Rosemary (<i>Rosmarinus officinalis</i>L.) Extract Regulates Glucose and Lipid Metabolism by Activating AMPK and PPAR Pathways in HepG2 Cells

Tu, Zheng; Moss‐Pierce, Tijuana; Ford, Paul W.; Jiang, Tingting

doi:10.1021/jf400298c

Cited by 103 publications

(58 citation statements)

References 49 publications

(101 reference statements)

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“…Statistical significance was set as * p < 0.05, **p < 0.01, or ***p < 0.001, ns: no significance. Tu et al, 2013). Adiponectin (Ad) plays a crucial role in hepatic lipid metabolism, which has been shown to activate the AMPK signaling pathway and mediates lipid metabolism in bovine hepatocytes in vitro by promoting lipid oxidation, suppressing lipid synthesis and reducing hepatic lipid accumulation .…”

Section: Discussionmentioning

confidence: 99%

“…LKB1, a crucial regulator of AMPK activation, is implicated in the glucose and lipid metabolism (Imai et al, 2006). Rosemary potentially increases liver glycolysis and fatty acid oxidation by activating AMPK and PPAR (Peroxisome Proliferator-Activated Receptors) pathways (Tu et al, 2013). On the other hand, the pharmaceutical inhibition of AMPK activity by atypical antipsychotic drugs (AAPD) deregulates hepatic lipid metabolism (Oh et al, 2011).…”

Section: Discussionmentioning

confidence: 99%

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Aspirin regulates hepatocellular lipid metabolism by activating AMPK signaling pathway

Peng

Duan

et al. 2015

J. Toxicol. Sci.

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-Aspirin has been reported to regulate lipid metabolism. However, the mechanism underlying the regulation is not clear. We presently investigated aspirin's promotion of AMP-activated protein kinase (AMPK) pathway activation in human hepatoma HepG2 cells by examining AMPK expression, the promotion of AMPK activation. Then we investigated the influence of aspirin-promoted AMPK signaling on fatty acid oxidation in HepG2 cells. The results demonstrated that aspirin treatment did not regulate the expression of AMPK and its downstream target, Acetyl-Coenzyme A Carboxylase (ACC), but activated the AMPK signaling pathway by promoting the phosphorylation of AMPK and ACC. And, interestingly, the promotion by aspirin is dependent of cellular esterase, which catalyzes aspirin to salicylate. Moreover, the activated AMPK signaling promoted the fatty acid oxidation, by promoting expression of Carnitine palmitoyltransferase I (CPT1) and Medium-Chain Acyl-CoA Dehydrogenase (MCAD) in both mRNA and protein levels. Thus, we confirmed in this study that aspirin promoted lipid oxidation by upregulating the AMPK signaling pathway.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Aspirin regulates hepatocellular lipid metabolism by activating AMPK signaling pathway

Peng

Duan

et al. 2015

J. Toxicol. Sci.

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“…25 C2C12 myocytes were treated with SE or metformin, resveratrol for 16 h. At that time, the medium was changed to unbuffered serum-free DMEM (Seahorse Bioscience) without glucose for 1 h. The measurement protocol used is as follows 25 : After four baseline measurements, 10 mM glucose and 100 mM 2-deoxyglucose (2-DG) were injected sequentially. For each injection, the ECAR value was monitored at four successive 4-min intervals, with a 2-min inter-measurement mixing.…”

Section: Glycolysis Assaymentioning

confidence: 99%

Syzygium aromaticumL. (Clove) Extract Regulates Energy Metabolism in Myocytes

Ford

2014

Journal of Medicinal Food

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The prevalence of metabolic syndrome and type 2 diabetes is increasing worldwide. Herbs and spices have been used for the treatment of diabetes for centuries in folk medicine. Syzygium aromaticum L. (Clove) extracts (SE) have been shown to perform comparably to insulin by significantly reducing blood glucose levels in animal models; however, the mechanisms are not well understood. We investigated the effects of clove on metabolism in C2C12 myocytes and demonstrated that SE significantly increases glucose consumption. The phosphorylation of AMP-activated protein kinase (AMPK), as well as its substrate, acetyl-CoA carboxylase (ACC) was increased by SE treatment. SE also transcriptionally regulates genes involved in metabolism, including sirtuin 1 (SIRT1) and PPARγ coactivator 1α (PGC1α). Nicotinamide, an SIRT1 inhibitor, diminished SE's effects on glucose consumption. Furthermore, treatment with SE dose-dependently increases muscle glycolysis and mitochondrial spare respiratory capacity. Overall, our study suggests that SE has the potential to increase muscle glycolysis and mitochondria function by activating both AMPK and SIRT1 pathways.

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“…3 Obesity, diabetes, hyperlipidemia, and the consumption of soft drinks are the potential risk factors of NAFLD. 4,5 Pharmaceutical anti-NAFLD drugs have been developed, but these drugs have limited effects, except for pioglitazone and vitamin E. Recently, many studies reported that natural products, such as rosemary extract, 6 were investigated as potential therapeutics for NAFLD. 7 AMP-activated protein kinase (AMPK) has been implicated as a regulator of lipid synthesis by decreasing free fatty acid delivery from hepatic cells 8,9 and mediating lipid metabolism through lipid-metabolism-related transcription factors, such as sterol regulatory element-binding protein-1 (SREBP-1).…”

Section: ■ Introductionmentioning

confidence: 99%

Fermented Rhus verniciflua Stokes Extract Exerts an Antihepatic Lipogenic Effect in Oleic-Acid-Induced HepG2 Cells via Upregulation of AMP-Activated Protein Kinase

Lee

Kim

Cho

et al. 2015

J. Agric. Food Chem.

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Rhus verniciflua Stokes has been used as a traditional medicine and food supplement in Korea. In the present study, fermented R. verniciflua Stokes extract (FRVE), an allergen-free extract of R. verniciflua Stokes fermented with the yeast Saccharomyces carlsbergensis, was assessed for its lipid-lowering potential in an in vitro non-alcoholic fatty liver disease model. FRVE markedly suppressed lipid accumulation and intracellular triglycerides (TGs) in the presence of oleic acid (OA). Additionally, FRVE decreased both mRNA and protein levels of lipid-synthesis- and cholesterol-metabolism-related factors, such as sterol regulatory element-binding protein-1 (SREBP-1), fatty acid synthase (FAS), glycerol-3-phosphate acyltransferase (GPAT), and 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMGCR), in OA-induced HepG2 cells. Moreover, FRVE activated low-density lipoprotein receptor (LDLR), AMP-activated protein kinase (AMPK), and fatty acid oxidation-related factors peroxisome proliferator activated receptor α (PPARα) and carnitine palmitoyltransferase 1 (CPT-1). Further, the AMPK inhibitor compound C suppressed the increased expression of AMPK phosphorylation induced by FRVE. Phenolics and cosanols in FRVE increased the phosphorylation of AMPK and decreased that of SREBP-1. Taken together, our findings suggest that FRVE has antilipogenic potential in non-alcoholic fatty livers via AMPK upregulation.

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Rosemary (Rosmarinus officinalisL.) Extract Regulates Glucose and Lipid Metabolism by Activating AMPK and PPAR Pathways in HepG2 Cells

Cited by 103 publications

References 49 publications

Aspirin regulates hepatocellular lipid metabolism by activating AMPK signaling pathway

Aspirin regulates hepatocellular lipid metabolism by activating AMPK signaling pathway

Syzygium aromaticumL. (Clove) Extract Regulates Energy Metabolism in Myocytes

Fermented Rhus verniciflua Stokes Extract Exerts an Antihepatic Lipogenic Effect in Oleic-Acid-Induced HepG2 Cells via Upregulation of AMP-Activated Protein Kinase

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