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  4. Resistant maltodextrin ameliorates altered hepatic lipid homeostasis via activation of AMP-activated protein kinase in a high-fat diet-fed rat model
 
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Resistant maltodextrin ameliorates altered hepatic lipid homeostasis via activation of AMP-activated protein kinase in a high-fat diet-fed rat model

Journal
Nutrients
Journal Volume
11
Journal Issue
2
Date Issued
2019
Author(s)
SHING-HWA LIU  
Chiu C.-Y.
Huang L.-H.
Chiang M.-T.
DOI
10.3390/nu11020291
URI
https://www.scopus.com/inward/record.uri?eid=2-s2.0-85060952535&doi=10.3390%2fnu11020291&partnerID=40&md5=429394915d00bb9b072f498629334032
https://scholars.lib.ntu.edu.tw/handle/123456789/431132
Abstract
Many studies have shown that resistant maltodextrin (RMD) possesses blood cholesterol lowering and anti-obesity effects. In order to investigate the effect of RMD on lipid metabolism in the liver, rats were fed with a high-fat (HF) diet for 7 weeks to induce hyperlipidemia and fatty liver. Normal control rats were fed with a normal diet. HF-diet-fed rats were treated with 5% RMD for 8 weeks. The results showed that the increased plasma aspartate aminotransferase (AST) and alanine aminotransferase (ALT) activities, the increased hepatic triglyceride and total cholesterol levels, and fatty liver in HF-diet-fed rats were significantly decreased after supplementation with RMD. Supplementation with RMD significantly (1) induced AMP-activated protein kinase (AMPK) phosphorylation; (2) inhibited the activities of acetyl-CoA carboxylase (ACC), fatty acid synthase (FAS), and HMG-CoA reductase (HMGCR); (3) suppressed the protein expression of peroxisome proliferator activated receptor (PPAR)-γ; (4) increased β-oxidation of fatty acids by increasing the protein expression carnitine palmitoyl transferase 1α (CPT-1α) in the livers of HF-diet-fed rats. Taken together, supplementation of RMD was capable of inhibiting lipogenic enzyme activities and inducing fatty acid β-oxidation through increasing AMPK activation, thereby reducing lipid accumulation in the liver. ? 2019 by the authors. Licensee MDPI, Basel, Switzerland.
Subjects
AMP-activated protein kinase; Fatty liver; Hepatic lipid metabolism; High-fat diet; Resistant maltodextrin
SDGs

[SDGs]SDG3

Other Subjects
alanine aminotransferase; aspartate aminotransferase; carboxylase; carnitine palmitoyltransferase I; cholesterol; fatty acid; hydroxymethylglutaryl coenzyme A reductase kinase; maltodextrin; peroxisome proliferator activated receptor gamma; hydroxymethylglutaryl coenzyme A reductase kinase; maltodextrin; polysaccharide; animal model; Article; body weight; cholesterol blood level; controlled study; diet supplementation; enzyme activity; enzyme linked immunosorbent assay; fatty acid oxidation; fatty liver; food intake; histology; hyperlipidemia; lipid diet; lipid homeostasis; lipid liver level; lipid metabolism; lipid storage; male; nonalcoholic fatty liver; nonhuman; nutritional parameters; obesity; protein expression; rat; signal transduction; Western blotting; animal; drug effect; enzymology; gene expression regulation; genetics; homeostasis; lipid diet; liver; metabolism; Sprague Dawley rat; AMP-Activated Protein Kinases; Animals; Diet, High-Fat; Gene Expression Regulation, Enzymologic; Homeostasis; Lipid Metabolism; Liver; Male; Polysaccharides; Rats; Rats, Sprague-Dawley
Publisher
MDPI AG
Type
journal article

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