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We previously demonstrated that monosodium glutamate (MSG) consumption increases trimethylamine (TMA) level in the renal tissue as well as dimethylamine and methylamine levels in urine of rats, suggesting the effects of MSG on humans. To better define the findings, we investigated whether MSG consumption alters serum trimethylamine N-oxide (TMAO) level, and as a consequence, induces kidney injury in the rat model. Adult male Wistar rats (n = 40) were randomized to be fed with a standard diet (control group) or a standard diet with 0.5, 1.5 or 3.0 g% MSG corresponding to 7, 21, or 42 g/day in 60 kg man, respectively in drinking water (MSG-treated groups), or a standard diet with 3.0 g% MSG in drinking water which was withdrawn after 4 weeks (MSG-withdrawal group). Blood and urine samples were collected to analyze the TMAO levels using 1H NMR and markers of kidney injury. Fecal samples were also collected for gut microbiota analysis. We found serum TMAO levels increased and urinary TMAO excretion decreased during MSG consumption, in parallel with the increase of the neutrophil gelatinase-associated lipocalin (NGAL) excretion which subsided with the withdrawal of MSG. The fecal 16 S rRNA analysis during MSG consumption showed gut microbiota changes with a consistent suppression of Akkermansia muciniphila, a mucin producing bacteria, but not of TMA-producing bacteria. In conclusions, our findings suggested that prolonged high dose MSG consumption may cause TMAO accumulation in the blood via reduction of renal excretion associated with acute kidney injury. The mechanisms by which MSG reduced TMAO excretion require further investigation.

Background: Opisthorchis viverrini (O. viverrini, Ov) infection and consumption of high-fat and high-fructose (HFF) diet exacerbate liver and kidney disease. Here, we investigated the effects of a combination of O. viverrini infection and HFF diet on kidney pathology via changes in the gut microbiome and host proteome in hamsters. Methodology/Principal findings: Twenty animals were divided into four groups; 1) fed a normal diet not infected with O. viverrini (normal group), 2) fed an HFF diet and not infected with O. viverrini (HFF), 3) fed a normal diet and infected with O. viverrini (Ov), and 4) fed an HFF diet and infected with O. viverrini (HFFOv). DNA was extracted from fecal samples and the V3–V4 region of the bacterial 16S rRNA gene sequenced on an Illumina MiSeq sequencing platform. In addition, LC/MS-MS analysis was done. Histopathological studies and biochemical assays were also conducted. The results indicated that the HFFOv group exhibited the most severe kidney injury, manifested as elevated KIM-1 expression and accumulation of fibrosis in kidney tissue. The microbiome of the HFFOv group was more diverse than in the HFF group: there were increased numbers of Ruminococcaceae, Lachnospiraceae, Desulfovibrionaceae and Akkermansiaceae, but fewer Eggerthellaceae. In total, 243 host proteins were identified across all groups. Analysis using STITCH predicted that host proteome changes may lead to leaking of the gut, allowing molecules such as soluble CD14 and p-cresol to pass through to promote kidney disease. In addition, differential expression of TGF-beta-activated kinase 1 and MAP3K7-binding protein 2 (Tab2, involving renal inflammation and injury) are predicted to be associated with kidney disease. Conclusions/Significance: The combination of HFF diet and O. viverrini infection may promote kidney injury through alterations in the gut microbiome and host proteome. This knowledge may suggest an effective strategy to prevent kidney disease beyond the early stages. [ABSTRACT FROM AUTHOR]

Head louse infestations remain a global public-health concern due to increased resistance of lice to artificial pediculicides. In Thailand, there is a lack of comparative data on the current efficacy of pediculicides for treating head lice. In this study, we explored the status of botanical and toxic synthetic pediculicides with that of 4% dimeticone liquid gel for treating head lice in Thailand. The ex-vivo pediculicidal activity of various pediculicidal shampoos available at drugstores in Thailand was assessed and compared with that of 4% dimeticone liquid gel. The shampoos chosen were based on active ingredients toxic to lice (1% permethrin, 0.6% carbaryl, 0.15% Stemona root crude extract, or mixed plant extracts), whereas dimeticone acts physically on lice. We found that exposure to 4% dimeticone liquid gel following the manufacturer's instructions completely killed 100% of head lice in 15 min, whereas other pediculicide products failed to kill the great majority of head lice, whether treatment was for 10 min (resulting in 0% to 50.0% mortality) or 30 min (resulting in 17.0% to 60.0% mortality). We also extended a clinical assessment to confirm the efficacy of 1% permethrin for treating head lice in infested schoolchildren. In this clinical assessment, none of the 26 children treated with 1% permethrin shampoo achieved a cure after two applications. These results highlight that 4% dimeticone demonstrated a higher ex-vivo pediculicidal efficacy compared to both chemical and botanical pediculicides in Thailand. Conversely, 1% permethrin showed low efficacy in both laboratory and clinical assessments. Given its physical mode of action, 4% dimeticone merits consideration as an alternative treatment option for lice in Thailand, particularly in cases where treatment with toxic pediculicides has proven ineffective. [ABSTRACT FROM AUTHOR]