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Extracts from Aralia elata (Miq) Seem alleviate hepatosteatosis via improving hepatic insulin sensitivity.

Hwang KA, Hwang YJ, Kim GR, Choe JS - BMC Complement Altern Med (2015)

Bottom Line: Treatment with AE extract significantly decreased body weight and the fasting glucose level, alleviated hyperinsulinism and hyperlipidemia, and reduced glucose levels, as determined by OGTT.Additionally, AE extract decreased PI3K and Akt activity.Our results suggest that treatment with AE extract ameliorated NAFLD by inhibiting insulin resistance through activation of the Akt/GLUT4 pathway.

View Article: PubMed Central - PubMed

Affiliation: Department of Agrofood Resources, National Academy of Agricultural Science, RDA, Wanju-Gun, Jeollabuk-do, 565-851, Republic of Korea. kah366@korea.kr.

ABSTRACT

Background: Non-alcoholic fatty liver disease (NAFLD) is a common liver disease that is strongly associated with obesity and dysregulation of insulin in the liver. However, currently no pharmacological agents have been established for the treatment of NAFLD. In this regard, we sought to evaluate the anti-NAFLD effects of Aralia elata (Miq) Seem (AE) extract and its ability to inhibit hepatic lipid accumulation and modulate cellular signaling in a high fat diet (HFD)-induced obese mouse model.

Methods: A model of hepatic steatosis in the HepG2 cells was induced by oleic acid. Intracellular lipid droplets were detected by Oil-Red-O staining, and the expression of sterol regulatory element-binding protein 1(SREBP-1), Fatty acid synthase (FAS), Acetyl-CoA carboxylase (ACC) 1 and 2, Peroxisome proliferator activated receptor-α (PPARα), and carnitine palmitoyl transferase 1(CPT-1) was analyzed by real time reverse transcription-Polymerase chain reaction (qRT-PCR). And glucose consumption was measured with commercial kit. Furthermore, Male C57BL/6 J mice were fed with HFD to induce NAFLD. Groups of mice were given plant extracts orally at 100 and 300 mg/kg at daily for 4 weeks. After 3 weeks of AE extract treatment, we performed oral glucose tolerance test (OGTT). Liver tissue was procured for histological examination, Phosphoinositide 3-kinase (PI3K) and Protein kinase B (PKB/Akt) activity.

Results: In the present study, AE extract was shown to reduce hepatic lipid accumulation and significantly downregulate the level of lipogenic genes and upregulate the expression of lipolysis genes in HepG2 cells. And also, AE extract significantly increased the glucose consumption, indicating that AE extract improved insulin resistance. Subsequently, we confirmed the inhibitory activity of AE extract on NAFLD, in vivo. Treatment with AE extract significantly decreased body weight and the fasting glucose level, alleviated hyperinsulinism and hyperlipidemia, and reduced glucose levels, as determined by OGTT. Additionally, AE extract decreased PI3K and Akt activity.

Conclusions: Our results suggest that treatment with AE extract ameliorated NAFLD by inhibiting insulin resistance through activation of the Akt/GLUT4 pathway.

No MeSH data available.


Related in: MedlinePlus

Cell viability effect of Aralia elata (Miq) Seem (AE) in HepG2 cells. HepG2 cells were treated with oleic aicd (2 mM) and AE extract (10, 50, 100, 500 and 1000 μg/mL). After treatment for 24 h, cell viability was quantified by measuring intracellular levels of ATP. Bars represent the mean ± SEM of 3 experiments done in triplicate
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Fig1: Cell viability effect of Aralia elata (Miq) Seem (AE) in HepG2 cells. HepG2 cells were treated with oleic aicd (2 mM) and AE extract (10, 50, 100, 500 and 1000 μg/mL). After treatment for 24 h, cell viability was quantified by measuring intracellular levels of ATP. Bars represent the mean ± SEM of 3 experiments done in triplicate

Mentions: The cytotoxicity of AE in HepG2 cells was determined measuring intracellular level of ATP after incubating cells with AE for 24 h. As shown in Fig. 1, AE exhibited 6.5 % and 13.1 % cytotoxicity in HepG2 cells at concentrations of 500 μg/mL and 1000 μg/mL, respectively. When cells were treated with OA for 24 h to induce conditions of hepatic steatosis, no cytotoxicity was observed in the cells. Therefore, 100 μg/mL of AE and 2.0 mM of OA were used to examine the effect of AE on OA-induced steatosis in HepG2 cell.Fig. 1


Extracts from Aralia elata (Miq) Seem alleviate hepatosteatosis via improving hepatic insulin sensitivity.

Hwang KA, Hwang YJ, Kim GR, Choe JS - BMC Complement Altern Med (2015)

Cell viability effect of Aralia elata (Miq) Seem (AE) in HepG2 cells. HepG2 cells were treated with oleic aicd (2 mM) and AE extract (10, 50, 100, 500 and 1000 μg/mL). After treatment for 24 h, cell viability was quantified by measuring intracellular levels of ATP. Bars represent the mean ± SEM of 3 experiments done in triplicate
© Copyright Policy - OpenAccess
Related In: Results  -  Collection

License 1 - License 2
Show All Figures
getmorefigures.php?uid=PMC4595215&req=5

Fig1: Cell viability effect of Aralia elata (Miq) Seem (AE) in HepG2 cells. HepG2 cells were treated with oleic aicd (2 mM) and AE extract (10, 50, 100, 500 and 1000 μg/mL). After treatment for 24 h, cell viability was quantified by measuring intracellular levels of ATP. Bars represent the mean ± SEM of 3 experiments done in triplicate
Mentions: The cytotoxicity of AE in HepG2 cells was determined measuring intracellular level of ATP after incubating cells with AE for 24 h. As shown in Fig. 1, AE exhibited 6.5 % and 13.1 % cytotoxicity in HepG2 cells at concentrations of 500 μg/mL and 1000 μg/mL, respectively. When cells were treated with OA for 24 h to induce conditions of hepatic steatosis, no cytotoxicity was observed in the cells. Therefore, 100 μg/mL of AE and 2.0 mM of OA were used to examine the effect of AE on OA-induced steatosis in HepG2 cell.Fig. 1

Bottom Line: Treatment with AE extract significantly decreased body weight and the fasting glucose level, alleviated hyperinsulinism and hyperlipidemia, and reduced glucose levels, as determined by OGTT.Additionally, AE extract decreased PI3K and Akt activity.Our results suggest that treatment with AE extract ameliorated NAFLD by inhibiting insulin resistance through activation of the Akt/GLUT4 pathway.

View Article: PubMed Central - PubMed

Affiliation: Department of Agrofood Resources, National Academy of Agricultural Science, RDA, Wanju-Gun, Jeollabuk-do, 565-851, Republic of Korea. kah366@korea.kr.

ABSTRACT

Background: Non-alcoholic fatty liver disease (NAFLD) is a common liver disease that is strongly associated with obesity and dysregulation of insulin in the liver. However, currently no pharmacological agents have been established for the treatment of NAFLD. In this regard, we sought to evaluate the anti-NAFLD effects of Aralia elata (Miq) Seem (AE) extract and its ability to inhibit hepatic lipid accumulation and modulate cellular signaling in a high fat diet (HFD)-induced obese mouse model.

Methods: A model of hepatic steatosis in the HepG2 cells was induced by oleic acid. Intracellular lipid droplets were detected by Oil-Red-O staining, and the expression of sterol regulatory element-binding protein 1(SREBP-1), Fatty acid synthase (FAS), Acetyl-CoA carboxylase (ACC) 1 and 2, Peroxisome proliferator activated receptor-α (PPARα), and carnitine palmitoyl transferase 1(CPT-1) was analyzed by real time reverse transcription-Polymerase chain reaction (qRT-PCR). And glucose consumption was measured with commercial kit. Furthermore, Male C57BL/6 J mice were fed with HFD to induce NAFLD. Groups of mice were given plant extracts orally at 100 and 300 mg/kg at daily for 4 weeks. After 3 weeks of AE extract treatment, we performed oral glucose tolerance test (OGTT). Liver tissue was procured for histological examination, Phosphoinositide 3-kinase (PI3K) and Protein kinase B (PKB/Akt) activity.

Results: In the present study, AE extract was shown to reduce hepatic lipid accumulation and significantly downregulate the level of lipogenic genes and upregulate the expression of lipolysis genes in HepG2 cells. And also, AE extract significantly increased the glucose consumption, indicating that AE extract improved insulin resistance. Subsequently, we confirmed the inhibitory activity of AE extract on NAFLD, in vivo. Treatment with AE extract significantly decreased body weight and the fasting glucose level, alleviated hyperinsulinism and hyperlipidemia, and reduced glucose levels, as determined by OGTT. Additionally, AE extract decreased PI3K and Akt activity.

Conclusions: Our results suggest that treatment with AE extract ameliorated NAFLD by inhibiting insulin resistance through activation of the Akt/GLUT4 pathway.

No MeSH data available.


Related in: MedlinePlus