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Polysaccharide-rich red algae (Gelidium amansii) hot-water extracts ameliorate the altered plasma cholesterol and hepatic lipid homeostasis in high-fat diet-fed rats

We have demonstrated that red algae Gelidium amansii (GA) hot-water extract (GHE) is a polysaccharide-rich fraction, containing 68.54% water-soluble indigestible carbohydrate polymers; the molecular weight of major polysaccharide is 892. Here, we investigated the mechanisms of GHE on plasma and hepa...

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Autores principales: Liu, Shing-Hwa, Hung, Hsin-I, Yang, Tsung-Han, Pan, Chorng-Liang, Chiang, Meng-Tsan
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Taiwan Food and Drug Administration 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9261851/
https://www.ncbi.nlm.nih.gov/pubmed/35696225
http://dx.doi.org/10.38212/2224-6614.1181
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author Liu, Shing-Hwa
Hung, Hsin-I
Yang, Tsung-Han
Pan, Chorng-Liang
Chiang, Meng-Tsan
author_facet Liu, Shing-Hwa
Hung, Hsin-I
Yang, Tsung-Han
Pan, Chorng-Liang
Chiang, Meng-Tsan
author_sort Liu, Shing-Hwa
collection PubMed
description We have demonstrated that red algae Gelidium amansii (GA) hot-water extract (GHE) is a polysaccharide-rich fraction, containing 68.54% water-soluble indigestible carbohydrate polymers; the molecular weight of major polysaccharide is 892. Here, we investigated the mechanisms of GHE on plasma and hepatic lipid metabolisms in high-fat (HF) diet-fed rats. Rats were divided into: normal diet group, HF-diet group, HF-diet+5% GHE group, and HF-diet+1% cholestyramine group. GHE supplementation for 8 weeks significantly decreased plasma cholesterol, LDL-C, and VLDL-C levels and increased the fecal triglyceride and bile acid excretion in HF diet-fed rats. GHE group has lower lipid contents in the liver and adipose tissues. GHE supplementation decreased the activities of acetyl-CoA carboxylase, fatty acid synthase, and HMG-CoA reductase in the livers. The levels of increased phosphorylated AMP-activated protein kinase (AMPK), peroxisome proliferator activated receptor (PPAR)-α, farnesoid-X receptor (FXR), low density lipoprotein receptor (LDLR), and cytochrome P450-7A1 (CYP7A1) protein expression, and the decreased PPAR-γ protein expression in the livers were observed in GHE group. These results suggest that GHE supplementation is capable of interfering in cholesterol metabolism and increasing hepatic LDLR and CYP7A1 expression to decrease blood cholesterol, and activating FXR and AMPK to inhibit lipogenic enzyme activities and reduce the hepatic lipid accumulation.
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spelling pubmed-92618512022-07-18 Polysaccharide-rich red algae (Gelidium amansii) hot-water extracts ameliorate the altered plasma cholesterol and hepatic lipid homeostasis in high-fat diet-fed rats Liu, Shing-Hwa Hung, Hsin-I Yang, Tsung-Han Pan, Chorng-Liang Chiang, Meng-Tsan J Food Drug Anal Original Article We have demonstrated that red algae Gelidium amansii (GA) hot-water extract (GHE) is a polysaccharide-rich fraction, containing 68.54% water-soluble indigestible carbohydrate polymers; the molecular weight of major polysaccharide is 892. Here, we investigated the mechanisms of GHE on plasma and hepatic lipid metabolisms in high-fat (HF) diet-fed rats. Rats were divided into: normal diet group, HF-diet group, HF-diet+5% GHE group, and HF-diet+1% cholestyramine group. GHE supplementation for 8 weeks significantly decreased plasma cholesterol, LDL-C, and VLDL-C levels and increased the fecal triglyceride and bile acid excretion in HF diet-fed rats. GHE group has lower lipid contents in the liver and adipose tissues. GHE supplementation decreased the activities of acetyl-CoA carboxylase, fatty acid synthase, and HMG-CoA reductase in the livers. The levels of increased phosphorylated AMP-activated protein kinase (AMPK), peroxisome proliferator activated receptor (PPAR)-α, farnesoid-X receptor (FXR), low density lipoprotein receptor (LDLR), and cytochrome P450-7A1 (CYP7A1) protein expression, and the decreased PPAR-γ protein expression in the livers were observed in GHE group. These results suggest that GHE supplementation is capable of interfering in cholesterol metabolism and increasing hepatic LDLR and CYP7A1 expression to decrease blood cholesterol, and activating FXR and AMPK to inhibit lipogenic enzyme activities and reduce the hepatic lipid accumulation. Taiwan Food and Drug Administration 2021-03-15 /pmc/articles/PMC9261851/ /pubmed/35696225 http://dx.doi.org/10.38212/2224-6614.1181 Text en © 2021 Taiwan Food and Drug Administration https://creativecommons.org/licenses/by-nc-nd/4.0/This is an open access article under the CC-BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/ (https://creativecommons.org/licenses/by-nc-nd/4.0/) ).
spellingShingle Original Article
Liu, Shing-Hwa
Hung, Hsin-I
Yang, Tsung-Han
Pan, Chorng-Liang
Chiang, Meng-Tsan
Polysaccharide-rich red algae (Gelidium amansii) hot-water extracts ameliorate the altered plasma cholesterol and hepatic lipid homeostasis in high-fat diet-fed rats
title Polysaccharide-rich red algae (Gelidium amansii) hot-water extracts ameliorate the altered plasma cholesterol and hepatic lipid homeostasis in high-fat diet-fed rats
title_full Polysaccharide-rich red algae (Gelidium amansii) hot-water extracts ameliorate the altered plasma cholesterol and hepatic lipid homeostasis in high-fat diet-fed rats
title_fullStr Polysaccharide-rich red algae (Gelidium amansii) hot-water extracts ameliorate the altered plasma cholesterol and hepatic lipid homeostasis in high-fat diet-fed rats
title_full_unstemmed Polysaccharide-rich red algae (Gelidium amansii) hot-water extracts ameliorate the altered plasma cholesterol and hepatic lipid homeostasis in high-fat diet-fed rats
title_short Polysaccharide-rich red algae (Gelidium amansii) hot-water extracts ameliorate the altered plasma cholesterol and hepatic lipid homeostasis in high-fat diet-fed rats
title_sort polysaccharide-rich red algae (gelidium amansii) hot-water extracts ameliorate the altered plasma cholesterol and hepatic lipid homeostasis in high-fat diet-fed rats
topic Original Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9261851/
https://www.ncbi.nlm.nih.gov/pubmed/35696225
http://dx.doi.org/10.38212/2224-6614.1181
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