Trigonella foenum-graecum Seed Extract, 4-Hydroxyisoleucine, and Metformin Stimulate Proximal Insulin Signaling and Increase Expression of Glycogenic Enzymes and GLUT2 in HepG2 Cells

2016 ◽  
Vol 14 (2) ◽  
pp. 114-120 ◽  
Author(s):  
Nikita Naicker ◽  
Savania Nagiah ◽  
Alisa Phulukdaree ◽  
Anil Chuturgoon
Keyword(s):  
Insulin Signaling ◽  
Hepg2 Cells ◽  
Seed Extract ◽  
Trigonella Foenum Graecum

scholarly journals Trigonella foenum-graecum seed extract modulates expression of lipid metabolism- related genes in HepG2 cells

2019 ◽  
Vol 9 (6) ◽  
pp. 240 ◽  
Author(s):  
MohammadReza Hajizadeh ◽  
Maryam Mohammad-Sadeghipour ◽  
Mehdi Mahmoodi ◽  
SoudehKhanamani Falahati-pour ◽  
Alireza Khoshdel ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Hepg2 Cells ◽  
Seed Extract ◽  
Trigonella Foenum Graecum

Biogenic synthesis of silver nanoparticles using Trigonella foenum-graecum seed extract: Characterization, photocatalytic and antibacterial activities

2021 ◽  
Vol 323 ◽  
pp. 112670 ◽  
Author(s):  
Manal A. Awad ◽  
Awatif A. Hendi ◽  
Khalid Mustafa Ortashi ◽  
Batool Alzahrani ◽  
Dina Soliman ◽  
...  
Keyword(s):  
Silver Nanoparticles ◽  
Antibacterial Activities ◽  
Seed Extract ◽  
Biogenic Synthesis ◽  
Trigonella Foenum Graecum

scholarly journals In vitro antioxidant effects of Trigonella foenum graecum (L.) Fenugreek seed extract on sheep red blood cells

2012 ◽  
Vol 6 (38) ◽  
pp. 5119-5127 ◽  
Author(s):  
Dinakaran Vasudevan ◽  
Sridharan Subhashree ◽  
Periyasamy Latha ◽  
Sudha Rani Sankaramoorthy
Keyword(s):  
Red Blood Cells ◽  
Blood Cells ◽  
Seed Extract ◽  
Trigonella Foenum Graecum ◽  
Fenugreek Seed ◽  
Sheep Red Blood Cells ◽  
Trigonella Foenum Graecum L ◽  
Antioxidant Effects

Morin Exerts Anti-Diabetic Effects in Human HepG2 Cells Via Down-Regulation of miR-29a

2018 ◽  
Vol 127 (09) ◽  
pp. 615-622 ◽  
Author(s):  
Toktam Razavi ◽  
Shideh Montasser Kouhsari ◽  
Khalil Abnous
Keyword(s):  
Insulin Signaling ◽  
High Glucose ◽  
Hepg2 Cells ◽  
Target Genes ◽  
Expression Level ◽  
Inhibitory Effects ◽  
Down Regulation ◽  
Insulin Mimetic ◽  
Important Regulator ◽  
First Time

Abstract Diabetes mellitus is a complex metabolic disease around the world that is characterized by hyperglycemia resulting from impaired insulin secretion, insulin action, or both. MicroRNA-29a is an important regulator of insulin signaling and gluconeogenesis pathways through IRS2, PI3K and PEPCK expressions which up regulates in Diabetes. Morin is a substantial bioflavonoid which has insulin mimetic effect, and interacting with nucleic acids and proteins. In this study HepG2 cells, were exposed to high glucose to induce diabetic condition. We have determined whether high glucose stimulation might promotes miR-29a expression level in HepG2 cells and subsequently evaluated the Morin treatment effects on this state. In HepG2 cells, high glucose increases miR-29a expression level and decreases its target genes, IRS2 and PI3K expression, and increases associated downstream gene in gluconeogenic pathway, PEPCK. Morin treatment down regulates miR-29a expression level and improves insulin signaling and glucose metabolism. To confirm the inhibitory effects of Morin on miR-29a, we have transfected cells with mimic and inhibitor-miR-29a. This study for the first time identifies that Morin improves diabetic condition through down regulation of the miR-29a level, and suggest that this new inhibitor of miR-29a may be a useful biomedicine to treat diabetes.

scholarly journals Efficacy of Trigonella foenum-graecum Seed Extract in Reducing Metabolic and Inflammatory Alterations Associated With Menopause

2015 ◽  
Vol 17 (11) ◽  
Author(s):  
Mahmood Abedinzade ◽  
Sima Nasri ◽  
Masome Jamal Omodi ◽  
Elham Ghasemi ◽  
Ahmad Ghorbani
Keyword(s):  
Seed Extract ◽  
Trigonella Foenum Graecum

Abstract 628: Hepatic Insulin Signaling Regulates ApoA-I Gene Expression Through the Type I Deiodinase.

2014 ◽  
Vol 34 (suppl_1) ◽  
Author(s):  
Jing Liu ◽  
Antonio Hernandez-Ono ◽  
Valerie Galton ◽  
Henry Ginsberg
Keyword(s):  
Insulin Signaling ◽  
Knockout Mice ◽  
Hepg2 Cells ◽  
Density Lipoprotein ◽  
Type I ◽  
Mrna Levels ◽  
Reverse T3 ◽  
Hepatic Insulin Signaling ◽  
Low Levels

People with low levels of high density lipoprotein cholesterol (HDLC) and apolipoprotein A-I (ApoA-I) have a higher risk of cardiovascular disease. Low levels of HDLC are common in individuals who are insulin resistant (IR), e.g., with metabolic syndrome and type 2 diabetes mellitus (T2DM). Despite the high prevalence of these two disorders, very little work has been reported regarding the molecular pathways linking insulin signaling or action and the levels of either HDLC or ApoA-1. We reported previously that liver specific insulin receptor (InsR) knockout mice (LIRKO) have markedly reduced plasma HDLC levels that increase after restoration of hepatic Akt signaling. In the present study, we created acute LIRKO mice by injecting an albumin-Cre adenovirus (Ad) into InsR floxed mice and observed marked reductions in HDLC, the expression of ApoA-I, and the expression of the gene coding Type1 iodothyronine deiodinase1, a selenoenzyme expressed highly in the liver that converts thyroxine to 3,5,3’-triiodothyronine (T3) or reverse T3. Deiodinase 1 knockout mice also had significantly reduced hepatic ApoA-I mRNA levels. Overexpression of Dio1 in LIRKO restored HDLC and significantly increased the expression of ApoA-I mRNA. In vitro studies showed that the expression of ApoA-I was significantly reduced after knockdown of either InsR or Dio1 expression in HepG2 cells. Moreover, overexpression of Dio1 restored ApoA-I promoter activity that had been decreased by knockdown of InsR. Deletion analysis of ApoAI promoter regions showed that insulin signaling regulated ApoA-I expression by acting on a region which does not contain any thyroid response elements. Pulse-chase experiments in HepG2 cells showed that deficiency of insulin signaling resulted in decreased synthesis and secretion of ApoAI. Our results indicates that defective hepatic insulin signaling results in reduced expression of Dio1 which, in turn, leads to reduced expression of ApoA-I and decreased synthesis and secretion of ApoA-I from hepatocytes. We believe our studies have defined a novel pathway from insulin signaling to ApoA-I synthesis that may lead to new approaches for increasing HDL levels in people with defective insulin signaling.

scholarly journals Visfatin Induces Inflammation and Insulin Resistance via the NF-κB and STAT3 Signaling Pathways in Hepatocytes

2019 ◽  
Vol 2019 ◽  
pp. 1-11 ◽  
Author(s):  
Yu Jung Heo ◽  
Sung-E Choi ◽  
Ja Young Jeon ◽  
Seung Jin Han ◽  
Dae Jung Kim ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Signaling Pathways ◽  
Western Blotting ◽  
Insulin Signaling ◽  
Proinflammatory Cytokine ◽  
Hepg2 Cells ◽  
Molecular Mechanisms ◽  
Immunocytochemical Staining ◽  
Mrna Levels ◽  
Rt Pcr

Background. It has been suggested that visfatin, which is an adipocytokine, exhibits proinflammatory properties and is associated with insulin resistance. Insulin resistance and inflammation are the principal pathogeneses of nonalcoholic fatty liver disease (NAFLD), but the relationship, if any, between visfatin and NAFLD remains unclear. Here, we evaluated the effects of visfatin on hepatic inflammation and insulin resistance in HepG2 cells and examined the molecular mechanisms involved. Methods. After treatment with visfatin, the inflammatory cytokines IL-6, TNF-α, and IL-1β were assessed by real-time polymerase chain reaction (RT-PCR) and immunocytochemical staining in HepG2 cells. To investigate the effects of visfatin on insulin resistance, we evaluated insulin-signaling pathways, such as IR, IRS-1, GSK, and AKT using immunoblotting. We assessed the intracellular signaling molecules including STAT3, NF-κB, IKK, p38, JNK, and ERK by western blotting. We treated HepG2 cells with both visfatin and either AG490 (a JAK2 inhibitor) or Bay 7082 (an NF-κB inhibitor); we examined proinflammatory cytokine mRNA levels using RT-PCR and insulin signaling using western blotting. Results. In HepG2 cells, visfatin significantly increased the levels of proinflammatory cytokines, reduced the levels of proteins (e.g., phospho-IR, phospho-IRS-1 (Tyr612), phospho-AKT, and phospho-GSK-3α/β) involved in insulin signaling, and increased IRS-1 S307 phosphorylation compared to controls. Interestingly, visfatin increased the activities of the JAK2/STAT3 and IKK/NF-κB signaling pathways but not those of the JNK, p38, and ERK pathways. Visfatin-induced inflammation and insulin resistance were regulated by JAK2/STAT3 and IKK/NF-κB signaling; together with AG490 or Bay 7082, visfatin significantly reduced mRNA levels of IL-6, TNF-α and IL-1β and rescued insulin signaling. Conclusion. Visfatin induced proinflammatory cytokine production and inhibited insulin signaling via the STAT3 and NF-κB pathways in HepG2 cells.

scholarly journals Antibacterial, anticancer and antioxidant potential of silver nanoparticles engineered using Trigonella foenum‐graecum seed extract

2018 ◽  
Vol 12 (4) ◽  
pp. 526-533 ◽  
Author(s):  
Shivangi Goyal ◽  
Nidhi Gupta ◽  
Ajeet Kumar ◽  
Sreemoyee Chatterjee ◽  
Surendra Nimesh
Keyword(s):  
Silver Nanoparticles ◽  
Seed Extract ◽  
Antioxidant Potential ◽  
Trigonella Foenum Graecum
Sign in / Sign up

Export Citation Format

Share Document