Effects of the Major Structured Triacylglycerols in Human Milk on Lipid Metabolism of Hepatocyte Cells in Vitro

2020 ◽  
Author(s):  
Yanping Wu ◽  
Niu Zhang ◽  
Ze-Yuan Deng ◽  
Hong Zhang ◽  
Jing Li
Keyword(s):  
Lipid Metabolism ◽  
Human Milk ◽  
Structured Triacylglycerols ◽  
Hepatocyte Cells

scholarly journals Differential impact of Holder and High Temperature Short Time pasteurization on the dynamic in vitro digestion of human milk in a preterm newborn model

2020 ◽  
Vol 328 ◽  
pp. 127126 ◽  
Author(s):  
Stefano Nebbia ◽  
Marzia Giribaldi ◽  
Laura Cavallarin ◽  
Enrico Bertino ◽  
Alessandra Coscia ◽  
...  
Keyword(s):  
High Temperature ◽  
Human Milk ◽  
In Vitro Digestion ◽  
Preterm Newborn ◽  
Differential Impact ◽  
High Temperature Short Time ◽  
Short Time

scholarly journals YAP1 overexpression contributes to the development of enzalutamide resistance by induction of cancer stemness and lipid metabolism in prostate cancer

Oncogene ◽  
2021 ◽  
Author(s):  
Hsiu-Chi Lee ◽  
Chien-Hui Ou ◽  
Yun-Chen Huang ◽  
Pei-Chi Hou ◽  
Chad J. Creighton ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Lipid Metabolism ◽  
Critical Issue ◽  
Castration Resistant Prostate Cancer ◽  
Cancer Stemness ◽  
New Treatment ◽  
Underlying Mechanisms ◽  
Transcriptional Complex

AbstractMetastatic castration-resistant prostate cancer (mCRPC) is a malignant and lethal disease caused by relapse after androgen-deprivation (ADT) therapy. Since enzalutamide is innovated and approved by US FDA as a new treatment option for mCRPC patients, drug resistance for enzalutamide is a critical issue during clinical usage. Although several underlying mechanisms causing enzalutamide resistance were previously identified, most of them revealed that drug resistant cells are still highly addicted to androgen and AR functions. Due to the numerous physical functions of AR in men, innovated AR-independent therapy might alleviate enzalutamide resistance and prevent production of adverse side effects. Here, we have identified that yes-associated protein 1 (YAP1) is overexpressed in enzalutamide-resistant (EnzaR) cells. Furthermore, enzalutamide-induced YAP1 expression is mediated through the function of chicken ovalbumin upstream promoter transcription factor 2 (COUP-TFII) at the transcriptional and the post-transcriptional levels. Functional analyses reveal that YAP1 positively regulates numerous genes related to cancer stemness and lipid metabolism and interacts with COUP-TFII to form a transcriptional complex. More importantly, YAP1 inhibitor attenuates the growth and cancer stemness of EnzaR cells in vitro and in vivo. Finally, YAP1, COUP-TFII, and miR-21 are detected in the extracellular vesicles (EVs) isolated from EnzaR cells and sera of patients. In addition, treatment with EnzaR-EVs induces the abilities of cancer stemness, lipid metabolism and enzalutamide resistance in its parental cells. Taken together, these results suggest that YAP1 might be a crucial factor involved in the development of enzalutamide resistance and can be an alternative therapeutic target in prostate cancer.

scholarly journals Placental 13C-DHA metabolism and relationship with maternal BMI, glycemia and birthweight

2021 ◽  
Vol 27 (1) ◽  
Author(s):  
Oliver C. Watkins ◽  
Preben Selvam ◽  
Reshma Appukuttan Pillai ◽  
Victoria K. B. Cracknell-Hazra ◽  
Hannah E. J. Yong ◽  
...  
Keyword(s):  
Mass Spectrometry ◽  
Liquid Chromatography ◽  
Lipid Metabolism ◽  
Metabolic Pathways ◽  
Liquid Chromatography Mass Spectrometry ◽  
Fasting Glycemia ◽  
Glucose Treatment ◽  
Maternal Bmi

Abstract Background Fetal docosahexaenoic acid (DHA) supply relies on preferential transplacental transfer, which is regulated by placental DHA lipid metabolism. Maternal hyperglycemia and obesity associate with higher birthweight and fetal DHA insufficiency but the role of placental DHA metabolism is unclear. Methods Explants from 17 term placenta were incubated with 13C-labeled DHA for 48 h, at 5 or 10 mmol/L glucose treatment, and the production of 17 individual newly synthesized 13C-DHA labeled lipids quantified by liquid chromatography mass spectrometry. Results Maternal BMI positively associated with 13C-DHA-labeled diacylglycerols, triacylglycerols, lysophospholipids, phosphatidylcholine and phosphatidylethanolamine plasmalogens, while maternal fasting glycemia positively associated with five 13C-DHA triacylglycerols. In turn, 13C-DHA-labeled phospholipids and triacylglycerols positively associated with birthweight centile. In-vitro glucose treatment increased most 13C-DHA-lipids, but decreased 13C-DHA phosphatidylethanolamine plasmalogens. However, with increasing maternal BMI, the magnitude of the glucose treatment induced increase in 13C-DHA phosphatidylcholine and 13C-DHA lysophospholipids was curtailed, with further decline in 13C-DHA phosphatidylethanolamine plasmalogens. Conversely, with increasing birthweight centile glucose treatment induced increases in 13C-DHA triacylglycerols were exaggerated, while glucose treatment induced decreases in 13C-DHA phosphatidylethanolamine plasmalogens were diminished. Conclusions Maternal BMI and glycemia increased the production of different placental DHA lipids implying impact on different metabolic pathways. Glucose-induced elevation in placental DHA metabolism is moderated with higher maternal BMI. In turn, findings of associations between many DHA lipids with birthweight suggest that BMI and glycemia promote fetal growth partly through changes in placental DHA metabolism.

scholarly journals Identification of the molecular regulation of differences in lipid deposition in dedifferentiated preadipocytes from different chicken tissues

BMC Genomics ◽  
2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Zheng Ma ◽  
Na Luo ◽  
Lu Liu ◽  
Huanxian Cui ◽  
Jing Li ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Lipid Metabolism ◽  
Lipid Content ◽  
Regulatory Network ◽  
Total Lipid Content ◽  
Fatty Acid Transport ◽  
Lipid Deposition ◽  
Ppar Signaling ◽  
The Difference

Abstract Background A body distribution with high intramuscular fat and low abdominal fat is the ideal goal for broiler breeding. Preadipocytes with different origins have differences in terms of metabolism and gene expression. The transcriptome analysis performed in this study of intramuscular preadipocytes (DIMFPs) and adipose tissue-derived preadipocytes (DAFPs) aimed to explore the characteristics of lipid deposition in different chicken preadipocytes by dedifferentiation in vitro. Results Compared with DAFPs, the total lipid content in DIMFPs was reduced (P < 0.05). Moreover, 72 DEGs related to lipid metabolism were screened, which were involved in adipocyte differentiation, fatty acid transport and fatty acid synthesis, lipid stabilization, and lipolysis. Among the 72 DEGs, 19 DEGs were enriched in the PPAR signaling pathway, indicating its main contribution to the regulation of the difference in lipid deposition between DAFPs and DIMFPs. Among these 19 genes, the representative APOA1, ADIPOQ, FABP3, FABP4, FABP7, HMGCS2, LPL and RXRG genes were downregulated, but the ACSL1, FABP5, PCK2, PDPK1, PPARG, SCD, SCD5, and SLC27A6 genes were upregulated (P < 0.05 or P < 0.01) in the DIMFPs. In addition, the well-known pathways affecting lipid metabolism (MAPK, TGF-beta and calcium) and the pathways related to cell communication were enriched, which may also contribute to the regulation of lipid deposition. Finally, the regulatory network for the difference in lipid deposition between chicken DAFPs and DIMFPs was proposed based on the above information. Conclusions Our data suggested a difference in lipid deposition between DIMFPs and DAFPs of chickens in vitro and proposed a molecular regulatory network for the difference in lipid deposition between chicken DAFPs and DIMFPs. The lipid content was significantly increased in DAFPs by the direct mediation of PPAR signaling pathways. These findings provide new insights into the regulation of tissue-specific fat deposition and the optimization of body fat distribution in broilers.

scholarly journals Isolation of lactic acid bacteria from swine milk and characterization of potential probiotic strains with antagonistic effects against swine-associated gastrointestinal pathogens

2016 ◽  
Vol 62 (6) ◽  
pp. 514-524 ◽  
Author(s):  
Sandra Rayén Quilodrán-Vega ◽  
Julio Villena ◽  
José Valdebenito ◽  
María José Salas ◽  
Cristian Parra ◽  
...  
Keyword(s):  
Lactic Acid ◽  
Lactic Acid Bacteria ◽  
Human Milk ◽  
Salmonella Enterica ◽  
Enterohemorrhagic Escherichia Coli ◽  
Salmonella Infection ◽  
Antagonistic Effects ◽  
Gastrointestinal Pathogens

Probiotics are usually isolated from the gastrointestinal tract of humans and animals. The search of probiotics in human milk is a recent field of research, as the existence of the human milk microbiome was discovered only about a decade ago. To our knowledge, no reports regarding the potential probiotic effect of bacteria from swine milk have been published. In this work, we isolated several lactic acid bacteria from swine milk and evaluated them for them potential as probiotics. Among the isolated strains, Lactobacillus curvatus TUCO-5E showed antagonistic effects against swine-associated gastrointestinal pathogens. TUCO-5E was able to reduce the growth of enterotoxigenic and enterohemorrhagic Escherichia coli strains as well as pathogenic salmonella. In vitro exclusion and displacement assays in intestinal epithelial cells showed a remarkable antagonistic effect for L. curvatus TUCO-5E against Salmonella sp. strain TUCO-I7 and Salmonella enterica ATCC 13096. Moreover, by using a mouse model of Salmonella infection, we were able to demonstrate that preventative administration of L. curvatus TUCO-5E for 5 consecutive days was capable of decreasing the number of Salmonella enterica serovar Typhimurium in the liver and spleen of treated mice, compared with the controls, and prevented dissemination of the pathogen to the blood stream. Therefore, we have demonstrated here that swine milk is an interesting source of beneficial bacteria. In addition, the results of this work suggest that L. curvatus TUCO-5E is a good candidate to study in vivo the protective effect of probiotics against intestinal infection and damage induced by Salmonella infection in the porcine host.

scholarly journals Human milk glycosaminoglycans inhibit in vitro the adhesion of Escherichia coli and Salmonella fyris to human intestinal cells

2015 ◽  
Vol 79 (4) ◽  
pp. 603-607 ◽  
Author(s):  
Giovanni V. Coppa ◽  
Bruna Facinelli ◽  
Gloria Magi ◽  
Emanuela Marini ◽  
Lucia Zampini ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Human Milk ◽  
Intestinal Cells ◽  
Human Intestinal Cells

Knockdown of PGM1 Synergistically Enhances Anticancer Effects of Orlistat in Gastric Cancer Under Glucose Deprivation

2021 ◽  
Author(s):  
Bo Cao ◽  
Huan Deng ◽  
Hao Cui ◽  
Ruiyang Zhao ◽  
Hanghang Li ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Proliferation ◽  
Lipid Metabolism ◽  
Fatty Acid Synthase ◽  
Enrichment Analysis ◽  
Glucose Deprivation ◽  
Metabolic Reprogramming ◽  
The Cancer Genome Atlas

Abstract Background Phosphoglucomutase 1 (PGM1) acts as an important regulator in glucose metabolism. However, the role of PGM1 in gastric cancer (GC) remains unclear. This study aims to investigate the role of PGM1 and develop novel regimens based on metabolic reprogramming in GC. MethodsCorrelation and enrichment analysis of PGM1 was conducted based on The Cancer Genome Atlas database. Data derived from the Kaplan-Meier Plotter database were analyzed for correlations between PGM1 expression and survival time of GC patients. CCK-8, EdU, flow cytometry assays, generation of subcutaneous tumor and lung metastasis mouse models were used to determine growth and metastasis in vitro and in vivo. Cell glycolysis was detected by a battery of glycolytic indicators, including lactate, pyruvic acid, ATP production and glucose uptake. Fatty Acid Synthase (FASN) activity and detection of lipid regulators levels by western blot were used to reflect on the cell lipid metabolism. ResultsCorrelation and enrichment analysis suggested that PGM1 was closely associated with cell proliferation and metabolism. PGM1 was overexpressed in GC tissues and cell lines. High PGM1 expression served as an indicator of shorter survival for specific subpopulation of GC patients, which was also correlated with some clinicopathological features, including T stage and TNM stage. Under low glucose conditions, knockdown of PGM1 significantly suppressed cell proliferation and glycolysis levels, whereas lipid metabolism was enhanced. Orlistat, as a drug that was designed to inhibit FASN activity for obesity treatment, effectively induced apoptosis, suppressed FASN activity. However, orlistat conversely increased glycolytic levels in GC cells. Orlistat exhibited more significant inhibitive effects on GC progression after knockdown of PGM1 under glucose deprivation due to combination of glycolysis and lipid metabolism. ConclusionsDownregulation of PGM1 expression under glucose deprivation synergistically enhanced anti-cancer effects of orlistat. This combination application may serve as a novel strategy for GC treatment.

Abstract 121: Pro-inflammatory Cytokine Ifng Modulates Hepatic Sortilin Expression and Lipid Metabolism.

2015 ◽  
Vol 35 (suppl_1) ◽  
Author(s):  
John Pirault ◽  
Konstantinos Polyzos ◽  
Daniel F Ketelhuth ◽  
Göran K Hansson
Keyword(s):  
Lipid Metabolism ◽  
Binding Sites ◽  
In Silico ◽  
In Silico Analysis ◽  
Lipid Uptake ◽  
Regulatory T Lymphocytes ◽  
Inflammatory Conditions ◽  
Ldl Particles ◽  
Inflammatory Milieu

Rationale: Hypercholesterolemia and immunity are two major risk factors for cardiovascular diseases (CVDs). Yet, we reported increased atherosclerosis upon depletion of regulatory T lymphocytes (Tregs). The effect was associated with increased hepatic inflammation and reduction of Sortilin expression and lipid uptake in the liver. Objective: To define how inflammatory milieu in the liver can modulate Sortilin and lipid metabolism. Methods: To reproduce the inflammatory milieu, hepatocytes (AML-12) were treated in vitro with IFNg. Expression of genes and proteins of interest were followed by qPCR and western blot. In silico method was used to find binding sites of signal transducer and activator of transcription (STAT1) on Sortilin, confirmed later by chromatin immune precipitation assays (Chip). Lipid uptake by hepatocytes was assessed via incubation of cells with radioactive lipoproteins. Results: Culture of AML-12 cells with IFNg induced the phosphorylation of STAT1 showing an active signaling pathway. In the same inflammatory conditions, Sort1 mRNA is decreased meanwhile its inhibitor (Atf3) expression is increased. Kinetic experiments revealed the reduction of Sortilin after 12 hours of culture, suggesting a post-transcriptional regulation of Sort1 by STAT1. In silico analysis revealed putative binding sites for STAT1 on Sortilin gene which was confirmed by chromatin immunoprecipitation assay (Chip). IFNg treated hepatocytes that were incubated with radioactive lipoproteins demonstrated a reduced uptake capacity of VLDL and LDL particles compared to control cultures. Conclusion: All together, these results suggest that inflammation through production of IFNg is able to directly modulate the lipid metabolism in hepatocytes by acting on Sortilin expression.

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