Effects of Pyrroloquinoline Quinone on Lipid Metabolism and Anti-Oxidative Capacity in a High-Fat-Diet Metabolic Dysfunction-Associated Fatty Liver Disease Chick Model

Abstract

Metabolic dysfunction-associated fatty liver disease (MAFLD) and its interaction with many metabolic pathways raises global public health concerns. This study aimed to determine the therapeutic effects of Pyrroloquinoline quinone (PQQ, provided by PQQ.Na2) on MAFLD in a chick model and primary chicken hepatocytes with a focus on lipid metabolism, anti-oxidative capacity, and mitochondrial biogenesis. The MAFLD chick model was established on laying hens by feeding them a high-energy low-protein (HELP) diet. Primary hepatocytes isolated from the liver of laying hens were induced for steatosis by free fatty acids (FFA) and for oxidative stress by hydrogen peroxide (H2O2). In the MAFLD chick model, the dietary supplementation of PQQ conspicuously ameliorated the negative effects of the HELP diet on liver biological functions, suppressed the progression of MAFLD mainly through enhanced lipid metabolism and protection of liver from oxidative injury. In the steatosis and oxidative stress cell models, PQQ functions in the improvement of the lipid metabolism and hepatocytes tolerance to fatty degradation and oxidative damage by enhancing mitochondrial biogenesis and then increasing the anti-oxidative activity and anti-apoptosis capacity. At both the cellular and individual levels, PQQ was demonstrated to exert protective effects of hepatocyte and liver from fat accumulation through the improvement of mitochondrial biogenesis and maintenance of redox homeostasis. The key findings of the present study provide an in-depth knowledge on the ameliorative effects of PQQ on the progression of fatty liver and its mechanism of action, thus providing a theoretical basis for the application of PQQ, as an effective nutrient, into the prevention of MAFLD.

The Imbalance of Mitochondrial Homeostasis of Peripheral Blood-Derived Macrophages Mediated by MAFLD May Impair the Walking Ability of Elderly Patients with Osteopenia

“…In the future, they will study how to prevent osteoporosis by protecting mitochondrial function [ 34 ]. Furthermore, recent studies indicate that mitochondrial regulators/nutrients from natural products can remedy mitochondrial dysfunction mediated by MAFLD [ 35 , 36 ]. Meanwhile, a number of researches nowadays are developing innovative drugs for the prevention and treatment of fatty liver diseases based on mitochondrial dysfunction [ 37 ].…”

Associations of the T329S Polymorphism in Flavin-Containing Monooxygenase 3 With Atherosclerosis and Fatty Liver Syndrome in 90-Week-Old Hens

“…Furthermore, the “two-hit hypothesis” of FLS states that fat deposition caused by abnormal fatty acid metabolism in the liver represents the “first hit,” and that increased levels of INS, inflammatory cytokines, and oxidative stress induced by fat deposition represent the “second hit” ( 49 – 51 ). The levels of antioxidant enzymes, such as GSH-Px, T-SOD, and CAT, and the oxidative biomarker MDA could further evaluate oxidative damage in the liver ( 52 ). During our study, TT hens had higher hepatic GSH-Px activity but lower hepatic T-SOD activity and a lower level of hepatic MDA than those in AA hens ( P < 0.05) ( Figure 4 ), suggesting that T329S is associated with hepatic oxidative damage of layers.…”

“…During our study, TT hens had higher hepatic GSH-Px activity but lower hepatic T-SOD activity and a lower level of hepatic MDA than those in AA hens ( P < 0.05) ( Figure 4 ), suggesting that T329S is associated with hepatic oxidative damage of layers. GSH-Px and T-SOD are normally used to scavenge reactive oxygen species, a class of substances that can disrupt the formation of biofilm, and therefore protect cells from oxidative damage ( 52 , 53 ). MDA is one of the final products of lipid oxidation and is strongly toxic to cells ( 52 ).…”

“…GSH-Px and T-SOD are normally used to scavenge reactive oxygen species, a class of substances that can disrupt the formation of biofilm, and therefore protect cells from oxidative damage ( 52 , 53 ). MDA is one of the final products of lipid oxidation and is strongly toxic to cells ( 52 ). Therefore, the increased activity of hepatic GSH-Px and the decrease in hepatic MDA levels could reduce oxidative injury in TT hens.…”

Effects of Selenium Conjugated to Insect Protein on Pharmacokinetics of Florfenicol and Enrofloxacin in Laying Hens

“…In the poultry industry, veterinary drugs such as antibiotics and antiparasitics are extensively used for disease prevention and treatment. Antibiotic growth promoters have been banned on livestock and poultry feed in China in 2020 adhering to the European Union in 2006, and a series of additives were explored to replace antibiotics for the healthy and sustainable development of the poultry industry (1)(2)(3). Nonetheless, the occurrences of residues in edible tissues and products caused by therapeutic drugs or contaminated feedstuffs also pose risks to human health, including direct toxic effects, allergic reactions, and increased bacterial resistance to common antibiotics (4).…”