Effects of endoplasmic reticulum stress, liver function, insulin resistance and vascular endothelial function in patients with nonalcoholic fatty liver disease

Abstract

It is aimed to compare whether there are differences in endoplasmic reticulum stress, liver function, insulin resistance, and vascular endothelial function in patients with nonalcoholic fatty liver disease (NAFLD) with and without type 2 diabetes mellitus (T2DM). Forty patients with NAFLD, 38 patients with NAFLD combined with T2DM, and 30 patients with normal liver tissue were selected. They were set as Group A, Group B and Group C respectively. The expression level of glucose-regulated protein 94 (GRP94) and biochemical indicators such as alanine aminotransferase (ALT), free fatty acids (FFA), triglycerides (TG), gamma-glutamyl transferase (GGT), aspartate aminotransferase (AST), fasting blood glucose (FBG), and fasting insulin (FINS) were measured. Also, the calculation of the homeostatic model assessment for insulin resistance (HOMA-IR) index was performed. The reactive hyperemia index (RHI) was detected to evaluate the vascular endothelial function of patients. The comparison between groups and multi-factor analysis of the influencing factors of RHI was conducted. Compared with Group C, the expressions in Group A and Group B were distinctly enhanced (P <0.05). Also, the expression of GRP94 protein in Group B was distinctly higher than that in Group A (P <0.05). The average optical density values of Groups A, B, and C were 0.327 ± 0.007, 0.350 ± 0.009, and 0.299 ± 0.006, respectively. A comparison between the three groups was performed. The differences had statistical significance (P <0.05). The differences in the TG, ALT, AST, GGT, FINS and HOMA-IR between Group A and Group B had statistical significance (P <0.05). The RHI values of Groups A, B, and C were 1.59 ± 0.23, 1.79 ± 0.32, and 2.05 ± 0.47, respectively. A comparison between the three groups was performed. The differences had statistical significance (P <0.05). FFA, ALT and FBG in patients with NAFLD are risk factors for endothelial dysfunction (P <0.05). The liver damage caused by NAFLD may be related to the expression of GRP94. FFA, ALT and FBG are risk factors for endothelial dysfunction in NAFLD patients.

Gut dysbiosis in nonalcoholic fatty liver disease: pathogenesis, diagnosis, and therapeutic implications

“…Therefore, LPS causes inflammation and serious metabolic changes in the body, such as increasing fat consumption, and elevating circulating free fatty acid (FFA) and triglyceride (TG). The deposition of FFA in the liver may also induce inflammation, and insulin resistance (IR), further contributing to the development of NAFLD ( Rennert et al., 2020 ; Zheng et al., 2022 ).…”

Identification of biomarkers associated with immune-propionate metabolism in nonalcoholic fatty liver disease

“…Non-alcoholic fatty liver disease (NAFLD) refers to hepatic steatosis caused by fat accumulation in the liver that is not caused by viral infection, alcohol consumption, or genetic factors (1). The main pathological feature of NAFLD is the accumulation of triglycerides and free cholesterol (2). Its pathogenesis is related to a variety of factors, such as altered intestinal flora, obesity, and disturbances in body lipid homeostasis (3).…”