Peptides released from bovine α-lactalbumin by simulated digestion alleviated free fatty acids-induced lipid accumulation in HepG2 cells

α-Lactalbumin peptide Asp-Gln-Trp alleviates hepatic insulin resistance and modulates gut microbiota dysbiosis in high-fat diet-induced NAFLD mice

“…27 Our previous study also showed that DQW improved lipid accumulation and inhibited ROS production by activating the PPARα pathway in HepG2 cells. 22 In the present study, our results indicated that the protective effects of DQW on liver injury and hepatic insulin resistance may be partly by activating PPARα.…”

“…18,21 In our previous study, we found that the peptide DQW released from α-lactalbumin could attenuate FFAs-induced lipid accumulation and oxidative stress by activating the peroxisome proliferator-activated receptor α (PPARα) in HepG2 cells. 22 Moreover, many studies have shown that the beneficial effects of food-derived bioactive peptides on the regulation of metabolic diseases are closely associated with gut microecology. 23 Therefore, we hypothesized that the peptide DQW may have a potential role in improving glucose homeostasis and gut microbiota.…”

Lactobacillus paracaseiIMC 502 ameliorates type 2 diabetes by mediating gut microbiota–SCFA–hormone/inflammation pathway in mice

“…Denatured proteins were loaded on SDS‐PAGE gels for separation and then transferred to nitrocellulose membranes. Subsequent membrane blocking, primary and secondary antibodies incubation and the appearance, detection and quantification of protein bands were performed 23 …”

Hypersampones A–C, Three Nor-Polycyclic Polyprenylated Acylphloroglucinols with Lipid-Lowering Activity from Hypericum sampsonii

“…The weights of compounds 1 and 3 are sufficient for the antilipid accumulation experiment in the oleic acid (OA)-treated HepG2 cell model, while the weight of compound 2 is insufficient for it to be involved in this experiment . First, MTT assay results implied that there was no obvious cytotoxicity of compounds 1 and 3 in OA-treated HepG2 cells (Figure A).…”

“…Acetyl-coenzyme A carboxylase (ACAC) and fatty acid synthase (FAS) are two key rate-limiting enzymes in the process of fatty acid and cholesterol synthesis. , The preliminary mechanism of compound 1 with respect to lipid-lowering effects was investigated. As shown in Figure A, Western blot results showed that in OA-induced cells, the levels of protein expression of FAS and acetyl-coenzyme A carboxylase α (ACACA) were significantly higher than that in the control group ( p < 0.001).…”