Oral uridine-5′-monophosphate (UMP) increases brain CDP-choline levels in gerbils

Cansev, Mehmet; Watkins, Carol J.; Beek, Eline M. van der; Wurtman, Richard J.

doi:10.1016/j.brainres.2005.07.054

Cited by 58 publications

(76 citation statements)

References 38 publications

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“…Research published by several authors confirm previous findings that uridine can positively affect phosphatide synthesis in neuron membranes (CANSEV et al, 2005;CANSEV, 2006). Uridine, a pyrimidine nucleoside, crosses the blood-brain barrier (BBB) easily, being a precursor of UTP and CTP (CANSEV et al, 2005;CANSEV, 2006).…”

Section: Sgarbieri V C; Pacheco M T Bsupporting

confidence: 65%

Premature or pathological aging: longevity

Sgarbieri

Pacheco

2017

Braz. J. Food Technol.

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The main objective of this literature review was to summarize and characterize the main factors and events that may negatively influence quality of life and human longevity. The factors that act on premature aging processes are essentially the same as those of natural or healthy aging, but in a more intense and uncontrolled manner. Such factors are: 1) genetic (genome); 2) metabolic (metabolome); 3) environmental (life conditions and style, including diet). Factors 1 and 2 are more difficult to control by individuals; once depending on socioeconomic, cultural and educational conditions. Differently of environmental factors that may be totally controlled by individuals. Unfamiliarity with these factors leads to chronic and/or degenerative diseases that compromise quality of life and longevity.Keywords: Human longevity; Metabolic changes; Aging; Life quality; Diet. ResumoO principal objetivo desta revisão da literatura foi resumir e caracterizar os principais fatores e eventos que podem influenciar negativamente a qualidade de vida e a longevidade humana. Os fatores que atuam nos processos de envelhecimento prematuro são essencialmente os mesmos que aqueles relacionados ao envelhecimento saudável ou natural, mas em uma maior intensidade ou maneira descontrolada. Tais fatores são: 1) genéticos (genoma); 2) metabólicos (metaboloma); 3) ambientais (condições e estilos de vida, incluindo a alimentação). Os fatores dos itens 1 e 2 são mais difíceis de ser controlados, pois dependem das condições socioeconômicas, culturais e educacionais. Diferentemente dos fatores ambientais que podem ser controlados pelo indivíduo. A falta de familiaridade com esses fatores leva a doenças crônicas e/ou degenerativas que comprometem a qualidade de vida e a longevidade. Palavras-chave:Longevidade; Alterações metabólicas; Envelhecimento; Qualidade de vida; Alimentação.

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Section: Sgarbieri V C; Pacheco M T Bsupporting

confidence: 65%

Premature or pathological aging: longevity

Sgarbieri

Pacheco

2017

Braz. J. Food Technol.

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“…That the source of the additional choline is choline bound in membrane phosphatides, mainly PtdCho, is suggested by the increased synthesis (Cansev et al, 2005) and levels and Fig. 4) of this phosphatide after chronic pretreatment with dietary UMP.…”

Section: Discussionmentioning

confidence: 95%

“…UMP pretreatment most likely affects membrane phosphatide production as well as neurite outgrowth in PC-12 cells and hippocampal dendritic spine formation in vivo (Sakamoto and Wurtman, 2006) by two mechanisms: by increasing CTP levels, it increases the formation of CDP-choline (Cansev et al, 2005); and by increasing brain UTP, it activates metabotropic P2Y receptors . Oral UMP is rapidly absorbed, appearing in the circulation as uridine (Sonoda and Tatibana, 1978).…”

Section: Discussionmentioning

confidence: 99%

“…Consumption of UMP (2000 mg) by humans raises plasma uridine levels by 3 fold (from 6.0 to 21.9 μM), for 5-6 hours (Cansev, 2006). Circulating uridine crosses the blood-brain barrier via an adenosine transporter (the concentrative nucleoside transporter type 2; CNT2) (Li et al, 2001), which is unsaturated at physiologic plasma uridine concentrations (Cansev et al, 2005). Thus, dietary UMP can increase brain levels of uridine and subsequently, as shown in gerbils, brain levels of UTP, CTP and CDP-choline (Cansev et al, 2005).…”

Section: Discussionmentioning

confidence: 99%

“…Giving rodents like Mongolian gerbils a single dose of the uridine source uridine-5′-monophosphate (UMP) by gavage, increases their brain levels of CDP-choline by 50% (Cansev et al, 2005); chronic consumption of UMP via the diet (0.5%, with or without gavaged DHA) increases by 13-48% brain levels of PtdCho and other phosphatides including phosphatidylethanolamine (PtdEtn), phosphatidylserine (PtdSer), and phosphatidylinositol (PtdIns) . Daily administration of UMP and DHA for two weeks also increases dendritic spine densities in the CA1 region of adult gerbil hippocampus (Sakamoto and Wurtman, 2006) and, after 3-4 weeks, the concentrations of synaptic proteins including synapsin-I and PSD-95 .…”

Section: Introductionmentioning

confidence: 99%

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Dietary supplementation with uridine-5′-monophosphate (UMP), a membrane phosphatide precursor, increases acetylcholine level and release in striatum of aged rat

2007

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The biosynthesis of brain membrane phosphatides, e.g., phosphatidylcholine (PtdCho), may utilize three circulating compounds: choline, uridine (a precursor for UTP, CTP, and CDP-choline), and a PUFA (e.g., docosahexaenoic acid); moreover oral administration of the uridine source uridine-5′-monophosphate (UMP) can significantly increase levels of the phosphatides throughout the rodent brain. Since PtdCho can provide choline for acetylcholine (ACh) synthesis, we determined whether UMP administration also affects ACh levels in striatum and striatal extracellular fluid, in aged and young rats. Among aged animals consuming a UMP-containing diet (2.5%, w/w) for 1 or 6 weeks, baseline ACh levels in striatal dialysates rose from 73 fmol/min to 148 or 197 fmol/min (P<0.05). Consuming a lower dose (0.5%) for 1 week produced a smaller but still significant increase (from 75 to 92 fmol/min, P<0.05), and elevated striatal Ach content (by 16%; P<0.05). Dietary UMP (0.5%, 1 week) also amplified the increase in ACh caused by giving atropine (10 μM in the aCSF); atropine alone increased ACh concentrations from 81 to 386 fmol/min in control rats and from 137 to 680 fmol/min in those consuming UMP (P<0.05). Young rats eating the UMP-containing diet exhibited similar increases in basal ECF ACh (from 105 to 118 fmol/min) and in the increase produced by atropine (from 489 to 560 fmol/min; P<0.05). These data suggest that giving a uridine source may enhance some cholinergic functions, perhaps by increasing brain phosphatide levels. Scope: Section 3 (Neurophysiology, Neuropharmacology and other forms of Intercellular Communication)

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