Limits...
Polyphenol-Rich Fraction of Ecklonia cava Improves Nonalcoholic Fatty Liver Disease in High Fat Diet-Fed Mice.

Park EY, Choi H, Yoon JY, Lee IY, Seo Y, Moon HS, Hwang JH, Jun HS - Mar Drugs (2015)

Bottom Line: Ecklonia cava (E. cava; CA) is an edible brown alga with beneficial effects in diabetes via regulation of various metabolic processes such as lipogenesis, lipolysis, inflammation, and the antioxidant defense system in liver and adipose tissue.Further, we analyzed hepatic gene expression related to inflammation and lipid metabolism.The mRNA expression levels of inflammatory cytokines and hepatic lipogenesis-related genes were decreased in G-CA-treated HFD mice.

View Article: PubMed Central - PubMed

Affiliation: College of Pharmacy, Mokpo National University, Muan-gun, Jeonnam 58554, Korea. parkey@mokpo.ac.kr.

ABSTRACT
Ecklonia cava (E. cava; CA) is an edible brown alga with beneficial effects in diabetes via regulation of various metabolic processes such as lipogenesis, lipolysis, inflammation, and the antioxidant defense system in liver and adipose tissue. We investigated the effect of the polyphenol-rich fraction of E. cava produced from Gijang (G-CA) on nonalcoholic fatty liver disease (NAFLD) in high-fat diet (HFD)-fed mice. C57BL6 mice were fed a HFD for six weeks and then the HFD group was administered 300 mg/kg of G-CA extracts by oral intubation for 10 weeks. Body weight, fat mass, and serum biochemical parameters were reduced by G-CA extract treatment. MRI/MRS analysis showed that liver fat and liver volume in HFD-induced obese mice were reduced by G-CA extract treatment. Further, we analyzed hepatic gene expression related to inflammation and lipid metabolism. The mRNA expression levels of inflammatory cytokines and hepatic lipogenesis-related genes were decreased in G-CA-treated HFD mice. The mRNA expression levels of cholesterol 7 alpha-hydroxylase 1 (CYP7A1), the key enzyme in bile acid synthesis, were dramatically increased by G-CA treatment in HFD mice. We suggest that G-CA treatment ameliorated hepatic steatosis by inhibiting inflammation and improving lipid metabolism.

Show MeSH

Related in: MedlinePlus

Effect of G-CA on metabolic gene expression in liver. Six weeks after beginning a high fat diet, C57BL6 mice were orally administered G-CA (300 mg/kg body weight) or PBS daily for 10 weeks (n = 5–6). (A) Tumor necrosis factor alpha (TNFα), interleukin-1 beta (IL-1β), and monocyte chemoattractant protein 1 (MCP-1) mRNA levels were analyzed by RT-qPCR and normalized to 18S rRNA expression; (B) Sterol regulatory element-binding protein 1c (SREBP-1c), fatty acid synthase (FAS), and acetyl-CoA carboxylase (ACC) mRNA levels were analyzed by RT-qPCR and normalized to 18S rRNA expression; (C) Hepatic cholesterol 7 alpha-hydroxylase 1 (CYP7A1), farnesoid X receptor (FXR), small heterodimer partner (SHP), hepatocyte nuclear factor 4 alpha (HNF4α), and liver X nuclear receptor alpha (LXRα) mRNA levels were analyzed by RT-qPCR and normalized to 18S rRNA expression. Values are expressed as fold change compared with the NC group. NC: untreated, normal chow diet; PBS-HFD: PBS-treated, high fat diet (HFD); G-CA-HFD: G-CA-treated, HFD. Values are mean ± SE. * p < 0.05, ** p < 0.01 vs. NC group; #p < 0.05, ##p < 0.01 vs. PBS-HFD group.
© Copyright Policy
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC4663557&req=5

marinedrugs-13-06866-f005: Effect of G-CA on metabolic gene expression in liver. Six weeks after beginning a high fat diet, C57BL6 mice were orally administered G-CA (300 mg/kg body weight) or PBS daily for 10 weeks (n = 5–6). (A) Tumor necrosis factor alpha (TNFα), interleukin-1 beta (IL-1β), and monocyte chemoattractant protein 1 (MCP-1) mRNA levels were analyzed by RT-qPCR and normalized to 18S rRNA expression; (B) Sterol regulatory element-binding protein 1c (SREBP-1c), fatty acid synthase (FAS), and acetyl-CoA carboxylase (ACC) mRNA levels were analyzed by RT-qPCR and normalized to 18S rRNA expression; (C) Hepatic cholesterol 7 alpha-hydroxylase 1 (CYP7A1), farnesoid X receptor (FXR), small heterodimer partner (SHP), hepatocyte nuclear factor 4 alpha (HNF4α), and liver X nuclear receptor alpha (LXRα) mRNA levels were analyzed by RT-qPCR and normalized to 18S rRNA expression. Values are expressed as fold change compared with the NC group. NC: untreated, normal chow diet; PBS-HFD: PBS-treated, high fat diet (HFD); G-CA-HFD: G-CA-treated, HFD. Values are mean ± SE. * p < 0.05, ** p < 0.01 vs. NC group; #p < 0.05, ##p < 0.01 vs. PBS-HFD group.

Mentions: Inflammation is an important risk factor for the progression of NAFLD [24]. Therefore, we analyzed whether G-CA treatment can improve inflammatory signaling in the liver of HFD-fed mice. The mRNA expression levels of the inflammatory marker genes, tumor necrosis factor alpha (TNF-α), interleukin 1 beta (IL-1β) and monocyte chemoattractant protein 1 (MCP-1) were significantly increased in the PBS-HFD mice as compared with NC mice. TNF-α, IL-1β, and MCP-1 mRNA levels were significantly reduced in the G-CA-HFD group compared with PBS-HFD group (Figure 5A).


Polyphenol-Rich Fraction of Ecklonia cava Improves Nonalcoholic Fatty Liver Disease in High Fat Diet-Fed Mice.

Park EY, Choi H, Yoon JY, Lee IY, Seo Y, Moon HS, Hwang JH, Jun HS - Mar Drugs (2015)

Effect of G-CA on metabolic gene expression in liver. Six weeks after beginning a high fat diet, C57BL6 mice were orally administered G-CA (300 mg/kg body weight) or PBS daily for 10 weeks (n = 5–6). (A) Tumor necrosis factor alpha (TNFα), interleukin-1 beta (IL-1β), and monocyte chemoattractant protein 1 (MCP-1) mRNA levels were analyzed by RT-qPCR and normalized to 18S rRNA expression; (B) Sterol regulatory element-binding protein 1c (SREBP-1c), fatty acid synthase (FAS), and acetyl-CoA carboxylase (ACC) mRNA levels were analyzed by RT-qPCR and normalized to 18S rRNA expression; (C) Hepatic cholesterol 7 alpha-hydroxylase 1 (CYP7A1), farnesoid X receptor (FXR), small heterodimer partner (SHP), hepatocyte nuclear factor 4 alpha (HNF4α), and liver X nuclear receptor alpha (LXRα) mRNA levels were analyzed by RT-qPCR and normalized to 18S rRNA expression. Values are expressed as fold change compared with the NC group. NC: untreated, normal chow diet; PBS-HFD: PBS-treated, high fat diet (HFD); G-CA-HFD: G-CA-treated, HFD. Values are mean ± SE. * p < 0.05, ** p < 0.01 vs. NC group; #p < 0.05, ##p < 0.01 vs. PBS-HFD group.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4663557&req=5

marinedrugs-13-06866-f005: Effect of G-CA on metabolic gene expression in liver. Six weeks after beginning a high fat diet, C57BL6 mice were orally administered G-CA (300 mg/kg body weight) or PBS daily for 10 weeks (n = 5–6). (A) Tumor necrosis factor alpha (TNFα), interleukin-1 beta (IL-1β), and monocyte chemoattractant protein 1 (MCP-1) mRNA levels were analyzed by RT-qPCR and normalized to 18S rRNA expression; (B) Sterol regulatory element-binding protein 1c (SREBP-1c), fatty acid synthase (FAS), and acetyl-CoA carboxylase (ACC) mRNA levels were analyzed by RT-qPCR and normalized to 18S rRNA expression; (C) Hepatic cholesterol 7 alpha-hydroxylase 1 (CYP7A1), farnesoid X receptor (FXR), small heterodimer partner (SHP), hepatocyte nuclear factor 4 alpha (HNF4α), and liver X nuclear receptor alpha (LXRα) mRNA levels were analyzed by RT-qPCR and normalized to 18S rRNA expression. Values are expressed as fold change compared with the NC group. NC: untreated, normal chow diet; PBS-HFD: PBS-treated, high fat diet (HFD); G-CA-HFD: G-CA-treated, HFD. Values are mean ± SE. * p < 0.05, ** p < 0.01 vs. NC group; #p < 0.05, ##p < 0.01 vs. PBS-HFD group.
Mentions: Inflammation is an important risk factor for the progression of NAFLD [24]. Therefore, we analyzed whether G-CA treatment can improve inflammatory signaling in the liver of HFD-fed mice. The mRNA expression levels of the inflammatory marker genes, tumor necrosis factor alpha (TNF-α), interleukin 1 beta (IL-1β) and monocyte chemoattractant protein 1 (MCP-1) were significantly increased in the PBS-HFD mice as compared with NC mice. TNF-α, IL-1β, and MCP-1 mRNA levels were significantly reduced in the G-CA-HFD group compared with PBS-HFD group (Figure 5A).

Bottom Line: Ecklonia cava (E. cava; CA) is an edible brown alga with beneficial effects in diabetes via regulation of various metabolic processes such as lipogenesis, lipolysis, inflammation, and the antioxidant defense system in liver and adipose tissue.Further, we analyzed hepatic gene expression related to inflammation and lipid metabolism.The mRNA expression levels of inflammatory cytokines and hepatic lipogenesis-related genes were decreased in G-CA-treated HFD mice.

View Article: PubMed Central - PubMed

Affiliation: College of Pharmacy, Mokpo National University, Muan-gun, Jeonnam 58554, Korea. parkey@mokpo.ac.kr.

ABSTRACT
Ecklonia cava (E. cava; CA) is an edible brown alga with beneficial effects in diabetes via regulation of various metabolic processes such as lipogenesis, lipolysis, inflammation, and the antioxidant defense system in liver and adipose tissue. We investigated the effect of the polyphenol-rich fraction of E. cava produced from Gijang (G-CA) on nonalcoholic fatty liver disease (NAFLD) in high-fat diet (HFD)-fed mice. C57BL6 mice were fed a HFD for six weeks and then the HFD group was administered 300 mg/kg of G-CA extracts by oral intubation for 10 weeks. Body weight, fat mass, and serum biochemical parameters were reduced by G-CA extract treatment. MRI/MRS analysis showed that liver fat and liver volume in HFD-induced obese mice were reduced by G-CA extract treatment. Further, we analyzed hepatic gene expression related to inflammation and lipid metabolism. The mRNA expression levels of inflammatory cytokines and hepatic lipogenesis-related genes were decreased in G-CA-treated HFD mice. The mRNA expression levels of cholesterol 7 alpha-hydroxylase 1 (CYP7A1), the key enzyme in bile acid synthesis, were dramatically increased by G-CA treatment in HFD mice. We suggest that G-CA treatment ameliorated hepatic steatosis by inhibiting inflammation and improving lipid metabolism.

Show MeSH
Related in: MedlinePlus