Beneficial effects of mangiferin on hyperlipidemia in high‐fat‐fed hamsters

Guo, Fuchuan; Huang, C. C.; Liao, Xi-Lu; Wang, Yemei; He, Ying; Feng, Rennan; Liu, Ying; Sun, Changhao

doi:10.1002/mnfr.201100392

Cited by 97 publications

(87 citation statements)

References 42 publications

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“…Mangiferin (50-150 mg/kg per day) has been demonstrated to have an effect on excessive hepatic triglyceride accumulation in high fat diet-fed hamsters (Guo et al, 2011) and Wistar rats (Niu et al, 2012), similar to that in WKY and SHR in the present study. However, the antisteatotic effect was accompanied by augmentation of high fat diet-stimulated overexpression of both hepatic and muscular CD36 mRNA in hamsters (Guo et al, 2011).…”

Section: Discussionsupporting

confidence: 84%

“…However, the underlying mechanisms of action are still largely unknown. We and others have reported that they improve numerous lipid metabolism-associated abnormalities, such as fatty liver, hyperlipidemia, excessive cardiac lipid accumulation and obesity (Huang et al, 2006a,b;Guo et al, 2011;Niu et al, 2012;Liu et al, 2013;Xing et al, 2014;Na et al, 2015). We hypothesized that regulation of lipid metabolism might be associated with the antidiabetic property of mangiferin.…”

Section: Introductionmentioning

confidence: 92%

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Mitigation of Insulin Resistance by Mangiferin in a Rat Model of Fructose-Induced Metabolic Syndrome Is Associated with Modulation of CD36 Redistribution in the Skeletal Muscle

Zhou

Pan

Chonan

et al. 2015

Journal of Pharmacology and Experimental Therapeutics

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Mangiferin is one of the prominent active components responsible for the antidiabetic property of many traditional herbs, but its underlying mechanisms of action remain unclear. CD36 in skeletal muscle is known to contribute to the etiology of insulin resistance by facilitating fatty acid uptake. This study investigated the effect of mangiferin on insulin resistance. The results showed that treatment of Wistar-Kyoto rats with mangiferin (15 mg/kg, once daily, by oral gavage) for 7 weeks inhibited chronic liquid fructose consumption-induced increases in plasma insulin concentrations at the baseline and during oral glucose tolerance test (OGTT), and the homeostasis model assessment of insulin resistance index. It also suppressed the increases in fasted plasma nonesterified fatty acid (NEFA) concentration and the adipose tissue insulin resistance index. Mechanistically, mangiferin neither affected intakes of fructose and chow, and the increase in epididymal and perirenal fat, nor attenuated fructose-induced hypertension. In contrast, mangiferin attenuated fructose-induced acceleration of plasma NEFA clearance during OGTT, and tended to decrease excessive triglyceride accumulation in gastrocnemius. Immunofluorescence staining and subsequent rating of CD36-expressing fibers in gastrocnemius revealed that mangiferin restored fructose-stimulated sarcolemmal CD36 overexpression and decreased intracellular CD36 distribution. In addition, the effects of mangiferin on the parameters associated with insulin resistance and abnormal fatty acid metabolism were absent in the spontaneously hypertensive rats carrying numerous nonfunctional mutations in the CD36 gene. Thus, these results suggest that mangiferin treatment mitigates insulin resistance in a rat model of fructose-induced metabolic syndrome by modulating sarcolemmal and intracellular CD36 redistribution in the skeletal muscle.

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Section: Discussionsupporting

confidence: 84%

Section: Introductionmentioning

confidence: 92%

Mitigation of Insulin Resistance by Mangiferin in a Rat Model of Fructose-Induced Metabolic Syndrome Is Associated with Modulation of CD36 Redistribution in the Skeletal Muscle

Zhou

Pan

Chonan

et al. 2015

Journal of Pharmacology and Experimental Therapeutics

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Section: Discussionmentioning

confidence: 59%

“…Similar effects of mangiferin in improving dyslipidemia were previously reported in streptozotocin diabetic rats (Guo et al 2011, Muruganandan et al 2005. Mangiferin may mediate its action on lipid profile through increasing fatty acid uptake in the liver via upregulation of the expression of fatty acid translocase (Guo et al 2011), downregulation of microsomal triglyceride transfer protein (MTP) and upregulation of hepatic PPAR-α expression (Guo et al 2011). According to the Randle's glucose-fatty acid cycle, increased plasma triglycerides and increased free fatty acid (FFA) oxidation impairs insulin action, glucose metabolism and utilization leading to hyperglycemia and consequently, reduction of triglycerides could participate to the hypoglycemic effect of mangiferin (Randle et al 1963).…”

Section: Discussionmentioning

confidence: 59%

Modulation of Diabetes and Dyslipidemia in Diabetic Insulin-Resistant Rats by Mangiferin: Role of Adiponectin and TNF-α

Saleh

El-Maraghy

Reda

et al. 2014

An. Acad. Bras. Ciênc.

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Mangiferin, present in Mangifera indica bark, was reported to produce hypoglycemic and antidiabetic activity in an animal model of genetic type 2 diabetes and in streptozotocin diabetic rats. Its effect on diabetic insulinresistant animals has not been investigated. The current work aimed to explore the effect of mangiferin on diabetic insulin-resistant rat model. Diabetes was induced by high-fat/high fructose diet for eight weeks followed by a subdiabetogenic dose of streptozotocin (HFD-Fr-STZ). Rats were treated with mangiferin (20 mg/kg i.p.) for 28 days starting one week after STZ and its effects were compared to the standard insulin sensitizer, rosiglitazone. HFD-Fr-STZ, induced obesity, hyperglycemia and insulin resistance accompanied by depletion in liver glycogen and dyslipidemia. Moreover, there was an elevation in serum TNF-α and a reduction in adiponectin. Mangiferin ameliorated the consequences of HFD-Fr-STZ and its actions were comparable to the effects of the standard insulin sensitizer, rosiglitazone. The results obtained in this study provide evidence that mangiferin is a possible beneficial natural compound for type 2 diabetes and metabolic disorders associated with the metabolic syndrome. This effect is mediated through improving insulin sensitivity, modulating lipid profile and reverting adipokine levels to normal.

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“…Alternatively HL can be induced by dietary means (e.g. chronic feeding of a high fat diet) (11,13,40,43) or by treatment with compounds such as Triton (14,26) or poloxamer 407 (P407) (16). P407, a non-ionic synthetic copolymer surfactant, provides an attractive means of inducing HL because of its rapid onset and seeming lack of overt toxicity; within 24 h of its intraperitoneal (i.p.)…”

Section: Introductionmentioning

confidence: 99%

The Single Dose Poloxamer 407 Model of Hyperlipidemia; Systemic Effects on Lipids Assessed Using Pharmacokinetic Methods, and its Effects on Adipokines

Chaudhary

Brocks

2013

J Pharm Pharm Sci

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-Purpose:The induction of hyperlipidemia using poloxamer 407 (P407) is gaining use for studying the effect of the condition on drug pharmacokinetics. Although a single intraperitoneal dose of P407 causes a rapid onset of hyperlipidemia, the initial lipid concentrations are much higher than seen in humans. The hyperlipidemia is also reversible in nature. Here, pharmacokinetic methods were used to assess the P407 dose response on serum lipids, adipokines and cytokines. Methods: Single 0.5 and 1 g/kg doses of P407 were injected into rats followed by blood collection at various times for up to 12 d. Serum was assayed for lipids, selected adipokines and cytokines. Results: As expected, large increases in lipid levels were seen by 36 h after dosing. Using area under the concentration vs. time curve as a measure of systemic lipid exposure, P407 increased serum baseline corrected serum lipids in a nearly dose proportional fashion. The maximum increase in lipids was observed at ~36 h, with most lipids remaining elevated for up to ~180 h, although for the 1 g/kg dose triglyceride concentrations had still not quite returned to baseline by 12 days postdose. In addition to changes in lipids, P407 significantly increased serum leptin and decreased the serum adiponectin concentrations but did not affect cytokine levels. Conclusion: Depending on study aims, for the use of the model it may be beneficial to perform single-dose assessments at time points later than 36 h when the lipoprotein concentrations will be more similar to those seen in patient with hyperlipidemia.

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Beneficial effects of mangiferin on hyperlipidemia in high‐fat‐fed hamsters

Abstract: The results suggest that mangiferin may ameliorate hypertriglyceridemia partly by modulating the expression levels of genes involved in lipid oxidation and lipogenesis.

Cited by 97 publications

References 42 publications

Mitigation of Insulin Resistance by Mangiferin in a Rat Model of Fructose-Induced Metabolic Syndrome Is Associated with Modulation of CD36 Redistribution in the Skeletal Muscle

Mitigation of Insulin Resistance by Mangiferin in a Rat Model of Fructose-Induced Metabolic Syndrome Is Associated with Modulation of CD36 Redistribution in the Skeletal Muscle

Modulation of Diabetes and Dyslipidemia in Diabetic Insulin-Resistant Rats by Mangiferin: Role of Adiponectin and TNF-α

The Single Dose Poloxamer 407 Model of Hyperlipidemia; Systemic Effects on Lipids Assessed Using Pharmacokinetic Methods, and its Effects on Adipokines

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