Homeostasis of Glucose and Lipid in Non-Alcoholic Fatty Liver Disease

Abstract

Industrialized society-caused dysregular human behaviors and activities such as overworking, excessive dietary intake, and sleep deprivation lead to perturbations in the metabolism and the development of metabolic syndrome. Non-alcoholic fatty liver disease (NAFLD), the most common chronic liver disease worldwide, affects around 30% and 25% of people in Western and Asian countries, respectively, which leads to numerous medical costs annually. Insulin resistance is the major hallmark of NAFLD and is crucial in the pathogenesis and for the progression from NAFLD to non-alcoholic steatohepatitis (NASH). Excessive dietary intake of saturated fats and carbohydrate-enriched foods contributes to both insulin resistance and NAFLD. Once NAFLD is established, insulin resistance can promote the progression to the more severe state of liver endangerment like NASH. Here, we review current and potential studies for understanding the complexity between insulin-regulated glycolytic and lipogenic homeostasis and the underlying causes of NAFLD. We discuss how disruption of the insulin signal is associated with various metabolic disorders of glucoses and lipids that constitute both the metabolic syndrome and NAFLD.

Factors associated with hepatic fibrosis and its deterioration among fatty liver elderly: a retrospective cohort study

“…The impact of chronic liver disease on hepatic lipid metabolism has been mentioned in several studies (10,11). One important nding in this study is that patients with severe NAFLD, as indicated by a FIB-4 score greater than 2.67, were found to have lower lipid levels, speci cally total cholesterol and LDL, than patients with moderate and mild FIB-4 scores.…”

“…Another interesting nding is that fasting glucose was higher in the mild versus moderate NAFLD group (p < 0.05), as shown in Table 1. Although the relationship between the metabolism of glucose and chronic liver disease is not fully understood, there have been several proposed mechanisms for glucose homeostasis in NAFLD (11). A possible explanation for a lower fasting glucose in moderate versus mild NAFLD group is that the liver's ability to mobilize and distribute glucose to peripheral tissues is diminished, this is especially seen in patients with cirrhosis where their liver is severely dysfunctional (14).…”

Chronic hepatitis B and non‐alcoholic fatty liver disease: Conspirators or competitors?

“…In fact, during NAFLD pathogenesis, hepatic steatosis occurs when fatty acid uptake and synthesis exceed oxidation and re‐secretion . In addition, downregulation of glycolysis and glycogen synthesis can also represent the manifestation of insulin resistance, which is closely related to NAFLD development . Therefore, these HBV‐related metabolic changes may participate in the occurrence of NAFLD.…”

The Impacts of Herbal Medicines and Natural Products on Regulating the Hepatic Lipid Metabolism

“…In the normal physiological status, high level of glucose promotes the secretion of insulin, activates carbohydrate-responsive elementbinding protein (ChREBP), and meanwhile, provides substrate to facilitate lipogenesis in the liver . In terms of insulin, it activates sterol regulatory element-binding protein 1c (SREBP-1c) to up-regulate lipogenic enzymes, and then promotes de novo lipogenesis (Eissing et al, 2013;Chao et al, 2019). Figure 2 shows the overview of lipogenesis in hepatocytes.…”