Ferulic Acid Mediates Metabolic Syndrome via the Regulation of Hepatic Glucose and Lipid Metabolisms and the Insulin/IGF-1 Receptor/PI3K/AKT Pathway in Palmitate-Treated HepG2 Cells.

Ferulic acid (FA) is one of the most abundant bound phenolics in whole grains, partly contributing to its preventive effects on metabolic syndrome (MetS). The study aims to investigate if FA mediates MetS through the regulation of hepatic metabolisms and the insulin receptor related pathways in the palmitate-treated HepG2 cells (MetS model). We found that FA (50, 100, and 200 µM) dramatically ameliorated the lipid accumulation in the MetS model. FA significantly decreased the activities of the gluconeogenic enzymes, G6Pase and PEPCK, downregulated the lipogenic enzyme FAS-1, and upregulated the lipolytic enzyme CPT-1 by regulating a series of transcriptional factors including HNF4α, FOXO-1, SREBP-1c, and PPAR-γ. Notably, we found that FA's ability to alleviate MetS is achieved by activating the insulin receptor/PI3K/AKT pathway. Our results validated the effects of FA on mediating the metabolic disorders of lipid and glucose pathways and unveiled its potential intracellular mechanisms for the prevention of MetS.

Molecular regulation of phenolic compounds on IGF-1 signaling cascade in breast cancer.

Breast cancer is a highly aggressive and heterogeneous disease with complex features that remains a major health problem and undermines the span and quality of life of women worldwide. Primary literature has shown the role of phenolic compounds in controlling the onset of breast cancer. The mechanism of action of phenolic compounds can be explained by their interaction with signal transduction pathways that regulate cell proliferation and induction of apoptosis. One of the targets of phenolic compounds is the insulin like growth factor 1 (IGF-1) signaling cascade, which plays a significant role in the growth and development of mammary tissues by leading proliferative and anti-apoptotic events. Increasing research evidence points to the function of the IGF-1 cascade system in the commencement, progression, and metastasis of breast tissue malignancy. In this review, we mainly discuss the function of the IGF-1 system, and the role of phenolic compounds in regulating the IGF-1 signaling cascade and curbing breast malignancies.

High-Dietary Fiber Intake Alleviates Antenatal Obesity-Induced Postpartum Depression: Roles of Gut Microbiota and Microbial Metabolite Short-chain Fatty Acid Involved.

Antenatal obesity increases the risk of postpartum depression. Previous research found that dietary fiber supplementation could alleviate mental behavioral disorders. The present study aims to uncover the effects of high-dietary fiber intake on high-fat diet (HFD)-induced depressive-like behaviors and its underlying mechanism. Female C57BL6/J mice were fed with HFD to establish an antenatal obese model. A high-dietary fiber intake (inulin, 0.037 g/kcal) significantly attenuated cognitive deficits and depressive-like behaviors in the maternal mice after the offspring weaning. High-dietary fiber intake upregulated the expression of 5-hydroxytryptamine (5-HT) and norepinephrine (NE) and suppressed neuroinflammation. Furthermore, high-dietary fiber intake restructured the gut microbiome and elevated the formation of short-chain fatty acids (SCFAs). Correlation analysis indicated that the increase in microbes such as Lactobacillus and S24-7, and SCFAs' levels were positively correlated with behavioral improvements. In conclusion, high-dietary fiber intake is a promising nutritional intervention strategy to prevent antenatal obesity-induced behavioral disorders via a microbiota-gut-brain axis.

Sea-Buckthorn Flavonoids Alleviate High-Fat and High-Fructose Diet-Induced Cognitive Impairment by Inhibiting Insulin Resistance and Neuroinflammation.

Sea-buckthorn flavonoids (SFs) have been used as functional food components for their bioactive potential in preventing metabolic complications caused by diet, such as obesity and inflammation. However, the protective effect of SFs on cognitive functions is not fully clear. In this study, a high-fat and high-fructose diet (HFFD)-induced obese mice model was treated with SFs for 14 weeks. It was found that the oral SF administration (0.06% and 0.31% w/w, mixed in diet) significantly reduced bodyweight gain and insulin resistance in the HFFD-fed mice. SFs significantly prevented HFFD-induced neuronal loss and memory impairment in behavioral tests. Additionally, SFs also suppressed the HFFD-induced synaptic dysfunction and neuronal damages by increasing the protein expressions of PSD-95. Furthermore, SF treatment activated the ERK/CREB/BDNF and IRS-1/AKT pathways and inactivated the NF-κB signaling and its downstream inflammatory mediator expressions. In conclusion, SFs are a potential nutraceutical to prevent high-energy density diet-induced cognitive impairments, which could be possibly explained by their mediating effects on insulin signaling and inflammatory responses in the brain.