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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

Aralia elata (Miq) Seem (AE) decreases insulin resistance in OGTT. On the 21th days after AE treatment, OGTT were performed on the animals. Blood samples were collected from tail vein for glucose measurement at 0, 30, 60, 90, 120, 180 and 240 min after glucose administration (po). *p < 0.05 compared with the HFD-fed group. Normal, Normal chaw-fed group; HFD, HFD-fed group; AE100, HFD + Aralia elata (Miq) Seem 100 mg/kg -treated group; AE300, HFD + Aralia elata (Miq) Seem 300 mg/kg -treated group; RV, HFD+ resveratrol 300 mg/kg-treated group
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Fig5: Aralia elata (Miq) Seem (AE) decreases insulin resistance in OGTT. On the 21th days after AE treatment, OGTT were performed on the animals. Blood samples were collected from tail vein for glucose measurement at 0, 30, 60, 90, 120, 180 and 240 min after glucose administration (po). *p < 0.05 compared with the HFD-fed group. Normal, Normal chaw-fed group; HFD, HFD-fed group; AE100, HFD + Aralia elata (Miq) Seem 100 mg/kg -treated group; AE300, HFD + Aralia elata (Miq) Seem 300 mg/kg -treated group; RV, HFD+ resveratrol 300 mg/kg-treated group

Mentions: To verify whether AE extract can decrease IR in vivo, we performed an animal study using the HFD-induced obese mice. The HFD-fed mice showed significantly higher body weight, serum fasting glucose, insulin levels, and TG levels compared to those observed in the normal group, and HOMA-IR—negatively correlated with insulin sensitivity—also increased in the HFD-fed group. Treatment with AE for 4 weeks resulted in a dose-dependent reduction in body weight and food intake and improved glucose and TG levels. AE extract also significantly decreased HOMA-IR and the serum insulin level, which means that AE reduced IR (Table 2). To supplement these results, the mitigating effect of AE on IR was measured by OGTT. As shown in Fig. 5, mice fed with HFD showed poor glucose tolerance and high fasting blood glucose level. However, the AE-treated groups showed improved glucose tolerance ability and reduced fasting blood glucose level. These results indicate that AE treatment ameliorated IR.Table 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)

Aralia elata (Miq) Seem (AE) decreases insulin resistance in OGTT. On the 21th days after AE treatment, OGTT were performed on the animals. Blood samples were collected from tail vein for glucose measurement at 0, 30, 60, 90, 120, 180 and 240 min after glucose administration (po). *p < 0.05 compared with the HFD-fed group. Normal, Normal chaw-fed group; HFD, HFD-fed group; AE100, HFD + Aralia elata (Miq) Seem 100 mg/kg -treated group; AE300, HFD + Aralia elata (Miq) Seem 300 mg/kg -treated group; RV, HFD+ resveratrol 300 mg/kg-treated group
© Copyright Policy - OpenAccess
Related In: Results  -  Collection

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

Fig5: Aralia elata (Miq) Seem (AE) decreases insulin resistance in OGTT. On the 21th days after AE treatment, OGTT were performed on the animals. Blood samples were collected from tail vein for glucose measurement at 0, 30, 60, 90, 120, 180 and 240 min after glucose administration (po). *p < 0.05 compared with the HFD-fed group. Normal, Normal chaw-fed group; HFD, HFD-fed group; AE100, HFD + Aralia elata (Miq) Seem 100 mg/kg -treated group; AE300, HFD + Aralia elata (Miq) Seem 300 mg/kg -treated group; RV, HFD+ resveratrol 300 mg/kg-treated group
Mentions: To verify whether AE extract can decrease IR in vivo, we performed an animal study using the HFD-induced obese mice. The HFD-fed mice showed significantly higher body weight, serum fasting glucose, insulin levels, and TG levels compared to those observed in the normal group, and HOMA-IR—negatively correlated with insulin sensitivity—also increased in the HFD-fed group. Treatment with AE for 4 weeks resulted in a dose-dependent reduction in body weight and food intake and improved glucose and TG levels. AE extract also significantly decreased HOMA-IR and the serum insulin level, which means that AE reduced IR (Table 2). To supplement these results, the mitigating effect of AE on IR was measured by OGTT. As shown in Fig. 5, mice fed with HFD showed poor glucose tolerance and high fasting blood glucose level. However, the AE-treated groups showed improved glucose tolerance ability and reduced fasting blood glucose level. These results indicate that AE treatment ameliorated IR.Table 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