Unsaponifiable Matter from Rice Bran Attenuates High Glucose-Induced Lipid Accumulation by Activating AMPK in HepG2 Cells

2016 ◽  
Vol 41 (2) ◽  
pp. e12313
Author(s):  
Hyeonmi Ham ◽  
Koan Sik Woo ◽  
Yu Young Lee ◽  
Byongwon Lee ◽  
In-Hwan Kim ◽  
...  
Keyword(s):  
Unsaponifiable Matter ◽  
Rice Bran ◽  
High Glucose ◽  
Lipid Accumulation ◽  
Hepg2 Cells

Houttuynia cordata Attenuates Lipid Accumulation via Activation of AMP-Activated Protein Kinase Signaling Pathway in HepG2 Cells

2014 ◽  
Vol 42 (03) ◽  
pp. 651-664 ◽  
Author(s):  
Hyun Kang ◽  
Sushruta Koppula
Keyword(s):  
Protein Kinase ◽  
High Glucose ◽  
Lipid Accumulation ◽  
Hepg2 Cells ◽  
Fatty Acid Synthase ◽  
Molecular Mechanisms ◽  
Regulatory Element ◽  
Adenosine Monophosphate ◽  
Perennial Herb ◽  
Houttuynia Cordata

Houttuynia cordata (H. cordata) from the family Saururaceae is a perennial herb native to Southeast Asia. It possesses a range of medicinal properties to treat several disease symptoms including allergic inflammation and anaphylaxis. In the present investigation, we provided the molecular mechanisms underlying the role of H. cordata extract (HCE) in the prevention of high glucose-induced lipid accumulation in human HepG2 hepatocytes. HepG2 cells were pre-treated with various concentrations of HCE (0, 10, 20, 40, and 80 μg/mL) and treated with serum-free medium with normal glucose (5 mM) for 1 h, followed by exposure to high glucose (25 mM D-glucose) for 24 h. HCE significantly and dose-dependently attenuated lipid accumulation in human HepG2 hepatocytes when exposed to high glucose (25 mM D-glucose) (p < 0.05, p < 0.01 and p < 0.001 at 20, 40, and 80 μg/mL concentrations, respectively). Further, HCE attenuated the expression of fatty acid synthase (FAS), sterol regulatory element-binding protein-1 and glycerol 3-phosphate acyltransferases (GPATs). The adenosine monophosphate-activated protein kinase (AMPK) was also activated by HCE treatment when exposed to high glucose (25 mM D-glucose) in human HepG2 hepatocytes. This study suggests the hypolipidemic effects of HCE by the inhibition of lipid biosynthesis mediated through AMPK signaling, which may play an active role and can be developed as an anti-obesity agent.

Rice bran protein hydrolysates prevented interleukin-6- and high glucose-induced insulin resistance in HepG2 cells

2015 ◽  
Vol 6 (2) ◽  
pp. 566-573 ◽  
Author(s):  
Kampeebhorn Boonloh ◽  
Upa Kukongviriyapan ◽  
Patchareewan Pannangpetch ◽  
Bunkerd Kongyingyoes ◽  
Laddawan Senggunprai ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Rice Bran ◽  
Interleukin 6 ◽  
High Glucose ◽  
Hepg2 Cells ◽  
Protein Hydrolysates ◽  
Rice Bran Protein

Rice bran protein hydrolysates prevent insulin resistance in HepG2 cells.

scholarly journals Nobiletin Inhibits Hepatic Lipogenesis via Activation of AMP-Activated Protein Kinase

2018 ◽  
Vol 2018 ◽  
pp. 1-8 ◽  
Author(s):  
Taewon Yuk ◽  
Younghwa Kim ◽  
Jinwoo Yang ◽  
Jeehye Sung ◽  
Heon Sang Jeong ◽  
...  
Keyword(s):  
Protein Kinase ◽  
High Glucose ◽  
Lipid Accumulation ◽  
Hepg2 Cells ◽  
Fatty Acid Synthase ◽  
Regulatory Element ◽  
Hepatic Lipogenesis ◽  
Nonalcoholic Fatty Liver ◽  
Compound C ◽  
Amp Activated Protein Kinase

We aimed to investigate the effects of nobiletin on hepatic lipogenesis in high glucose-induced lipid accumulation in HepG2 cells. Nobiletin, a citrus polymethoxyflavonoid with six methoxy groups, is present abundantly in the peels of citrus fruits. HepG2 cells were incubated in Dulbecco’s modified Eagle’s medium containing high glucose (25 mM) and subsequently treated with nobiletin at different concentrations (5, 25, and 50 μM). Results showed that nobiletin markedly inhibited high glucose-induced hepatic lipid accumulation in HepG2 cells. In addition, it reduced the protein expression of lipogenic factors, including sterol regulatory element-binding protein 1c (SREBP-1c) and fatty acid synthase (FAS). Nobiletin significantly increased the phosphorylation of AMP-activated protein kinase (AMPK) and acetyl-CoA carboxylase. Pretreatment with compound C, an AMPK inhibitor, abolished the inhibitory effects of nobiletin on SREBP-1c and FAS expression. These results suggested that nobiletin might attenuate high glucose-induced lipid accumulation in HepG2 hepatocytes via modulation of AMPK signaling pathway. Therefore, nobiletin might be useful for the prevention and treatment of nonalcoholic fatty liver diseases.

Role of salt inducible kinase 1 in high glucose-induced lipid accumulation in HepG2 cells and metformin intervention

Life Sciences ◽  
2017 ◽  
Vol 173 ◽  
pp. 107-115 ◽  
Author(s):  
Yue Zhang ◽  
Hiroshi Takemori ◽  
Chang Wang ◽  
JiaHui Fu ◽  
MingWang Xu ◽  
...  
Keyword(s):  
High Glucose ◽  
Lipid Accumulation ◽  
Hepg2 Cells

Anti-obesity Effect of Gold Nanoparticles from Dendropanax morbifera Léveille by Suppression of Triglyceride Synthesis and Downregulation of PPARγ and CEBPα Signaling Pathways in 3T3-L1 Mature Adipocytes and HepG2 Cells

2020 ◽  
Vol 16 (2) ◽  
pp. 196-203 ◽  
Author(s):  
Myoung Hi Yi ◽  
Shakina Yesmin Simu ◽  
Sungeun Ahn ◽  
Verónica Castro Aceituno ◽  
Chao Wang ◽  
...  
Keyword(s):  
Gold Nanoparticles ◽  
Fatty Liver ◽  
Lipid Accumulation ◽  
Hepg2 Cells ◽  
Cellular Level ◽  
Dendropanax Morbifera ◽  
Immunoblotting Assay ◽  
Triglyceride Content ◽  
20 Nm ◽  
Proliferation Assays

Background: Biosynthesis of gold nanoparticles from medicinal plants has become an interesting strategy in biomedical research due to its exclusive properties including less toxic cellular level through its ecofriendly biological function. Objective: To examine the anti-lipid accumulation effect of spherical gold nanoparticles (size 10-20 nm) synthesized from Dendropanax morbifera Léveille (D-AuNPs) in both 3T3-L1 and HepG2 cells. Method: 3T3-L1 preadipocytes and HepG2 hepatocytes were stimulated with cocktail media to generate obese and fatty liver disease models. Cell cytotoxicity and cell proliferation assays were performed in adipocytes at different stages of growth. An anti-lipid accumulation assay was performed in 3T3-L1 obese and HepG2 fatty liver models using different doses of D-AuNPs. Expression of adipogenic genes of PPARγ, CEBPα, Jak2, STAT3, and ap2 and hepatogenic genes PPARα, FAS, and ACC was measured by real-time PCR. In addition, protein expression of PPARγ and CEBPα was evaluated by immunoblotting assay. Result: We found that D-AuNPs (size 10–20 nm) at concentrations up to 100 µg/ml were nontoxic to 3T3-L1 and HepG2 at post-confluent and mature stages. In addition, pretreatment of D-AuNPs at post-confluent stage reduced triglyceride content. In addition, the adipogenesis process was negatively controlled by D-AuNPs, with downregulated PPARγ, CEBPα, Jak2, STAT3, and ap2 expression in 3T3-L1 cells and FAS and ACC levels in HepG2 cells. Conclusion: These data indicated that D-AuNPs exert antiadipogenic properties. We hypothesize that Dendropanax contains a large amount of phenolic compound that coats the surface of gold nanoparticles and has the ability to reduce the excess amount of lipid in both cell lines.

scholarly journals Aqueous Extract of Pepino Leaves Ameliorates Palmitic Acid-Induced Hepatocellular Lipotoxicity via Inhibition of Endoplasmic Reticulum Stress and Apoptosis

Antioxidants ◽  
2021 ◽  
Vol 10 (6) ◽  
pp. 903
Author(s):  
Jen-Ying Hsu ◽  
Hui-Hsuan Lin ◽  
Charng-Cherng Chyau ◽  
Zhi-Hong Wang ◽  
Jing-Hsien Chen
Keyword(s):  
Fatty Acid ◽  
Palmitic Acid ◽  
Er Stress ◽  
Lipid Accumulation ◽  
Hepg2 Cells ◽  
Target Genes ◽  
Liver Lipid ◽  
Antioxidant Response ◽  
Long Chain Fatty Acid ◽  
Nrf2 Expression

Saturated fatty acid is one of the important nutrients, but contributes to lipotoxicity in the liver, causing hepatic steatosis. Aqueous pepino leaf extract (AEPL) in the previous study revealed alleviated liver lipid accumulation in metabolic syndrome mice. The study aimed to investigate the mechanism of AEPL on saturated long-chain fatty acid-induced lipotoxicity in HepG2 cells. Moreover, the phytochemical composition of AEPL was identified in the present study. HepG2 cells treated with palmitic acid (PA) were used for exploring the effect of AEPL on lipid accumulation, apoptosis, ER stress, and antioxidant response. The chemical composition of AEPL was analyzed by HPLC-ESI-MS/MS. AEPL treatment reduced PA-induced ROS production and lipid accumulation. Further molecular results revealed that AEPL restored cytochrome c in mitochondria and decreased caspase 3 activity to cease apoptosis. In addition, AEPL in PA-stressed HepG2 cells significantly reduced the ER stress and suppressed SREBP-1 activation for decreasing lipogenesis. For defending PA-induced oxidative stress, AEPL promoted Nrf2 expression and its target genes, SOD1 and GPX3, expressions. The present study suggested that AEPL protected from PA-induced lipotoxicity through reducing ER stress, increasing antioxidant ability, and inhibiting apoptosis. The efficacy of AEPL on lipotoxicity was probably concerned with kaempferol and isorhamnetin derived compounds.

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