Cytokine · 2020
Combination of asprosin and adiponectin as a novel marker for diagnosing non-alcoholic fatty liver disease.
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Ke Fan, Xue Guohui, Jiang Xueling, Li Fangfang, Lai Xiaoyang, Zhang Meiying, Shen Yunfeng, Gao Ling
Аннотация
BACKGROUND AND OBJECTIVE: Patients with non-alcoholic fatty liver disease (NAFLD) have insulin resistance and are at an increased risk of diabetes. Recent evidence suggests that asprosin-a novel hormone secreted by white adipose tissue-may play a role in the pathogenesis of insulin resistance. However, the role of asprosin in NAFLD remains unclear. This study aimed to determine whether serum asprosin level could be used as a biochemical marker for NAFLD diagnosis.
METHODS: Forty-three untreated NAFLD patients and 50 sex- and age-matched healthy controls were included. Circulating serum asprosin and adiponectin (another adipokine) levels were detected by ELISA. Other metabolic parameters related to NAFLD were also determined.
RESULTS: Increased circulating serum asprosin and decreased serum adiponectin levels were found in NAFLD patients unlike in healthy controls. A positive correlation was observed between asprosin and platelet counts (PLT) (r = 0.3653, p = 0.015), fasting blood glucose (FBG) (r = 0.3592, p = 0.017), triglyceride (TG) levels (r = 0.3383, p = 0.025), serum albumin (ALB) levels (r = 0.3273, p = 0.030), and insulin resistance (HOMA-IR) (r = 0.4799, p = 0.001), whereas a negative correlation existed between adiponectin and TG levels in the NAFLD group. Multivariate linear regression showed that FBG and HOMA-IR were independently related to asprosin levels. Receiver operating characteristic (ROC) curves showed that asprosinAUC and adiponectinAUC were 0.735 (95%CI 0.633-0.836, P < 0.0001) and 0.702 (95%CI 0.597-0.807, p = 0.0007) respectively. Moreover, the combination of both biomarkers showed good sensitivity and specificity with AUC of 0.827, which was better than the single detection of asprosin or adiponectin.
CONCLUSION: High serum asprosin and low adiponectin level might be associated with the presence of insulin resistance in NAFLD, and the combination of asprosin and adiponectin could be a novel biomarker for diagnosing NAFLD. These data needed to be confirmed and extended in further large-population, well-designed clinical studies.
METHODS: Forty-three untreated NAFLD patients and 50 sex- and age-matched healthy controls were included. Circulating serum asprosin and adiponectin (another adipokine) levels were detected by ELISA. Other metabolic parameters related to NAFLD were also determined.
RESULTS: Increased circulating serum asprosin and decreased serum adiponectin levels were found in NAFLD patients unlike in healthy controls. A positive correlation was observed between asprosin and platelet counts (PLT) (r = 0.3653, p = 0.015), fasting blood glucose (FBG) (r = 0.3592, p = 0.017), triglyceride (TG) levels (r = 0.3383, p = 0.025), serum albumin (ALB) levels (r = 0.3273, p = 0.030), and insulin resistance (HOMA-IR) (r = 0.4799, p = 0.001), whereas a negative correlation existed between adiponectin and TG levels in the NAFLD group. Multivariate linear regression showed that FBG and HOMA-IR were independently related to asprosin levels. Receiver operating characteristic (ROC) curves showed that asprosinAUC and adiponectinAUC were 0.735 (95%CI 0.633-0.836, P < 0.0001) and 0.702 (95%CI 0.597-0.807, p = 0.0007) respectively. Moreover, the combination of both biomarkers showed good sensitivity and specificity with AUC of 0.827, which was better than the single detection of asprosin or adiponectin.
CONCLUSION: High serum asprosin and low adiponectin level might be associated with the presence of insulin resistance in NAFLD, and the combination of asprosin and adiponectin could be a novel biomarker for diagnosing NAFLD. These data needed to be confirmed and extended in further large-population, well-designed clinical studies.