Salacia oblonga extract increases glucose transporter 4-mediated glucose uptake in L6 rat myotubes: Role of mangiferin

Girón, María D.; Sevillano, Natalia; Salto, Rafael; Haı̈dour, Ali; Manzano, Manuel; Jiménez, María Luisa Martín; Rueda, Ricardo; López-Pedrosa, J.M.

doi:10.1016/j.clnu.2009.04.018

Cited by 69 publications

(50 citation statements)

References 27 publications

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“…Following this treatment, plates were processed as described 27, 28. The protein concentration of the supernatants was measured using a bicinchoninic acid method (Bio‐Rad, Madrid, Spain).…”

Section: Methodsmentioning

confidence: 99%

Conversion of leucine to β-hydroxy-β-methylbutyrate by α-keto isocaproate dioxygenase is required for a potent stimulation of protein synthesis in L6 rat myotubes

Girón

Rienda

Salto

et al. 2015

Journal of Cachexia, Sarcopenia and Muscle

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BackgroundL‐Leu and its metabolite β‐hydroxy‐β‐methylbutyrate (HMB) stimulate muscle protein synthesis enhancing the phosphorylation of proteins that regulate anabolic signalling pathways. Alterations in these pathways are observed in many catabolic diseases, and HMB and L‐Leu have proven their anabolic effects in in vivo and in vitro models. The aim of this study was to compare the anabolic effects of L‐Leu and HMB in myotubes grown in the absence of any catabolic stimuli.MethodsStudies were conducted in vitro using rat L6 myotubes under normal growth conditions (non‐involving L‐Leu‐deprived conditions). Protein synthesis and mechanistic target of rapamycin signalling pathway were determined.ResultsOnly HMB was able to increase protein synthesis through a mechanism that involves the phosphorylation of the mechanistic target of rapamycin as well as its downstream elements, pS6 kinase, 4E binding protein‐1, and eIF4E. HMB was significantly more effective than L‐Leu in promoting these effects through an activation of protein kinase B/Akt. Because the conversion of L‐Leu to HMB is limited in muscle, L6 cells were transfected with a plasmid that codes for α‐keto isocaproate dioxygenase, the key enzyme involved in the catabolic conversion of α‐keto isocaproate into HMB. In these transfected cells, L‐Leu was able to promote protein synthesis and mechanistic target of rapamycin regulated pathway activation equally to HMB. Additionally, these effects of leucine were reverted to a normal state by mesotrione, a specific inhibitor of α‐keto isocaproate dioxygenase.ConclusionOur results suggest that HMB is an active L‐Leu metabolite able to maximize protein synthesis in skeletal muscle under conditions, in which no amino acid deprivation occurred. It may be proposed that supplementation with HMB may be very useful to stimulate protein synthesis in wasting conditions associated with chronic diseases, such as cancer or chronic heart failure.

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Section: Methodsmentioning

confidence: 99%

Conversion of leucine to β-hydroxy-β-methylbutyrate by α-keto isocaproate dioxygenase is required for a potent stimulation of protein synthesis in L6 rat myotubes

Girón

Rienda

Salto

et al. 2015

Journal of Cachexia, Sarcopenia and Muscle

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“…It has been reported that mangiferin increased PPAR-g response element-driven luciferase activity in L6-myotubes (Girón et al, 2009). However, a gene reporter assay demonstrated that mangiferin did not affect ciglitazone-induced activation of all three isoforms of PPARs (PPAR-g; PPAR-a, PPAR-b) (Wilkinson et al, 2008).…”

Section: Discussionmentioning

confidence: 99%

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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“…Mangiferin has been investigated extensively because of its remarkable pharmacological effects, including antioxidant [7,8], anti-inflammatory [9], antidiabetic [10], anticancer [11], antibacterial [12], anti-HIV [13], and radioprotective activities [14]. Notably, neomangiferin is likely biotransformed to mangiferin in vivo [7].…”

Section: Introductionmentioning

confidence: 99%

The Pharmacokinetics and Metabolism of Neomangiferin, a Major Bioactive Component in Anemarrhena asphodeloides

Gao¹,

Liu²

2016

Med chem

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Salacia oblonga extract increases glucose transporter 4-mediated glucose uptake in L6 rat myotubes: Role of mangiferin

Cited by 69 publications

References 27 publications

Conversion of leucine to β-hydroxy-β-methylbutyrate by α-keto isocaproate dioxygenase is required for a potent stimulation of protein synthesis in L6 rat myotubes

Conversion of leucine to β-hydroxy-β-methylbutyrate by α-keto isocaproate dioxygenase is required for a potent stimulation of protein synthesis in L6 rat myotubes

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

The Pharmacokinetics and Metabolism of Neomangiferin, a Major Bioactive Component in Anemarrhena asphodeloides

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