Department of Nutrition, School of Public Health, Anhui Medical University, Hefei, China.
Key Laboratory of Population Health Across Life Cycle (Anhui Medical University), Ministry of Education of the People's Republic of China, Anhui, China.
Liver Int. 2022 Jan;42(1):69-79. doi: 10.1111/liv.15057. Epub 2021 Sep 18.
Hyperinsulinaemia and insulin resistance play a central role in the progression of hepatic steatosis and fibrosis, and diet can modulate insulin response. We thus hypothesised that diet with higher insulinaemic potential is associated with an increased risk of these conditions.
Two empirically dietary indices for hyperinsulinaemia (EDIH) and insulin resistance (EDIR) were derived to identify food groups most predictive of fasting concentrations of C-peptide and insulin and homeostatic model assessment for insulin resistance respectively. Hepatic steatosis and fibrosis were defined by controlled attenuation parameter and liver stiffness measurement using transient elastography (TE). Odds ratios (ORs) and 95% confidence intervals (CIs) were calculated by logistic regression.
Of the 4171 participants with TE examination, 1436 (age-standardised prevalence, 33.8%) were diagnosed with steatosis, 255 (5.6%) with advanced fibrosis and 101 (2.2%) with cirrhosis. The multivariable-adjusted ORs for participants comparing the highest to the lowest EDIH tertile were 1.17 (95% CI: 0.99-1.39, P = .005) for steatosis, 1.74 (95% CI: 1.24-2.44, P = .001) for advanced fibrosis and 2.05 (95% CI: 1.21-3.46, P = .004) for cirrhosis. Similar associations were observed for EDIR with ORs of 1.32 (95% CI: 1.11-1.55, P < .001) for steatosis and 1.43 (95% CI: 1.03-1.99, P = .006) for advance fibrosis. These positive associations remained among never drinkers and individuals who were free of hepatitis B and/or C.
Our findings suggest that hyperinsulinaemia and insulin resistance may partially underlie the influence of diet on hepatic steatosis and fibrosis, and highlight the importance of reducing or avoiding insulinaemic dietary pattern.
高胰岛素血症和胰岛素抵抗在肝脂肪变性和纤维化的进展中起着核心作用,而饮食可以调节胰岛素反应。因此,我们假设具有更高胰岛素生成潜力的饮食与这些疾病的风险增加有关。
我们得出了两个用于高胰岛素血症(EDIH)和胰岛素抵抗(EDIR)的经验性饮食指数,以确定最能预测空腹 C 肽和胰岛素浓度以及稳态模型评估胰岛素抵抗的食物组。使用瞬态弹性成像(TE),通过受控衰减参数和肝硬度测量来定义肝脂肪变性和纤维化。通过逻辑回归计算比值比(OR)和 95%置信区间(CI)。
在接受 TE 检查的 4171 名参与者中,1436 名(年龄标准化患病率为 33.8%)被诊断为脂肪变性,255 名(5.6%)为晚期纤维化,101 名(2.2%)为肝硬化。与 EDIH 三分位最高组相比,参与者的多变量调整 OR 分别为 1.17(95%CI:0.99-1.39,P = 0.005)为脂肪变性,1.74(95%CI:1.24-2.44,P = 0.001)为晚期纤维化,2.05(95%CI:1.21-3.46,P = 0.004)为肝硬化。EDIR 也观察到类似的关联,OR 分别为 1.32(95%CI:1.11-1.55,P < 0.001)为脂肪变性和 1.43(95%CI:1.03-1.99,P = 0.006)为晚期纤维化。在从未饮酒者和未感染乙型肝炎和/或丙型肝炎的个体中,这些阳性关联仍然存在。
我们的研究结果表明,高胰岛素血症和胰岛素抵抗可能部分解释了饮食对肝脂肪变性和纤维化的影响,并强调了减少或避免胰岛素生成饮食模式的重要性。