Li Xue1, Xiaolan Lu2, Juntao He1, Ting Zhang3, Xiaokang Wu1, Yanping Zhang1, Ningning Wang4, Zhe An1, Jiru Xu5, Yan Geng6. 1. Department of Laboratory, The Second Affiliated Hospital of Medical College of Xi'an Jiaotong University, Xi'an, Shaanxi 710004, PR China. 2. Department of Gastroenterology, The Second Affiliated Hospital, Xi'an Jiaotong University, Xi'an, Shaanxi 710004, PR China. 3. Department of Laboratory, Wuxi Maternity and Child Health Care Hospital Affiliated to Nanjing Medical University, Wuxi, Jiangsu 214002, PR China. Electronic address: zhangting040715@163.com. 4. Department of Infection Control, The Second Affiliated Hospital, Xi'an Jiaotong University, Xi'an, Shaanxi 710004, PR China. Electronic address: ninglian2000@163.com. 5. Department of Immunology and Pathogenic Biology, Health Science Center, Xi'an Jiaotong University, Xi'an, Shaanxi 710061, PR China. Electronic address: xujiru@mail.xjtu.edu.cn. 6. Department of Laboratory, The Second Affiliated Hospital of Medical College of Xi'an Jiaotong University, Xi'an, Shaanxi 710004, PR China. Electronic address: gengyanjyk@126.com.
Abstract
BACKGROUND: CK 18-M30 was increased in patients with NAFLD. However, little is known about the relationship between CK 18-M30 and NAFLD progression. We aimed to analyze the variety of CK 18-M30 and other metabolism indices during NAFLD progression. Meanwhile, we aimed to investigate the correlation between CK 18-M30 and liver pathology during NAFLD progression. MATERIALS AND METHODS: Rats were fed with high sucrose and high fat diet for building NAFLD models. We detected liver pathology by hematoxylin-eosin (HE) staining. We also detected serum CK 18-M30 and metabolism indices including liver enzymes, serum lipids and glycometabolism indices. RESULTS: The aggravating degree of liver pathology appeared with prolonged feeding period. The relevance of CK 18-M30 to the severity of liver pathology were higher relative to other indices. CONCLUSION: Our results suggested the significance of CK 18-M30 in the progression of NAFLD and provided new evidence for the early diagnosis and prognostic estimation of NAFLD.
BACKGROUND:CK 18-M30 was increased in patients with NAFLD. However, little is known about the relationship between CK 18-M30 and NAFLD progression. We aimed to analyze the variety of CK 18-M30 and other metabolism indices during NAFLD progression. Meanwhile, we aimed to investigate the correlation between CK 18-M30 and liver pathology during NAFLD progression. MATERIALS AND METHODS:Rats were fed with high sucrose and high fat diet for building NAFLD models. We detected liver pathology by hematoxylin-eosin (HE) staining. We also detected serum CK 18-M30 and metabolism indices including liver enzymes, serum lipids and glycometabolism indices. RESULTS: The aggravating degree of liver pathology appeared with prolonged feeding period. The relevance of CK 18-M30 to the severity of liver pathology were higher relative to other indices. CONCLUSION: Our results suggested the significance of CK 18-M30 in the progression of NAFLD and provided new evidence for the early diagnosis and prognostic estimation of NAFLD.