Oleofoams stabilized by monoacylglycerides: Impact of chain length and concentration.

Oleofoams are plant oil based whipped systems which have drawn academic and industry attention in recent years. The aim of this study was to determine the effect of fatty acid chain length and monoacylglyceride (MAG) concentration on the performance and structural properties of MAG-based oleofoams. Four different MAGs (monolaurin, monomyrystin, monopalmitin, and monostearin) were studied at three concentration levels (5, 10, and 15 wt%). The fatty acid chain length had a statistically significant impact on the size and shape of crystals formed, while higher MAG concentrations led to higher numbers of crystals in the continuous oil phase. These differences affected the performance and physical properties of the oleofoams: compared to other MAGs, monostearin based oleofoams were harder and exhibited higher values of G' and G″, had higher overrun and showed better stability. Lastly, through microscopy techniques it was successfully proved that monostearin-based oleofoams are stabilized by both bulk and Pickering stabilization.

Structural, functional properties, and volatile profile of hemp protein isolate as affected by extraction method: Alkaline extraction-isoelectric precipitation vs salt extraction.

The utilization of industrial hemp in food is gaining popularity. This study aimed to comprehensively investigate the impact of alkaline extraction-isoelectric precipitation (AE-IEP) and salt extraction (SE) dialysis on structural, functional properties and the volatile profile of hemp protein isolate (HPI). A higher protein content (97.21%) in SE extracted HPI (SE-HPI) was obtained than the AE-IEP extracted HPI (93.37%). In particular, protein subunit composition, structural properties were strongly influenced by the extraction methods. For example, SE-HPI exhibited a larger percentage of albumin (46.53%) and a lower amount of ß-sheet (52.65%) than its counterpart (albumin 20.92%, ß-sheet 54.46%). Consequently, SE-HPI showed the higher solubility, emulsion activity, and thermal stability. Interestingly, the volatile profile of the proteins showed that SE-HPI exhibited a lower number (21) of volatile compounds when compared to its counterpart (25). This study highlights the importance of establishing the relationships between extraction methods and functional attributes of HPI.

Autophagy Induced by Palmitic Acid Regulates Neutrophil Adhesion Through the Granule-Dependent Degradation of αMß2 Integrin in Dairy Cows With Fatty Liver.

ß2 integrins are critical for neutrophil firm adhesion, trans-endothelial migration, and the recruitment to the inflamed tissue. Autophagy is implicated in cell migration and tumor metastasis through facilitating the turnover of ß1 integrins; however, whether autophagy is able to control neutrophil migration by promoting the degradation of ß2 integrins is unexplored. Here, we show that high blood levels of palmitic acid (PA) strongly triggered neutrophil autophagy activation, leading to adhesion deficiency in dairy cows with fatty liver. The three neutrophil granule subtypes, namely, azurophil granules (AGs), specific granules (SGs), and gelatinase granules (GGs), were engulfed by the autophagosomes for degradation, resulting in an increased vacuolation in fatty liver dairy cow neutrophils. Importantly, the adhesion-associated molecules CD11b and CD18 distributed on AGs, SGs, and GGs were degraded with the three granule subtypes by autophagy. Moreover, FGA, Hsc70, and TRIM21 mediated the degradation of cytosolic oxidized-ubiquitinated CD11b and CD18. Collectively, our results demonstrate that high blood PA triggers neutrophil autophagy-dependent vacuolation and granule-dependent adhesion deficiency, decreasing neutrophil mobility, and impairing the innate immune system of dairy cow with fatty liver. This theory extends the category of autophagy in maintaining granule homeostasis and provides a novel strategy to improve the immune of dairy cows with metabolic disease.

Epigallocatechin-3-gallate protects against 1,3-dichloro-2-propanol-induced lipid accumulation in C57BL/6J mice.

AIMS: Chloropropanol is a contaminant produced during food processing, and 1,3-dichloro-2-propanol (1,3-DCP) is one of the most-studied and most common chloropropanol-related food contaminants. Epigallocatechin-3-gallate (EGCG) is the most abundant ester catechin in tea polyphenols. We studied the potential therapeutic effect of EGCG on 1,3-DCP-induced lipid accumulation in the liver of mice, and determined the related regulatory mechanisms. MATERIALS AND METHODS: The effects of EGCG were investigated in 6-8-week-old adult male C57BL/6J mice that were given 1,3-DCP (1 mg/kg bw/day; i.g.) for 6 weeks. EGCG (10, 31.6 and 100 mg/kg bw/day i.g.) was administered daily in the 1,3-DCP-treated mice for 10 days. Total cholesterol (TC) and triglyceride (TG) were measured in serum and liver. For histological examination, HE staining and oil red O experiments were performed. Western blot and quantitative RT-PCR were subsequently used to study the molecular mechanisms. KEY FINDINGS: Increasing concentrations of EGCG significantly lowered TC and TG levels compared with those of the model group. Furthermore, EGCG dramatically increased expression of cAMP, P-PKA and P-CREBP, -AMPKα (Tr172), LKB1, P-ACC (Ser79) and lowered expression of CD36, SREBP-2, HMGCR, SREBP-1, GPAT in 1,3-DCP-treated mice livers. Quantitative RT-PCR experiments showed that EGCG regulated gene transcription of AMPK, SREBF-2, HMGCR and SREBP-1c. SIGNIFICANCE: These data suggested that EGCG intervention restored 1,3-DCP-altered protein levels and reduced hepatic lipid levels to normal. The mechanism was mediated by the AMPK and PKA pathways. EGCG may be developed as a candidate natural agent for the treatment of 1,3-DCP-induced lipid accumulation.

Alliin attenuates 1, 3-dichloro-2-propanol-induced lipogenesis in HepG2 cells through activation of the AMP-activated protein kinase-dependent pathway.

Accumulating evidence reveals the association of 1, 3-dichloro-2-propanol (1, 3-DCP) exposure and lipogenesis. Alliin, the most abundant sulphur compound in garlic, has been demonstrated to exhibit hypoglycemic, antioxidant and anti-inflammatory activities. Here, we showed that alliin attenuated lipogenesis induced by 1,3-DCP and that the reduction was due to activation of the AMPK pathway. HepG2 cells exposed to 1,3-DCP exhibited significant increase of triglyceride(TG) and total cholesterol(TC), and alliin reduced the accumulation. Most importantly, alliin could up-regulate the phosphorylation of AMPK and down-regulate protein and gene expressions of SREBP-1; FAS; SREBP-2;HMGCR in 1,3-DCP-induced HepG2 cells. The results demonstrated that alliin was effective on attenuating 1,3-DCP-induced lipogenesis via activation of the AMPK-SREBPs signaling pathway in HepG2 cells.

Protective effects of allicin on 1,3-DCP-induced lipid metabolism disorder in HepG2 cells.

Allicin (2-propene-1-sulfinothioic acid S-2-propenyl ester), with quite a good range of hepatoprotective and antineoplastic properties, is a functional substance from garlic (Allium sativum L.) The purpose of this study was to provide evidence that allicin could protect 1,3-DCP-induced lipid metabolism disorder in HepG2 cells. Allicin reduced the accumulation of triglycerides (TG) and total cholesterol (TC) in 1,3-DCP-induced HepG2 cells. Allicin significantly increased the phosphorylation of AMP-activated protein kinase (AMPK) and down-regulated the levels of sterol regulatory element binding protein-1 (SREBP-1) and sterol regulatory element binding protein-2 (SREBP-2) in 1,3-DCP-induced HepG2 cells. Additionally, allicin had obvious recovery influence on the phosphorylation level of PKA and CREB in 1,3-DCP-induced HepG2 cells. These observations indicated that allicin alleviated lipid metabolism disorder induced by 1,3-DCP in HepG2 cells by regulating AMPK-SREBPs and PKA-CREB signaling pathways.

1,3-dichloro-2-propanol induced lipid accumulation in HepG2 cells through cAMP/protein kinase A and AMP-activated protein kinase pathways via Gi/o-coupled receptors.

1,3-dichloro-2-propanol (1,3-DCP) is a food born hepatoxic chloropropanol contaminant that has been detected in a wide range of foods. In the present study, we investigated the effects and mechanisms of 1,3-DCP on lipid accumulation in HepG2 cells. The data showed 1,3-DCP significantly increased intracellular content of triglyceride (TG) and total cholesterol (TC) at 0.5-2µg/mL. Further results showed that 1,3-DCP greatly decreased cyclic AMP (cAMP) level. In addition, 1,3-DCP inhibited PKA and AMPK signaling pathway, but had no influence on intracellular calcium and regulated proteins. Moreover, Gi/o protein inhibitor PTX significantly inhibited 1,3-DCP induced decrease of cAMP, p-PKA and p-AMPK expression. Furthermore, 1,3-DCP significantly decreased GPR41 and GPR43 expression, but had no effect on GPR109B.Thus, we concluded that 1,3-DCP induced lipid accumulation in HepG2 cells through cAMP/PKA and AMPK signaling pathways via Gi/o-coupled receptor.

Antibacterial Effect of Gallic Acid against Aeromonas hydrophila and Aeromonas sobria Through Damaging Membrane Integrity.

In the study, we investigated the antibacterial activity and mechanism of gallic acid against Aeromonas hydrophila and Aeromonas sobria. Gallic acid showed strong antimicrobial activity against the two bacteria. Furthermore, the antibacterial mechanism of gallic acid (0, 3, 6, 12 mM) was performed by membrane integrity assay and scanning electron microscopy (SEM) assay. The results showed that gallic acid notably increased the released material absorption value at 260, 280 nm and electric conductivity in a dose-dependent manner. Moreover, the SEM assay showed that gallic acid induced severe shrink of bacterial intima and irregular morphology in a dose-dependent manner. The SDS-PAGE profiles further confirmed that gallic acid could damage bacterial cells. These results indicated gallic acid exhibited antibacterial effect by destroying membrane integrity of A. hydrophila and A. sobria. Hence, gallic acid has great potential as a new natural food preservative in food fresh-keeping and storage.

A 4-week study of four 3-monochloropropane-1,2-diol diesters on lipid metabolism in C57BL/6J mice.

3-Monochloropropane-1,2-diol (3-MCPD) esters have been detected in many foods, which have become a new safety issue worldwide. In the study, we investigated the effect of four 3-MCPD diesters (palmitate diester: CDP; stearate diester: CDS; oleate diester: CDO; linoleate diester: CDL) on lipid metabolism in C57BL/6J mice. The results showed that CDP, CDS, CDO and CDL significantly increased the serum TC, LDL-C levels and liver TG, TC levels at dose of 16.5µmol/kg/day. These results indicated that 3-MCPD diesters could potentially cause hyperlipidemia in C57BL/6J mice. Moreover, oil red O staining confirmed fat accumulation in liver induced by 3-MCPD diesters. Our work will provide more information for safety evaluation of 3-MCPD diesters. However, whether free 3-MCPD or free fatty acids or combined action compensates for the hyperlipidemia effects should be elucidated in the future.

Nonalcoholic fatty liver disease induced by 13-week oral administration of 1,3-dichloro-2-propanol in C57BL/6J mice.

1,3-Dichloro-2-propanol (1,3-DCP) is a food born chloropropanol contaminant that has been detected during the production process of a wide range of foods. In this study, we investigated the effect of 1,3-DCP on lipid metabolism of mice after 13-week subchronic exposure. The data showed that 1,3-DCP (0.05-0.5mg/kg/day) could induce nonalcoholic fatty liver disease (NAFLD) in C57BL/6J mice and the NOAEL was 0.01mg/kg/day. In addition, we studied the signaling pathway to see how 1,3-DCP worked. The data showed that NAFLD induced by 1,3-DCP was due to the dysregulation of AMPK signaling pathway. As far as we are aware, this is the first study to use 13-week subchronic toxicology to investigate the effect of 1,3-DCP on the development of NAFLD in mice. Our study provided evidence for diet contaminants in the development of NAFLD and furthered the safety evaluation of 1,3-DCP through subchronic exposure.

Immunosuppressive activity of alpinetin on activation and cytokines secretion of murine T lymphocytes.

Abstract Alpinetin, a flavonoid compound extracted from the seeds of Alpinia katsumadai Hayata, has been known to possess antibacterial, anti-inflammatory and other important therapeutic activities. In the current study, we investigated alpinetin for its immunosuppressive effect on activation and cytokines secretion of murine T lymphocytes. The data showed that alpinetin markedly suppressed ConA-induced murine splenocyte proliferation, Th1/Th2 cytokines production, CD4(+) T-cell populations and ratio of CD4(+)/CD8(+). This inspired us to further study the effects of alpinetin in vivo. The results showed that administration of alpinetin suppressed T-cell-mediated delayed-type hypersensitivity reaction in mice. In addition, we studied signal transduction pathways about T-cell activation on puried murine T lymphocytes by Western-blot assay. The data revealed that alpinetin could shock the activation of NF-κB, NFAT2 signal transduction pathways. These observations indicated that alpinetin have potential effects in downregulating the immune system and might be developed as a useful immunosuppressive agent in treating undesired immune responses.