Abstract

The short- and long-term consumption of monosodium glutamate (MSG) increases urinary pH but the effects on the metabolic pathways in the liver, kidney and the gut microbiota remain unknown. To address this issue, we investigated adult male Wistar rats allocated to receive drinking water with or without 1 g% MSG for 2 weeks (n = 10, each). We performed a Nuclear Magnetic Resonance (NMR) spectroscopy-based metabolomic study of the jejunum, liver, and kidneys, while faecal samples were collected for bacterial DNA extraction to investigate the gut microbiota using 16S rRNA gene sequencing. We observed significant changes in the liver of MSG-treated rats compared to controls in the levels of glucose, pyridoxine, leucine, isoleucine, valine, alanine, kynurenate, and nicotinamide. Among kidney metabolites, the level of trimethylamine (TMA) was increased, and pyridoxine was decreased after MSG-treatment. Sequencing of the 16S rRNA gene revealed that MSG-treated rats had increased Firmicutes, the gut bacteria associated with TMA metabolism, along with decreased Bifidobacterium species. Our data support the impact of MSG consumption on liver and kidney metabolism. Based on the gut microbiome changes, we speculate that TMA and its metabolites such as trimethylamine-N-oxide (TMAO) may be mediators of the effects of MSG on the kidney health.

Highlights

  • The gut bacteria produce TMA from dietary fish or it can be generated from other nutrients including choline and carnitine, which are abundant in eggs and red meat [16]

  • The major part of TMA is enzymatically converted to the odourless trimethylamine-N-oxide (TMAO), and high TMAO plasma levels are associated with cardiovascular disease (CVD) [17], chronic kidney disease (CKD) [18] and diabetes [19]

  • monosodium glutamate (MSG)-treated and control rats had a similar amount of food intake

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Summary

Introduction

Attempts have been made to reveal the effects of MSG on metabolic organs of animals by either parenteral [9,10] or oral intake [11,12]. In one of such efforts to investigate the effects of MSG in rat kidneys, the results showed that both short- [13] and longterm [11] MSG consumption caused alkaline urine in rats, the mechanism of urine alkalinization is not established. The short-term MSG consumption caused specific changes in urinary metabolites including dimethylamine (DMA) and methylamine (MA), which are gut-derived metabolites from trimethylamine (TMA). The major part of TMA is enzymatically converted to the odourless trimethylamine-N-oxide (TMAO), and high TMAO plasma levels are associated with cardiovascular disease (CVD) [17], chronic kidney disease (CKD) [18] and diabetes [19]

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