2023
DOI: 10.1016/j.lfs.2023.121414
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Intestinal microbiome diversity of diabetic and non-diabetic kidney disease: Current status and future perspective

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Cited by 5 publications
(3 citation statements)
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“…In a diabetic context, a shift from glucose to protein metabolism takes place. Thus, PCS is a protein-bound uremic solute that is produced in the small intestine following the phenylalanine-to-p-cresol route [ 34 ]. PCS excretion occurs by glomerular filtration and proximal tubule reabsorption through OAT receptors on the baso-lateral membrane of proximal tubular epithelial cells [ 35 ].…”
Section: Discussionmentioning
confidence: 99%
“…In a diabetic context, a shift from glucose to protein metabolism takes place. Thus, PCS is a protein-bound uremic solute that is produced in the small intestine following the phenylalanine-to-p-cresol route [ 34 ]. PCS excretion occurs by glomerular filtration and proximal tubule reabsorption through OAT receptors on the baso-lateral membrane of proximal tubular epithelial cells [ 35 ].…”
Section: Discussionmentioning
confidence: 99%
“…The research has revealed that the reduced abundance of Akkermansia muciniphila in T2D patients may be associated with blood glucose fluctuations. Das et al (2023) [ 19 ] has suggested the identification of novel biomarkers for early detection of diabetic kidney disease (DKD), as well as potential therapies to modulate the gut microbiota and improve host immune response. Ye et al (2023) [ 20 ] has identified the inadequacy of circulating dopamine, imbalanced short-chain fatty acid (SCFA) production, and excessive metabolic inflammation as multiple parallel impacts driven by the gut microbiota in the development of gestational diabetes mellitus (GDM).…”
Section: Discussionmentioning
confidence: 99%
“…Экспериментальное удаление УТ, в том числе низкомолекулярных (фосфат, триметиламин-N-оксид), крупномолекулярных (фактор роста фибробластов-23, цитокины -ИЛ-1, 6 и 18, ФНО-α и конечные продукты повышенного гликирования белков) и связанных с белками УТ (ИС, п-крезилсульфат -п-КС), уменьшает выраженность КС [9]. Ряд недавних исследований показал, что воздействие ФНО-α, ИЛ-6, ИЛ-18 и интерферона индуцирует кальцификацию КГМС на клеточных моделях и что данный процесс обратим при противовоспалительном лечении [10,11]. Совокупное воздействие крупномолекулярных УТ объясняет повышенный риск васкулопатии, особенно КC, наблюдаемой у пациентов с ХБП и ТПН [12].…”
Section: Discussionunclassified