Abstract

Insulin resistance is associated with increased risk of death and liver transplantation in the cirrhotic population, independent of disease aetiology. However, factors accounting for insulin resistance in the context of cirrhosis are incompletely understood. This study aimed to investigate the association between adiponectin and leptin with insulin resistance in cirrhotic patients and to assess the influence of disease severity on insulin resistance and metabolic status. This cross-sectional study included 126 non-diabetic cirrhotic transplant candidates. The homeostasis model assessment 2 model was used to determine the insulin resistance index, and fasting adiponectin, leptin, insulin, c-peptide, glucose, HbA1c, and lipid profiles were analysed. Insulin resistance was detected in 83% of subjects and associated with increased leptin, fasting plasma glucose and body mass index, and lower triglyceride levels. Logistic regression analysis identified leptin and triglycerides as independent predictors of insulin resistance (OR 1.247, 95% CI 1.076–1.447, p = 0.003; OR 0.357, 95% CI 0.137–0.917, p = 0.032.). Leptin levels remained unchanged, whereas adiponectin levels increased (p < 0.001) with disease progression, and inversely correlated with HbA1c (ρ = −0.349, p < 0.001). Our results indicate that leptin resistance, as indicated by elevated leptin levels, can be regarded as a contributing factor to insulin resistance in cirrhotic patients, whereas triglycerides elicited a weak protective effect. Progressively increasing adiponectin levels elicited a positive effect on glucose homeostasis, but not insulin sensitivity across disease stages.

Highlights

  • When higher circulating insulin levels are necessary to achieve glucose-lowering responses, a subject is considered insulin resistant [1]

  • This study aimed to investigate the association between adiponectin and leptin with insulin resistance in patients with liver cirrhosis, as well as to assess the influence of disease severity on insulin resistance and metabolic status

  • Our results reveal a high prevalence of insulin resistance in patients with liver cirrhosis clinically evaluated for liver transplantation

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Summary

Introduction

When higher circulating insulin levels are necessary to achieve glucose-lowering responses, a subject is considered insulin resistant [1]. To overcome insulin resistance and maintain normal metabolic functions, insulin secretion is increased, leading to a state of compensatory hyperinsulinemia [2]. This metabolic dysfunction is associated with a cluster of abnormalities with serious clinical consequences, including type 2 diabetes and cardiovascular disease [3,4]. IR tends to be an early event in the course of the disease, possibly explained by insufficient clearance of insulin due to reduced hepatocellular function. Both disease progression with further hepatocellular dysfunction and portal hypertension-related portosystemic shunting of insulin aggravate hyperinsulinemia [10,11]. Transition to overt diabetes mellitus is primarily driven by beta-cell dysfunction and the inability to compensate for the insulin resistance [14]

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