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Middle‐ and high‐molecular weight adiponectin levels in relation to nonalcoholic fatty liver disease

OBJECTIVE: Adiponectin (APN) circulates as high‐molecular weight (HMW), medium‐molecular weight (MMW), and low‐molecular weight (LMW) forms. Nonalcoholic fatty liver disease (NAFLD) is a common cause of chronic liver disease. Currently, the role of LMW, MMW, and HMW APN remains largely unclear in NA...

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Detalles Bibliográficos
Autores principales: Lian, Kun, Feng, Yu‐Nan, Li, Rong, Liu, Hao‐Lin, Han, Peng, Zhou, Lei, Li, Cheng‐Xiang, Wang, Qin
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7171302/
https://www.ncbi.nlm.nih.gov/pubmed/31880002
http://dx.doi.org/10.1002/jcla.23148
Descripción
Sumario:OBJECTIVE: Adiponectin (APN) circulates as high‐molecular weight (HMW), medium‐molecular weight (MMW), and low‐molecular weight (LMW) forms. Nonalcoholic fatty liver disease (NAFLD) is a common cause of chronic liver disease. Currently, the role of LMW, MMW, and HMW APN remains largely unclear in NAFLD. METHODS: We examined the variation of these forms and analyzed the related clinical characteristics in NAFLD. A total of 63 male NAFLD patients (mean age: 43.00 ± 6.10 years) and 70 healthy male subjects (mean age: 42.53 ± 7.98 years) were included in the study. Total APN and other clinical characteristics were measured. The changes in HMW, MMW, and LMW APN were determined in NAFLD patients and NAFLD patients on a high‐fat diet, and the association between the groups was further analyzed. RESULTS: Decreased levels of total APN and three APN isoforms were found in NAFLD. Significantly decreased levels of HMW (P < .01) and MMW (P < .001) were observed in NAFLD of high‐fat diet patients. In NAFLD patients, height (R = −.270, P = .032) and N‐epsilon‐(carboxymethyl) lysine (R = −.259, P = .040) significantly correlated with total APN. HMW APN was significantly associated with fasting plasma glucose (R = .350, P = .016), alanine aminotransferase (R = −.321, P = .029), and aspartate aminotransferase (R = −.295, P = .045). Additionally, MMW APN was significantly associated with total cholesterol (R = .357, P = .014) and high‐density lipoprotein (R = .556, P < .0001). Low‐density lipoprotein (R = −.283, P = .054) was also clearly associated with LMW APN in NAFLD patients. CONCLUSION: These results suggest that HMW and MMW APN may be involved in the pathogenesis and progression of NAFLD.