Abstract

BackgroundFructose-mediated protein glycation (fructation) has been linked to an increase in diabetic and cardiovascular complications due to over consumption of high-fructose containing diets in recent times. The objective of the present study is to evaluate the protective effect of (R)-α-lipoic acid (ALA) against fructose-induced myoglobin fructation and the formation of advanced glycation end products (AGEs) in vitro.MethodsThe anti-glycation activity of ALA was determined using the formation of AGEs fluorescence intensity, iron released from the heme moiety of myoglobin and the level of fructosamine. The fructation-induced myoglobin oxidation was examined using the level of protein carbonyl content and thiol group estimation.ResultsThe results showed that co-incubation of myoglobin (1 mg/mL), fructose (1 M) and ALA (1, 2 and 4 mM) significantly inhibited the formation of AGEs during the 30 day study period. ALA markedly decreased the levels of fructosamine, which is directly associated with the reduction of AGEs formation. Furthermore, ALA significantly reduced free iron release from myoglobin which is attributed to the protection of myoglobin from fructose-induced glycation. The results also demonstrated a significant protective effect of ALA on myoglobin oxidative damages, as seen from decreased protein carbonyl content and increased protein thiols.ConclusionThese findings provide new insights into the anti-glycation properties of ALA and emphasize that ALA supplementation is beneficial in the prevention of AGEs-mediated diabetic and cardiovascular complications.

Highlights

  • Fructose-mediated protein glycation has been linked to an increase in diabetic and cardiovascular complications due to over consumption of high-fructose containing diets in recent times

  • Effect of α-lipoic acid on fluorescent advanced glycation end products (AGEs) formation The effect of (R)-αLipoic acid (ALA) on the formation of fluorescent AGEs in myoglobin-fructose glycation system was observed on day-30 of incubation

  • ALA co-treatment in the myoglobin-fructose glycation system at 1, 2 and 4 mM concentrations elicited significant (p < 0.01) concentration-dependent inhibition of fluorescent AGEs formation with a maximum reduction of 49.7% (4641.7 ± 590.2 vs 9226.7 ± 398.4) at 4 mM concentration compared with the fructated control

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Summary

Introduction

Fructose-mediated protein glycation (fructation) has been linked to an increase in diabetic and cardiovascular complications due to over consumption of high-fructose containing diets in recent times. The objective of the present study is to evaluate the protective effect of (R)-α-lipoic acid (ALA) against fructose-induced myoglobin fructation and the formation of advanced glycation end products (AGEs) in vitro. The Amadori product undergoes oxidative cleavage, generating dicarbonyl compounds to form cross-linked structures termed advanced glycation end products (AGEs). In a high glucose and/or fructose environment, Ghelani et al BMC Complementary and Alternative Medicine (2018) 18:13 the amino group of myoglobin readily undergoes a nonenzymatic reaction which results in its structural and functional modification in vitro [13, 14]. Glucose and fructose-mediated glycation induces oxidative modification of myoglobin by generating protein carbonyl compounds which may be associated with oxidative stress [13, 17]. Intracellular myoglobin glycation in muscles cell, in hyperglycaemic condition and its implications in the development of complications, is still not known

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