Abstract
Our data about pathogenesis of hepatic steatosis after liver transplantation is scarce. This study aimed to investigate the association between serum adipokines and insulin resistance with hepatic steatosis in liver transplant recipients. We investigated the association between insulin resistance, serum adiponectin, insulin, and leptin with hepatic steatosis in a cohort of liver transplant recipients. Homeostatic model assessment of insulin resistance 2 (HOMA 2-IR) was used for estimation of insulin resistance. Hepatic steatosis was determined using ultrasound and controlled attenuation parameter (CAP). A total of 178 patients were included. 79 patients (44.4%) had hepatic steatosis. Serum adiponectin (OR: 0.912; 95% CI 0.869–0.957; P < 0.001), serum leptin (OR: 1.060; 95% CI 1.017–1.102; P = 0.005), HOMA2-IR (OR: 1.671; 95% CI 1.049–2.662; P = 0.031), and post-transplant diabetes mellitus (PTDM) (OR: 5.988; 95% CI 1.680–21.276; P = 0.006) were independently associated with hepatic steatosis after liver transplantation. CAP values were negatively correlated with serum adiponectin (P = 0.011) and positively correlated with serum insulin (P = 0.001), leptin (P < 0.001) and HOMA2-IR (P < 0.001). Insulin resistance and alterations in adipokines might have central role in pathogenesis of hepatic steatosis after liver transplantation and can be targeted for diagnostic and therapeutic purposes.
Highlights
Our data about pathogenesis of hepatic steatosis after liver transplantation is scarce
Association of hepatic steatosis with serum adipokines and insulin resistance after liver trans‐ plantation. 178 liver transplant recipients were included in the study
Serum adiponectin (OR: 0.912; 95% CI 0.869-0.957; P < 0.001), serum leptin (OR: 1.060; 95% CI 1.017–1.102; P = 0.005), HOMA2-IR as a marker of insulin resistance (OR: 1.671; 95% CI 1.049–2.662; P = 0.031), and post-transplant diabetes mellitus (PTDM) (OR: 5.988; 95% CI 1.680–21.276; P = 0.006), were independently associated with hepatic steatosis after liver transplantation (Table 2)
Summary
Our data about pathogenesis of hepatic steatosis after liver transplantation is scarce. This study aimed to investigate the association between serum adipokines and insulin resistance with hepatic steatosis in liver transplant recipients. We investigated the association between insulin resistance, serum adiponectin, insulin, and leptin with hepatic steatosis in a cohort of liver transplant recipients. Serum adiponectin (OR: 0.912; 95% CI 0.869–0.957; P < 0.001), serum leptin (OR: 1.060; 95% CI 1.017–1.102; P = 0.005), HOMA2-IR (OR: 1.671; 95% CI 1.049–2.662; P = 0.031), and post-transplant diabetes mellitus (PTDM) (OR: 5.988; 95% CI 1.680–21.276; P = 0.006) were independently associated with hepatic steatosis after liver transplantation. Non-alcoholic fatty liver disease (NAFLD) is rapidly surpassing other indications of liver transplantation during recent years and is going to become the leading cause of liver transplantation w orldwide[1] This is mainly due to the increasing prevalence of NAFLD secondary to the epidemics of metabolic syndrome and obesity[2]. Serum leptin level is increased and serum adiponectin is decreased in patients with NAFLD in parallel to the severity of d isease[15]
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