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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

Effects of Aralia elata (Miq) Seem (AE) on steatosis in HepG2 cells stimulated with oleic acid (OA). a HepG2 cells were treated with 100 μg/mL AE. After treatment for 24 h, lipid accumulation was measured by staining with Oil-red-O. b Lipid accumulation in HepG2 cell was determined by ORO-based colorimetric assay. Results are the mean ± SEM. *p < 0.05 compared with the OA group. DMEM, control group; OA, oleic acid-treated group; AE, OA + Aralia elata (Miq) Seem-treated group; RV, OA+ resveratrol-treated group
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Fig2: Effects of Aralia elata (Miq) Seem (AE) on steatosis in HepG2 cells stimulated with oleic acid (OA). a HepG2 cells were treated with 100 μg/mL AE. After treatment for 24 h, lipid accumulation was measured by staining with Oil-red-O. b Lipid accumulation in HepG2 cell was determined by ORO-based colorimetric assay. Results are the mean ± SEM. *p < 0.05 compared with the OA group. DMEM, control group; OA, oleic acid-treated group; AE, OA + Aralia elata (Miq) Seem-treated group; RV, OA+ resveratrol-treated group

Mentions: Incubation of HepG2 cells, for 24 h with 2 mM OA led to increased amounts of intracellular lipid accumulation. Microscopic examination revealed that HepG2 cells treated with OA exhibited significant morphological changes in lipid droplet formation. When cells were treated with AE and OA simultaneously for 24 h, hepatic lipid accumulation significantly decreased (Fig. 2a). There was also a significant decrease in lipid levels by 2.6 folds in AE-treated HepG2 cells (Fig. 2b).Fig. 2


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)

Effects of Aralia elata (Miq) Seem (AE) on steatosis in HepG2 cells stimulated with oleic acid (OA). a HepG2 cells were treated with 100 μg/mL AE. After treatment for 24 h, lipid accumulation was measured by staining with Oil-red-O. b Lipid accumulation in HepG2 cell was determined by ORO-based colorimetric assay. Results are the mean ± SEM. *p < 0.05 compared with the OA group. DMEM, control group; OA, oleic acid-treated group; AE, OA + Aralia elata (Miq) Seem-treated group; RV, OA+ resveratrol-treated group
© Copyright Policy - OpenAccess
Related In: Results  -  Collection

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

Fig2: Effects of Aralia elata (Miq) Seem (AE) on steatosis in HepG2 cells stimulated with oleic acid (OA). a HepG2 cells were treated with 100 μg/mL AE. After treatment for 24 h, lipid accumulation was measured by staining with Oil-red-O. b Lipid accumulation in HepG2 cell was determined by ORO-based colorimetric assay. Results are the mean ± SEM. *p < 0.05 compared with the OA group. DMEM, control group; OA, oleic acid-treated group; AE, OA + Aralia elata (Miq) Seem-treated group; RV, OA+ resveratrol-treated group
Mentions: Incubation of HepG2 cells, for 24 h with 2 mM OA led to increased amounts of intracellular lipid accumulation. Microscopic examination revealed that HepG2 cells treated with OA exhibited significant morphological changes in lipid droplet formation. When cells were treated with AE and OA simultaneously for 24 h, hepatic lipid accumulation significantly decreased (Fig. 2a). There was also a significant decrease in lipid levels by 2.6 folds in AE-treated HepG2 cells (Fig. 2b).Fig. 2

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