, Republic of Korea; Division of Endocrinology and Metabolism, Department of Internal Medicine, Yonsei University College of Medicine, Seoul, Republic of Korea. 3. Department of Internal Medicine, Yonsei University College of Medicine, Seoul, Republic of Korea; Institute of Gastroenterology, Yonsei University College of Medicine, Seoul, Republic of Korea; Liver Cirrhosis Clinical Research Center, Seoul, Republic of Korea. 4. Department of Orthopaedic Surgery, Clinical Research Center, Gangnam Severance Hospital, Yonsei University College of Medicine, Seoul, Republic of Korea. 5. Division of Endocrinology and Metabolism, Department of Internal Medicine, Yonsei University College of Medicine, Seoul, Republic of Korea. 6. Division of Endocrinology and Metabolism, Department of Internal Medicine, Yonsei University College of Medicine, Seoul, Republic of Korea. Electronic address: bwanlee@yuhs.ac.
Abstract
OBJECTIVE: The pathogenesis of non-alcoholic fatty liver disease (NAFLD) involves multiple concomitant events induced by obesity and metabolic health condition. This study aimed to assess the risk of NAFLD according to metabolic health and obesity status using transient elastography (TE). MATERIALS AND METHODS: A total of 2198 asymptomatic adults without chronic liver disease and who underwent a medical health check-up were recruited. Subjects were categorized into four groups according to metabolic health and obesity statuses: metabolically healthy non-obese (MHNO); metabolically unhealthy non-obese (MUNO); metabolically healthy obese (MHO); and metabolically unhealthy obese (MUO). Hepatic steatosis was defined as controlled attenuation parameter (CAP)≥238dB/m, and significant liver fibrosis was defined as liver stiffness measurement (LSM) >7.0kPa, as defined by TE. RESULTS: Compared with MHNO group, the odds ratios (ORs) [95% confidence interval (CI)] for hepatic steatosis were 2.94 [2.32-3.71], 4.62 [3.52-6.07], and 12.02 [9.08-15.92] in the MUNO, MHO, and MUO groups, respectively (P<0.001) in crude model. Regarding liver fibrosis, there was no significant difference in the ORs in MUNO group (ORs: 0.95 [95% CI, 0.33-2.78], P value = 0.929), whereas there was a significant increase in the ORs in MHO group compared with MHNO group (ORs: 4.32 [95% CI, 1.73-10.76], P=0.002) in the fully adjusted model. CONCLUSION: Our results show that MHO was associated with both liver steatosis and fibrosis assessed by transient elastography. Our results suggest that a healthy metabolic profile does not protect obese adults from hepatic steatosis or fibrosis, indicating that obesity itself might contribute to liver fibrosis. Copyright Â
OBJECTIVE: The pathogenesis of non-alcoholic fatty liver disease (NAFLD) involves multiple concomitant events induced by obesity and metabolic health condition. This study aimed to assess the risk of NAFLD according to metabolic health and obesity status using transient elastography (TE). MATERIALS AND METHODS: A total of 2198 asymptomatic adults without chronic liver disease and who underwent a medical health check-up were recruited. Subjects were categorized into four groups according to metabolic health and obesity statuses: metabolically healthy non-obese (MHNO); metabolically unhealthy non-obese (MUNO); metabolically healthy obese (MHO); and metabolically unhealthy obese (MUO). Hepatic steatosis was defined as controlled attenuation parameter (CAP)≥238dB/m, and significant liver fibrosis was defined as liver stiffness measurement (LSM) >7.0kPa, as defined by TE. RESULTS: Compared with MHNO group, the odds ratios (ORs) [95% confidence interval (CI)] for hepatic steatosis were 2.94 [2.32-3.71], 4.62 [3.52-6.07], and 12.02 [9.08-15.92] in the MUNO, MHO, and MUO groups, respectively (P<0.001) in crude model. Regarding liver fibrosis, there was no significant difference in the ORs in MUNO group (ORs: 0.95 [95% CI, 0.33-2.78], P value = 0.929), whereas there was a significant increase in the ORs in MHO group compared with MHNO group (ORs: 4.32 [95% CI, 1.73-10.76], P=0.002) in the fully adjusted model. CONCLUSION: Our results show that MHO was associated with both liver steatosis and fibrosis assessed by transient elastography. Our results suggest that a healthy metabolic profile does not protect obese adults from hepatic steatosis or fibrosis, indicating that obesity itself might contribute to liver fibrosis. Copyright Â