Fucosterol inhibits adipogenesis through the activation of AMPK and Wnt/β-catenin signaling pathways

Food Science and Biotechnology - Fucosterol is a sterol constituent primarily derived from brown algae. Recently, the antiadipogenic effect of fucosterol has been reported; however, its molecular...     

Effect of Chrysanthemum indicum Linné extract on melanogenesis through regulation of TGF-β/JNK signaling pathway

Food Science and Biotechnology - Although several physiological effects of Chrysanthemum indicum Linné (CL) have been researched, the specific effect and molecular mechanism of CL as a...     

Xanthigen attenuates high-fat diet-induced obesity through down-regulation of PPARγ and activation of the AMPK pathway

Xanthigen, a mixture of brown seaweed and pomegranate seed extracts, has weight loss properties and lipid-lowering effects in mice and humans. This study elucidated the Xanthigen mechanism of an anti-obesity activity in high-fat diet (HFD)-fed mice. Xanthigen decreased expression of peroxisome proliferator-activated receptor γ (PPARγ) in the adipose tissue of HFD-fed mice. The serum leptin level and the adipose tissue leptin expression in mice fed HFD plus Xanthigen were significantly decreased, compared to HFD-fed mice. Phosphorylation of AMPactivated protein kinase (AMPK) α and β and acetyl-CoA carboxylase (ACC) in the adipose tissue of HFD plus Xanthigen-fed mice was elevated, and HMG-CoA reductase (HMGCR) expression was decreased. Xanthigen may have an anti-obesity activity by down-regulation of PPARγ and activation of the AMPK pathway.     

β-Hydroxybutyrate inhibits apoptosis in bovine neutrophils through activating ERK1/2 and AKT signaling pathways

Ketosis in dairy cows, a common metabolic disorder during the peripartal period, is accompanied by systemic inflammation and high concentrations of blood β-hydroxybutyrate (BHB). Neutrophil apoptosis plays a key role in maintaining the balance of inflammation and functional capacity of circulating neutrophils in ketotic cows. The kinases ERK1/2 and AKT, as well as their downstream Bcl-2 family-mediated mitochondrial signaling, are important apoptosis-regulating pathways in neutrophils. The objective of our study was to investigate the effects of BHB on neutrophil apoptosis and the underlying regulatory mechanisms during ketosis. Neutrophils were isolated from 5 multiparous cows (within 3 wk postpartum) with serum BHB concentrations <0.6 mM and glucose concentrations >3.5 mM. In a series of experiments, neutrophils were treated with increasing concentrations of BHB (0, 0.6, 2, and 3 mM for 10 h) and time (0, 2, 4, 6, 8, and 10 h with 2 mM). Subsequently, a 2 mM BHB dose was used to challenge neutrophils for 8 h. Apoptosis rate of neutrophils and protein abundance of cleaved caspase 3 were lower after BHB treatment. Treatment with BHB decreased protein and mRNA abundance of the pro-apoptotic genes Bax (BAX) and Bad (BAD), whereas it increased mitochondrial membrane potential (MMP) and protein and mRNA of the anti-apoptotic genes Bcl-xL (BCL2L1) and Mcl-1 (MCL1). This indicated that a mitochondrial pathway was involved in the inhibition of neutrophil apoptosis via BHB. In addition, both SCH772984 (an inhibitor of the ERK1/2 signaling pathway) and MK-2206 (an inhibitor of the AKT signaling pathway) alleviated the BHB-induced anti-apoptotic function of the Bcl-2 family and the inhibition of MMP. Overall, our data demonstrated that high concentrations of BHB inhibit apoptosis in bovine neutrophils by activating the ERK1/2 and AKT signaling pathways. These findings provide a theoretical basis for the understanding of systemic inflammation in ketotic cows.     

Lithium chloride’s inhibition of 3T3-L1 cell differentiation by regulating the Wnt/β-catenin pathway and enhancing villin 2 expression

Food Science and Biotechnology - The aim of this study is to reveal the relation among villin 2, Wnt/β-catenin, and adipogenesis by adding appropriate lithium chloride (LiCl). The study...     

Effects of high hydrostatic pressure on microstructure,physicochemical properties and in vitro digestibility of oat starch/β-glucan mixtures

Oats do not contain gluten protein, and oat dough structure is formed mainly through the hydrogen bonding of starch and β-glucan. As a non-thermal processing technology, high hydrostatic pressure (HHP) is mainly used to modify starch and protein in food processing. This study investigated the effects of HHP treatment on the morphological, structural, thermal, pasting and in vitro digestion properties of oat starch/β-glucan mixtures. Results showed that β-glucan interconnects with amylose through hydrogen bonding and has a protective effect on the crystalline region of oat starch. Effect of HHP treatment on the crystal structure of mixture system goes through crystal structure perfection stage, crystallisation disintegration and gelatinisation stage. After 300–400 MPa treatment, the changes in particle surface were not obvious, the phase transition temperature, the ΔH_gel and the PT of mixtures increased, while the particle size, viscosity and BD values decreased. After 500–600 MPa treatment, mixtures were completely gelatinised, most of the particles swelled and deformed, the particle size increased significantly. The principal component analysis results show that the complexes were distributed in the same region with similar properties after the 300–400 MPa and 500–600 MPa treatments, respectively.     

αs-casein inhibits the pressure-induced aggregation of β-lactoglobulin through its molecular chaperone-like properties

In this work, the effects of α_s-casein (α_s-CN) on the pressure-induced aggregation of β-lactoglobulin (β-Lg) were studied. α_s-CN depressed the pressure-induced aggregation of β-Lg, and this function was dependent on the concentration of α_s-CN and the pressure holding time. Furthermore, α_s-CN altered the aggregation process of β-Lg by suppressing the transition of the aggregate from the soluble phase to the insoluble phase and, as a result, the fraction of insoluble aggregates was decreased. During this process, α_s-CN formed stable complexes with the denatured β-Lg and the formation of complexes prevented further aggregation of β-Lg and solubilized aggregated β-Lg to a small degree of polymerization. These results indicate that α_s-CN exhibits a chaperone-like activity under high pressure, and provide an insight into the possible mechanism by which α_s-CN accomplishes the task of stabilizing proteins to resist the pressure-induced aggregation of β-Lg.     

Methylglyoxal-derived advanced glycation end products induce matrix metalloproteinases through activation of ERK/JNK/NF-κB pathway in kidney proximal epithelial cells

Food Science and Biotechnology - The accumulation of reactive α-dicarbonyl leading to advanced glycation end products (AGEs) have been linked to pathophysiological diseases in many studies,...     

Optimal ratios of essential amino acids stimulate β-casein synthesis via activation of the mammalian target of rapamycin signaling pathway in MAC-T cells and bovine mammary tissue explants

Amino acids are the building blocks of proteins and serve as key molecular components upstream of the signaling pathways that regulate protein synthesis. The objective of this study was to systematically investigate the effect of essential AA ratios on milk protein synthesis in vitro and to elucidate some of the underlying mechanisms. Triplicate cultures of MAC-T cells and bovine mammary tissue explants (MTE) were incubated with the optimal AA ratio (OPAA; Lys:Met, 2.9:1; Thr:Phe, 1.05:1; Lys:Thr, 1.8:1; Lys:His, 2.38:1; and Lys:Val, 1.23:1) in the presence of rapamycin (control), OPAA, a Lys:Thr ratio of 2.1:1, a Lys:Thr ratio of 1.3:1, a Lys:His ratio of 3.05:1, or a Lys:Val ratio of 1.62:1 for 12 h; the other AA concentrations were equal to OPAA. In some experiments, the cells were cultured with OPAA with or without rapamycin (100 ng/mL) or with mammalian target of rapamycin (mTOR) small interference RNA, and the MTE were exposed to OPAA with rapamycin for β-casein expression. Among the treatments, the expression of β-casein was greatest in the MTE cultured with OPAA. In MAC-T cells, the OPAA upregulated the mRNA expression of SLC1A5 and SLC7A5 but downregulated the expression of IRS1, AKT3, EEF1A1, and EEF2 compared with the control. The OPAA had no effect on the mTOR phosphorylation status but increased the phosphorylation of S6K1 and RPS6. When the MTE were treated with rapamycin in the presence of OPAA, the expression of β-casein was markedly decreased. The phosphorylation of RPS6 and 4EBP1 also was reduced in MAC-T cells. A similar negative effect on the expression of RPS6KB1 and EIF4EBP1 was detected when the cells were cultured with either rapamycin or mTOR small interference RNA. The optimal AA ratio stimulated β-casein expression partly by enhancing the transport of AA into the cells, cross-talk with insulin signaling and a subsequent enhancement of mTOR signaling, or translation elongation in both MAC-T cells and bovine MTE.     

The human milk oligosaccharide 2′-fucosyllactose attenuates β-lactoglobulin–induced food allergy through the miR-146a–mediated toll-like receptor 4/nuclear factor-κB signaling pathway

Our previous experiments have confirmed that human milk oligosaccharides (HMO) and its main component 2′-fucosyllactose (2′-FL), as prebiotics, could effectively alleviate cow milk allergy by regulating the intestinal microecology. This study intended to further explore the molecular mechanism of HMO regulating intestinal immunity. The results of the allergic mouse model showed that oral administration of 2′-FL or HMO reduced β-lactoglobulin (β-LG)–induced serum-specific IgE secretion and mast cell degranulation, while reducing the inflammatory cytokines, TNF-α, IL-4, and IL-6 production and promoting the miR-146a expression. In vitro results further confirmed that 2′-FL or HMO treatment reduced allergen–induced secretion of iNOS, NO, pro-inflammatory cytokines and reactive oxygen species in RAW264.7 cells. At the same time, in contrast to the β-LG group, 2′-FL dose-dependently inhibited the TLR4/NF-κB inflammatory pathway and upregulated miR-146a expression, and the effect of the 2′-FL mid-dose group was similar to that of the HMO intervention group. In particular, adding miR-146a inhibitors to macrophages attenuated the inhibitory effect of 2′-FL on the expression of TRAF6 and IRAKI in the TLR4 pathway, suggesting that miR-146a might be involved in the immune regulation of 2′-FL. The above results indicated that 2′-FL had a similar effect to HMOs, and its effect of reducing β-LG allergy might be related to the regulation of miR-146a to inhibit TLR4/NF-κB signaling pathway.