Mangiferin decreases plasma free fatty acids through promoting its catabolism in liver by activation of AMPK
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Mangiferin has been shown to have the effect of improving dyslipidemia. Plasma free fatty acids (FFA) are closely associated with blood lipid metabolism as well as many diseases including metabolic syndrome. This study is to investigate whether mangiferin has effects on FFA metabolism in hyperlipidemic rats. Wistar rats were fed a high-fat diet and administered mangiferin simultaneously for 6 weeks. Mangiferin (50, 100, 150 mg/kg BW) decreased dose-dependently FFA and triglycerides (TG) levels in plasma, and their accumulations in liver, but increased the β-hydroxybutyrate levels in both plasma and liver of hyperlipidemic rats. HepG2 cells were treated with oleic acid (OA, 0.2 mmol/L) to simulate the condition of high level of plasma FFA in vitro, and were treated with different concentrations of mangiferin simultaneously for 24 h. We found that mangiferin significantly increased FFA uptake, significantly decreased intracellular FFA and TG accumulations in HepG2 cells. Mangiferin significantly increased AMP-activated protein kinase (AMPK) phosphorylation and its downstream proteins involved in fatty acid translocase (CD36) and carnitine palmitoyltransferase 1 (CPT1), but significantly decreased acyl-CoA: diacylgycerol acyltransferase 2 (DGAT2) expression and acetyl-CoA carboxylase (ACC) activity by increasing its phosphorylation level in both in vivo and in vitro studies. Furthermore, these effects were reversed by Compound C, an AMPK inhibitor in HepG2 cells. For upstream of AMPK, mangiferin increased AMP/ATP ratio, but had no effect on LKB1 phosphorylation. In conclusion, mangiferin decreased plasma FFA levels through promoting FFA uptake and oxidation, inhibiting FFA and TG accumulations by regulating the key enzymes expression in liver through AMPK pathway. Therefore, mangiferin is a possible beneficial natural compound for metabolic syndrome by improving FFA metabolism.
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In Wistar rats and HepG2 cells, levels of intracellular FFA and TG accumulation were decreased in HepG2 cells.
“Similarly, it was also observed in Wistar rats and HepG2 cells that levels of intracellular FFA and TG accumulation was decreased in HepG2 cells.”
From Mangiferin: An effective therapeutic agent against several disorders (Review) (2018) · cites this paper as [86]
The Results section reports that mangiferin decreased intracellular oleic acid (an FFA) and triglycerides in HepG2 cells. The Materials and Methods section confirms a rat experiment but does not identify the rats as Wistar, so that specific breed is not supported by our copy. (LLM, conf=0.85)
Experimental — accuracy not yet measuredMangiferin upregulates mRNA levels of PPAR-alpha, CD36 and CPT-1.
“It was observed that mangiferin upregulates the mRNA levels of peroxisome proliferator-activated receptor-α, fatty acid translocase (CD36) and carnitine palmitoyl transferase 1 (CPT-1) (86).”
From Mangiferin: An effective therapeutic agent against several disorders (Review) (2018) · cites this paper as [86]
The Results report increased CD36 and CPT-1 protein levels after mangiferin treatment in hyperlipidemic rats and HepG2 cells. The Methods specify that these proteins were measured by western blot; our copy does not report increased mRNA levels for them or for PPAR-α. (LLM, conf=0.88)
Experimental — accuracy not yet measuredIn Wistar rats fed a high-fat diet and administered mangiferin (50, 100, 150 mg/kg) for 6 weeks, mangiferin improves FFA metabolism in a dose-dependent manner through promoting FFA uptake and oxidation.
“Wistar rats were fed a high-fat diet and administered mangiferin (50, 100, 150 mg/kg) simultaneously for 6 weeks, which confirmed that mangiferin improves FFA metabolism in a dose-dependent manner through promoting FFA uptake and oxidation (86).”
From Mangiferin: An effective therapeutic agent against several disorders (Review) (2018) · cites this paper as [86]
Mangiferin promotes AMPK phosphorylation and upregulates expression of CD36 and CPT-1.
“Furthermore, mangiferin promotes AMPK phosphorylation, and upregulates the expression of CD36 and CPT-1 (86).”
From Mangiferin: An effective therapeutic agent against several disorders (Review) (2018) · cites this paper as [86]
Mangiferin increases the AMP/ATP ratio upstream of AMPK, decreases DGAT2 expression, and decreases ACC activity.
“Mangiferin increases the AMP/ATP ratio upstream of AMPK, decreases acyl-CoA:diacyl gycerol acyltransferase 2 (DGAT2) expression, decreases acetyl-CoA carboxylase (ACC) activity.”
From Mangiferin: An effective therapeutic agent against several disorders (Review) (2018) · cites this paper as [86]
The AMPK pathway is associated with the therapeutic effect of mangiferin.
“Furthermore, the AMPK pathway is associated with this therapeutic effect of mangiferin (86).”
From Mangiferin: An effective therapeutic agent against several disorders (Review) (2018) · cites this paper as [86]
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- Authors
- Niu, Y., Li, S., Na, L., Feng, R., Liu, L., Li, Y., & Sun, C.
- Affiliations
- Harbin Medical University (CN)
- Corresponding author
- Sun, Changhao
- Venue
- PLoS ONE
- Publisher
- Public Library of Science (PLoS)
- Published
- 2012-01-23
- Volume
- 7
- Issue
- 1
- Pages
- e30782
- ISSN
- 1932-6203 (ISSN-L)
- PMC
- PMC3264633
- OpenAlex
- W2073563008
- Cited by
- 116
- References
- 32
- Citations by year
- 2026: 2 · 2025: 8 · 2024: 8 · 2023: 4 · 2022: 5 · 2021: 4 · 2020: 7 · 2019: 13 · 2018: 7 · 2017: 9 · 2016: 10 · 2015: 14 · 2014: 12 · 2013: 10 · 2012: 3
- FWCI
- 30.39
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- PLoS ONE (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Figshare (submittedVersion, cc-by)
- Funders
- National Natural Science Foundation of China (2010AA023002)
- National High-tech Research and Development Program (2010AA023002)
- National Institute on Alcohol Abuse and Alcoholism (K99AA023002, R00AA023002)
- Topics
- Health Sciences › Medicine › Complementary and alternative medicine › Mangiferin and Mango Extracts
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Natural Antidiabetic Agents Studies
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
- Keywords
- mangiferin, plasma free fatty acids, AMPK, fatty acid degradation, hyperlipidemia, hepatic triglyceride accumulation, fatty acid uptake, fatty acid oxidation, CD36, carnitine palmitoyltransferase 1, DGAT2, acetyl-CoA carboxylase, metabolic syndrome, high-fat diet, oleic acid, beta-hydroxybutyrate
- MeSH terms
- Adenylate Kinase, Animals, Enzyme Activation, Fatty Acids, Nonesterified, Female, Humans, Hyperlipidemias, Hypoglycemic Agents, Liver, Male, Metabolism, Triglycerides, Down-Regulation, Rats, Wistar, Xanthones, Lipid Metabolism, Rats, Hep G2 Cells
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