Abstract
As a sugar additive, fructose is widely used in processed foods and beverages. Excessive fructose consumption can cause hepatic steatosis and dyslipidemia, leading to the development of metabolic syndrome. Recent research revealed that fructose-induced nonalcoholic fatty liver disease (NAFLD) is related to several pathological processes, including: (1) augmenting lipogenesis; (2) leading to mitochondrial dysfunction; (3) stimulating the activation of inflammatory pathways; and (4) causing insulin resistance. Cellular signaling research indicated that partial factors play significant roles in fructose-induced NAFLD, involving liver X receptor (LXR)α, sterol regulatory element binding protein (SREBP)-1/1c, acetyl-CoA carboxylase (ACC), fatty acid synthase (FAS), stearoyl-CoA desaturase (SCD), peroxisome proliferator–activated receptor α (PPARα), leptin nuclear factor-erythroid 2-related factor 2 (Nrf2), nuclear factor kappa B (NF-κB), tumor necrosis factor α (TNF-α), c-Jun amino terminal kinase (JNK), phosphatidylinositol 3-kinase (PI3K) and adenosine 5′-monophosphate (AMP)-activated protein kinase (AMPK). Until now, a series of natural products have been reported as regulators of NAFLD in vivo and in vitro. This paper reviews the natural products (e.g., curcumin, resveratrol, and (−)-epicatechin) and their mechanisms of ameliorating fructose-induced NAFLD over the past years. Although, as lead compounds, natural products usually have fewer activities compared with synthesized compounds, it will shed light on studies aiming to discover new drugs for NAFLD.
Highlights
Fructose— known as fruit sugar—is a ketonic monosaccharide present in many plants, such as sugar cane, sugar beets, and corn
Fructose enters hepatocytes through a transporter, especially glucose transporter 2 (Glut2), Glut5, Glut8 [11], or possibly Glut9 [12], where it is preferentially metabolized by fructokinase to generate fructose-1-phophate, serves as a relatively unregulated source providing carbon atoms for both the glycerol and the acyl portions of triglycerides [13]
The results indicated that S. cochinchinensis ethanol extract decreased the expression of stearoyl-CoA desaturase (SCD)-1, sterol regulatory element binding protein (SREBP)-1c, and fatty acid synthase (FAS) to modulate lipid accumulation and attenuate hepatic insulin resistance [25]
Summary
Fructose— known as fruit sugar—is a ketonic monosaccharide present in many plants, such as sugar cane, sugar beets, and corn It has been appreciated for many years that fructose is applied as a sugar additive, typically in high fructose corn syrup, the main ingredient of soft drinks, pastries, desserts, and other daily processed foods. Exploratory observational pilot studies showed that over-consumption of fructose in NAFLD patients may increase risk of liver. Patients with NAFLD tend to suffer from non-alcoholic steatohepatitis, hepatic fibrosis, cirrhosis, hepatoma, and metabolic syndrome, meaning that it is a leading health risk in this population [16,17]. This paper reviewed the bioactive natural products on NAFLD recently reported in the literature, which can serve as a lead for new drugs research and diary supplement development
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