scholarly journals Dietary Trivalent Chromium Exposure Up-Regulates Lipid Metabolism in Coral Trout: The Evidence From Transcriptome Analysis

2021 ◽  
Vol 12 ◽  
Author(s):  
Lu Wei ◽  
Yu Li ◽  
Hengzhen Ye ◽  
Juan Xiao ◽  
Christer Hogstrand ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Essential Element ◽  
Trivalent Chromium ◽  
Functional Enrichment ◽  
Chromium Picolinate ◽  
High Dose ◽  
Potential Toxicity ◽  
Steroid Biosynthesis ◽  
Qrt Pcr ◽  
Coral Trout

Diet quality greatly affects an animal’s performance and metabolism. Despite the fact that trivalent chromium [Cr(III)] is considered an essential element and is widely used in nutritional supplements for animals and humans, the potential toxicity of Cr(III) is unclear. Here, liver transcriptome sequencing was performed on coral trout (Plectropomus leopardus) exposed to 200 mg kg–1 of dietary organic Cr(III) [as chromium picolinate (CrPic)] for 8 weeks. One-hundred-and thirteen differentially expressed genes (DEGs) were identified in response to Cr(III) stress, in comparison to the control, including 31 up-regulated and 82 down-regulated DEGs. Clusters of Orthologous Groups of proteins (COG) classifies DEGs into 15 functional categories, with the predominant category being related to lipid transport and metabolism (9.73%). The Kyoto Encyclopedia of Genes and Genomes (KEGG) assigned DEGs to six major categories with robust DEGs as part of the lipid metabolism pathway (18.58%). Moreover, KEGG functional enrichment analysis showed that these DEGs are primarily related to steroid biosynthesis, terpenoid backbone biosynthesis, and steroid hormone biosynthesis pathways, of which steroid biosynthesis was the most significant pathway, and 12 key up-regulated DEGs (dhcr7, dhcr24, ebp, lss, msmo1, sqle, cyp51, tm7sf2, sc5dl, fdft1, nsdhl, and hsd17b7) were found for steroid biosynthesis pathways. To validate the RNA sequencing data using quantitative real-time PCR (qRT-PCR), qRT-PCR results indicate that the expression of genes encoding HMGCR, TM7SF2, TRYP2, CTRL, EBP, LSS, and CYP51 were induced, while those encoding THRSP, LCE, and MCM5 were reduced, consistent with RNA-seq results. This findings provides the first evidence that a long-term high dose of Cr(III) intake causes lipid metabolism disorder and potential toxicity in fish. Cautious health risk assessment of dietary Cr(III) intake is therefore highly recommended for the commercial and/or natural diets of aquatic animals, which has previously largely been ignored.

scholarly journals High-dose Glycerol Monolaurate Up-Regulated Beneficial Indigenous Microbiota without Inducing Metabolic Dysfunction and Systemic Inflammation: New Insights into Its Antimicrobial Potential

Nutrients ◽  
2019 ◽  
Vol 11 (9) ◽  
pp. 1981 ◽  
Author(s):  
Qiufen Mo ◽  
Aikun Fu ◽  
Lingli Deng ◽  
Minjie Zhao ◽  
Yang Li ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Systemic Inflammation ◽  
Body Weight Gain ◽  
High Dose ◽  
Dependent Manner ◽  
Glucose And Lipid Metabolism ◽  
Glycerol Monolaurate ◽  
Indigenous Microbiota ◽  
Anti Inflammatory ◽  
Dose Dependent

Glycerol monolaurate (GML) has potent antimicrobial and anti-inflammatory activities. The present study aimed to assess the dose-dependent antimicrobial-effects of GML on the gut microbiota, glucose and lipid metabolism and inflammatory response in C57BL/6 mice. Mice were fed on diets supplemented with GML at dose of 400, 800 and 1600 mg kg−1 for 4 months, respectively. Results showed that supplementation of GML, regardless of the dosages, induced modest body weight gain without affecting epididymal/brown fat pad, lipid profiles and glycemic markers. A high dose of GML (1600 mg kg−1) showed positive impacts on the anti-inflammatory TGF-β1 and IL-22. GML modulated the indigenous microbiota in a dose-dependent manner. It was found that 400 and 800 mg kg−1 GML improved the richness of Barnesiella, whereas a high dosage of GML (1600 mg kg−1) significantly increased the relative abundances of Clostridium XIVa, Oscillibacter and Parasutterella. The present work indicated that GML could upregulate the favorable microbial taxa without inducing systemic inflammation and dysfunction of glucose and lipid metabolism.

Abstract 11983: Auraptene, a Coumaric Compounds Analogous, Improved the Worsening of Systolic Function by Activating Mitochondrial Function After Myocardial Infarction in Rats

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Yoichi Sunagawa ◽  
Miho Suzuki ◽  
Masafumi Funamoto ◽  
Yasufumi Katanasaka ◽  
Hidetoshi Suzuki ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Heart Failure ◽  
Lipid Metabolism ◽  
Mitochondrial Function ◽  
Low Dose ◽  
Systolic Function ◽  
Pharmacological Therapy ◽  
Vehicle Group ◽  
High Dose ◽  
Related Gene

Introduction: Heart failure is associated with pathological growth and mitochondrial dysfunction of constituent cardiomyocytes. To achieve effective oral pharmacological therapy for heart failure, we screened compounds isolated from natural products and found that auraptene derived from the peel of Citrus Hassaku may be applicable to pharmacological therapy for heart failure. Hypothesis: We assessed the hypothesis that auraptene could improve the deterioration of mitochondrial function and the development of heart failure in rats with myocardial infarction (MI). Methods and Results: In cultured cardiomyocytes, auraptene (2.5-10 μM) dose-dependently repressed phenylephrine-induced hypertrophic responses such as increase in cell size and ANF and ET-1 promoter activations. Auraptene also activated mitochondrial- and lipid metabolism-related gene transcriptions, such as PGC1α, PPARα/γ, mCPT1, UCP3, and PDK4. One week after operation, 22 rats with a moderate size of MI (Fractional shortening (FS) < 40%) were then randomly assigned to vehicle (n=8), auraptene low-dose (5 mg/kg/day, n=7), or high-dose (50 mg/kg/day, n=7). Oral daily treatments with these agents were continued for 6 weeks. There were no differences in left ventricle (LV) geometric and functional data among the 3 MI groups before treatment. After treatment, LVFS was significantly higher in the auraptene low-dose (21%, p < 0.0001) and high-dose (26%, p < 0.0001) groups than the vehicle group (16%). LV wall thickness in the remote non-infarct area was significantly thinner in the auraptene low-dose (1.4 mm, p < 0.01) and high-dose (1.2 mm, p < 0.0001) groups than the vehicle group (2.5 mm). Histological analysis demonstrated that auraptene treatment significantly suppressed MI-induced increases in myocardial cell diameter and perivascular fibrosis compared with vehicle treatment. Moreover, auraptene also prevented the activations of ANF and MCP-1 mRNA levels and up-regulated mitochondrial- and lipid metabolism-related gene transcriptions in LV. Conclusions: Auraptene treatment prevents the worsening of LV systolic function and represses hypertrophy after MI in adult rats. A natural compound, auraptene is expected as a novel useful agent for heart failure therapy in humans.

scholarly journals Integrative Identification of Hub Genes Associated With Immune Cells in Atrial Fibrillation Using Weighted Gene Correlation Network Analysis

2021 ◽  
Vol 7 ◽  
Author(s):  
Tao Yan ◽  
Shijie Zhu ◽  
Miao Zhu ◽  
Chunsheng Wang ◽  
Changfa Guo
Keyword(s):  
Atrial Fibrillation ◽  
Network Analysis ◽  
Molecular Mechanism ◽  
Immune Cells ◽  
Bioinformatics Analysis ◽  
Functional Enrichment ◽  
Correlation Network ◽  
Hub Genes ◽  
Qrt Pcr ◽  
Gene Correlation

Background: Atrial fibrillation (AF) is the most common tachyarrhythmia in the clinic, leading to high morbidity and mortality. Although many studies on AF have been conducted, the molecular mechanism of AF has not been fully elucidated. This study was designed to explore the molecular mechanism of AF using integrative bioinformatics analysis and provide new insights into the pathophysiology of AF.Methods: The GSE115574 dataset was downloaded, and Cibersort was applied to estimate the relative expression of 22 kinds of immune cells. Differentially expressed genes (DEGs) were identified through the limma package in R language. Weighted gene correlation network analysis (WGCNA) was performed to cluster DEGs into different modules and explore relationships between modules and immune cell types. Functional enrichment analysis was performed on DEGs in the significant module, and hub genes were identified based on the protein-protein interaction (PPI) network. Hub genes were then verified using quantitative real-time polymerase chain reaction (qRT-PCR).Results: A total of 2,350 DEGs were identified and clustered into eleven modules using WGCNA. The magenta module with 246 genes was identified as the key module associated with M1 macrophages with the highest correlation coefficient. Three hub genes (CTSS, CSF2RB, and NCF2) were identified. The results verified using three other datasets and qRT-PCR demonstrated that the expression levels of these three genes in patients with AF were significantly higher than those in patients with SR, which were consistent with the bioinformatic analysis.Conclusion: Three novel genes identified using comprehensive bioinformatics analysis may play crucial roles in the pathophysiological mechanism in AF, which provide potential therapeutic targets and new insights into the treatment and early detection of AF.

scholarly journals The key role of a glucagon-like peptide-1 receptor agonist in body fat redistribution

2019 ◽  
Vol 240 (2) ◽  
pp. 271-286 ◽  
Author(s):  
Li Zhao ◽  
Chunfang Zhu ◽  
Meng Lu ◽  
Chi Chen ◽  
Xiaomin Nie ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Body Fat ◽  
Visceral Fat ◽  
Subcutaneous Fat ◽  
Control Group ◽  
Acid Oxidation ◽  
High Dose ◽  
Fat Depots ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1

Glucagon-like peptide-1 receptor agonists (GLP-1RAs) are an ideal therapy for type 2 diabetes and, as of recently, for obesity. In contrast to visceral fat, subcutaneous fat appears to be protective against metabolic diseases. Here, we aimed to explore whether liraglutide, a GLP-1RA, could redistribute body fat via regulating lipid metabolism in different fat depots. After being fed a high-fat diet for 8 weeks, 50 male Wistar and Goto-Kakizaki rats were randomly divided into a normal control group, a diabetic control group, low- and high-dose liraglutide-treated groups and a diet-control group. Different doses of liraglutide (400 μg/kg/day or 1200 μg/kg/day) or an equal volume of normal saline were administered to the rats subcutaneously once a day for 12 weeks. Body composition and body fat deposition were measured by dual-energy X-ray absorptiometry and MRI. Isotope tracers were infused to explore lipid metabolism in different fat depots. Quantitative real-time PCR and Western blot analyses were conducted to evaluate the expression of adipose-related genes. The results showed that liraglutide decreased visceral fat and relatively increased subcutaneous fat. Lipogenesis was reduced in visceral white adipose tissue (WAT) but was elevated in subcutaneous WAT. Lipolysis was also attenuated, and fatty acid oxidation was enhanced. The mRNA expression levels of adipose-related genes in different tissues displayed similar trends after liraglutide treatment. In addition, the expression of browning-related genes was upregulated in subcutaneous WAT. Taken together, the results suggested that liraglutide potentially redistributes body fat and promotes browning remodeling in subcutaneous WAT to improve metabolic disorders.

scholarly journals Acetyl-CoA Synthetase 2 Promotes Cell Migration and Invasion of Renal Cell Carcinoma by Upregulating Lysosomal-Associated Membrane Protein 1 Expression

2018 ◽  
Vol 45 (3) ◽  
pp. 984-992 ◽  
Author(s):  
Lv Yao ◽  
Xiaoqiang Guo ◽  
Yaoting Gui
Keyword(s):  
Cell Proliferation ◽  
Cell Migration ◽  
Lipid Metabolism ◽  
Western Blotting ◽  
Renal Cell ◽  
Migration And Invasion ◽  
Cancer Tissue ◽  
Acetyl Coa ◽  
Cell Migration And Invasion ◽  
Qrt Pcr

Background/Aims: Reprogramming energy metabolism is an emerging hallmark of many cancers, and this alteration is especially evident in renal cell carcinomas (RCCs). However, few studies have been conducted on lipid metabolism. This study investigated the function and mechanism of lipid metabolism-related acetyl-CoA synthetase 2 (ACSS2) in RCC development, cell migration and invasion. Methods: Quantitative real-time PCR (qRT-PCR) was used to determine the expression of ACSS2 in cancer tissue and adjacent tissue. The inhibition of ACSS2 expression was achieved by RNA interference, which was confirmed by qRT-PCR and Western blotting. Cell proliferation and apoptosis were detected by a CCK8 assay and a flow cytometry analysis, respectively. Cell migration and invasion were determined by the scratch and transwell assays. Following the knockdown of ACSS2 expression, the expression of the autophagy-related factor LAMP1 was measured by qRT-PCR and Western blotting. Results: Compared to adjacent tissues, ACSS2 expression was upregulated in RCC cancer tissues and positively correlated with metastasis. Inhibition of ACSS2 had no effect on RCC cell proliferation or apoptosis. However, decreased ACSS2 expression was found to inhibit RCC cell migration and invasion. ACSS2 was determined to promote the expression of LAMP1, which can also promote cell migration. This pathway may be considered a potential mechanism through which ACSS2 participates in RCC development. Conclusion: These data suggest that ACSS2 is an important factor for promoting RCC development and is essential for cell migration and invasion, which it promotes by increasing the expression of LAMP1. Taken together, these findings reveal a potential target for the diagnosis and treatment of RCC.

The conception of the probable role of the biological active chromium in the emergence of insulin resistance and alimentary obesity

2021 ◽  
Vol 1 (223) ◽  
pp. 34-38
Author(s):  
Bolat Abishev ◽  
Keyword(s):  
Insulin Resistance ◽  
Structural Organization ◽  
Redox State ◽  
Metabolic Response ◽  
Essential Element ◽  
Insulin Receptors ◽  
Trivalent Chromium ◽  
Manual Search ◽  
Alimentary Obesity ◽  
Search And Selection

The conception of probable alimentary chromium role in connection with metabolic reasons emergence of insulin resistance in the alimentary obesity and type 2 diabetes is represented. The violation of insulin receptors structural organization and conformation with these pathological conditions in connection with redox states of chromium is supposed. Based on information from general chemistry and chromium metabolism, higher biological activity of hexavalent chromium when compared to the activity of trivalent chromium is assumed in insulin-resistant conditions. Aim. To analyze the literature data on the a supposed participation of chromium in food and chromium nutraceuticals in connection with insulin resistance at the metabolic level. Material and methods. The analysis of the literature was carried out by the method of manual search and selection of the most important and significant for the analyzed issue monographs and articles up to 60 years in depth. The search criteria were works directly related to the association of food chromium with the insulin-dependent metabolic response of cells and the activity of insulin receptors. No works published over the past 10 years that introduce principled novelty and are of principled importance for the present problem have not been identified. Results and discussion. The concept of the supposed participation of chromium as an essential element in connection with the metabolic reasons for the formation of insulin resistance and the structural organization of insulin receptors depending on the redox state of chromium is presented. Keywords: hexavalent and trivalent chromium, insulin resistance, redox state, insulin receptor, alimentary obesity, diabetes.

scholarly journals Immunological pathways of macrophage response to Brucella ovis infection

2020 ◽  
Vol 26 (7) ◽  
pp. 635-648
Author(s):  
Zhixiong Zhou ◽  
Guojing Gu ◽  
Yichen Luo ◽  
Wenjie Li ◽  
Bowen Li ◽  
...  
Keyword(s):  
Immune Response ◽  
Molecular Mechanisms ◽  
Group Versus ◽  
Enrichment Analysis ◽  
Functional Enrichment Analysis ◽  
Functional Enrichment ◽  
Sequencing Data ◽  
Brucella Ovis ◽  
Qrt Pcr ◽  
Raw264.7 Macrophage

As the molecular mechanisms of Brucella ovis pathogenicity are not completely clear, we have applied a transcriptome approach to identify the differentially expressed genes (DEGs) in RAW264.7 macrophage infected with B. ovis. The DEGs related to immune pathway were identified by Kyoto Encyclopedia of Genes and Genomes (KEGG) and Gene Ontology (GO) functional enrichment analysis. Quantitative real-time PCR (qRT-PCR) was performed to validate the transcriptome sequencing data. In total, we identified 337 up-regulated and 264 down-regulated DEGs in B. ovis-infected group versus mock group. Top 20 pathways were enriched by KEGG analysis and 20 GO by functional enrichment analysis in DEGs involved in the molecular function, cellular component, and biological process and so on, which revealed multiple immunological pathways in RAW264.7 macrophage cells in response to B. ovis infection, including inflammatory response, immune system process, immune response, cytokine activity, chemotaxis, chemokine-mediated signaling pathway, chemokine activity, and CCR chemokine receptor binding. qRT-PCR results showed Ccl2 (ENSMUST00000000193), Ccl2 (ENSMUST00000124479), Ccl3 (ENSMUST00000001008), Hmox1 (ENSMUST00000005548), Hmox1 (ENSMUST00000159631), Cxcl2 (ENSMUST00000075433), Cxcl2 (ENSMUST00000200681), Cxcl2 (ENSMUST00000200919), and Cxcl2 (ENSMUST00000202317). Our findings firstly elucidate the pathways involved in B. ovis-induced host immune response, which may lay the foundation for revealing the bacteria–host interaction and demonstrating the pathogenic mechanism of B. ovis.

scholarly journals Regulation of microRNAs in high-fat diet induced hyperlipidemic hamsters

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Teodora Barbalata ◽  
◽  
Lu Zhang ◽  
Madalina D. Dulceanu ◽  
Camelia S. Stancu ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
High Fat Diet ◽  
Molecular Mechanisms ◽  
Bioinformatics Analysis ◽  
Discrete Distribution ◽  
Functional Enrichment ◽  
High Fat ◽  
Fat Cell ◽  
Specific Distribution ◽  
Different Tissues

AbstractDyslipidemia is a documented risk factor for cardiovascular diseases and other metabolic disorders. Therefore, the analysis of hyperlipidemia (HL)-related miRNAs is a potential approach for achieving new prognostic markers in lipid-metabolism related diseases. We aimed to analyze specific distribution of miRNAs in different tissues from HL animals. Golden Syrian hamsters were fed either regular chow (NL) or high-fat diet (HL) for 12 weeks. Microarray miRNAs profiling was performed in liver, heart and small intestine and data analyzed by R-studio software. Functional enrichment bioinformatics analysis was performed using miRWalk and DAVID tools. We observed a dysregulation of miRNAs in HL tissues evidencing a discrete distribution in the heart-liver axis and three lipid metabolism-related miRNAs were identified: hsa-miR-223-3p, hsa-miR-21-5p, and hsa-miR-146a-5p. Expression levels of these miRNAs were increased in HL livers and hearts. Functional bioinformatics analysis showed involvement of these miRNAs in the regulation of biological processes altered in HL conditions such as lipid metabolic process, fat cell differentiation, regulation of smooth muscle cells and cardiac septum development. We identified a set of miRNAs dysregulated in different tissues of HFD-induced HL hamsters. These findings motivate further studies aiming to investigate novel molecular mechanisms of lipid metabolism and atherogenic HL.

Effects of resistance training and chromium picolinate on body composition and skeletal muscle in older men

1999 ◽  
Vol 86 (1) ◽  
pp. 29-39 ◽  
Author(s):  
Wayne W. Campbell ◽  
Lyndon J. O. Joseph ◽  
Stephanie L. Davey ◽  
Deanna Cyr-Campbell ◽  
Richard A. Anderson ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Body Composition ◽  
Resistance Training ◽  
Muscle Power ◽  
Older Men ◽  
Muscle Size ◽  
Whole Body ◽  
Chromium Picolinate ◽  
High Dose ◽  
Repetition Maximum

The effects of chromium picolinate (CrPic) supplementation and resistance training (RT) on skeletal muscle size, strength, and power and whole body composition were examined in 18 men (age range 56–69 yr). The men were randomly assigned (double-blind) to groups ( n = 9) that consumed either 17.8 μmol Cr/day (924 μg Cr/day) as CrPic or a low-Cr placebo for 12 wk while participating twice weekly in a high-intensity RT program. CrPic increased urinary Cr excretion ∼50-fold ( P < 0.001). RT-induced increases in muscle strength ( P < 0.001) were not enhanced by CrPic. Arm-pull muscle power increased with RT at 20% ( P = 0.016) but not at 40, 60, or 80% of the one repetition maximum, independent of CrPic. Knee-extension muscle power increased with RT at 20, 40, and 60% ( P < 0.001) but not at 80% of one repetition maximum, and the placebo group gained more muscle power than did the CrPic group (RT by supplemental interaction, P < 0.05). Fat-free mass ( P < 0.001), whole body muscle mass ( P < 0.001), and vastus lateralis type II fiber area ( P < 0.05) increased with RT in these body-weight-stable men, independent of CrPic. In conclusion, high-dose CrPic supplementation did not enhance muscle size, strength, or power development or lean body mass accretion in older men during a RT program, which had significant, independent effects on these measurements.

scholarly journals Quercetin Improves Glucose and Lipid Metabolism of Diabetic Rats: Involvement of Akt Signaling and SIRT1

2017 ◽  
Vol 2017 ◽  
pp. 1-10 ◽  
Author(s):  
Jing Peng ◽  
Qingde Li ◽  
Keye Li ◽  
Li Zhu ◽  
Xiaoding Lin ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Lipid Metabolism ◽  
Fasting Blood Glucose ◽  
Akt Signaling ◽  
Hepatic Glycogen ◽  
High Dose ◽  
Lipid Metabolism Disorder ◽  
Metabolism Disorder ◽  
Glucose And Lipid Metabolism ◽  
Quercetin Treatment

Glucose and lipid metabolism disorder in diabetes mellitus often causes damage to multiple tissues and organs. Diabetes mellitus is beneficially affected by quercetin. However, its concrete mechanisms are yet to be fully elucidated. In our study, diabetes was induced in Sprague-Dawley rats by STZ injection. The rats were randomly divided into normal control, diabetic model, low-dose quercetin treatment, high-dose quercetin treatment, and pioglitazone treatment groups. Fasting blood glucose was collected to evaluate diabetes. Immunohistochemistry and fluorometric assay were performed to explore SIRT1. Akt levels were measured through immunoprecipitation and Western blot. After 12 weeks of quercetin treatment, the biochemical parameters of glucose and lipid metabolism improved to varying degrees. Hepatic histomorphological injury was alleviated, and hepatic glycogen content was increased. The expression and activity of hepatic SIRT1 were enhanced, and Akt was activated by phosphorylation and deacetylation. These results suggested that the beneficial effects of quercetin on glucose and lipid metabolism disorder are probably associated with the upregulated activity and protein level of SIRT1 and its influence on Akt signaling pathway. Hence, quercetin shows potential for the treatment of glucose and lipid metabolism disorder in diabetes mellitus.

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