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PubMed2003

Imaging of gynecologic tumors: comparison of (11)C-choline PET with (18)F-FDG PET.

UNLABELLED: This study was designed to compare the value of PET using (11)C-choline with that of PET using (18)F-FDG for the diagnosis of gynecologic tumors. METHODS: We examined 21 patients, including 18 patients with untreated primary tumors and 3 patients with suspected recurrence of ovarian cancer. (11)C-choline PET and (18)F-FDG PET were performed within 2 wk of each other on each patient. The patients fasted for at least 5 h before the PET examinations, and PET was performed 5 min ((11)C-choline) and 60 min ((18)F-FDG) after injection of each tracer. PET images were corrected for the transmission data, and the reconstructed images were visually analyzed. Then, the standardized uptake value (SUV) was calculated for quantitative assessment of tumor uptake. PET results were compared with surgical histology or >6 mo of clinical observations. RESULTS: Of 18 untreated patients, (11)C-choline PET correctly detected primary tumors in 16 patients, whereas (18)F-FDG PET detected them in 14 patients. In 1 patient with small uterine cervical cancer and 1 diabetic patient with uterine corpus cancer, only (11)C-choline PET was true-positive. Both tracers were false-negative for atypical hyperplasia of the endometrium in 1 patient and were false-positive for pelvic inflammatory disease in 1 patient. For the diagnosis of recurrent ovarian cancer (n = 3), (11)C-choline PET and (18)F-FDG PET were true-positive in 1 patient, whereas neither tracer could detect cystic recurrent tumor and microscopic peritoneal disease in the other 2 patients. In the 15 patients with true-positive results for both tracers, tumor SUVs were significantly higher for (18)F-FDG than for (11)C-choline (9.14 +/- 3.78 vs. 4.61 +/- 1.61, P < 0.0001). In 2 patients with uterine cervical cancer, parailiac lymph node metastases were clearly visible on (18)F-FDG PET but were obscured by physiologic bowel uptake on (11)C-choline PET. CONCLUSION: The use of (11)C-choline PET is feasible for imaging of gynecologic tumors. Unlike (18)F-FDG PET, interpretation of the primary tumor on (11)C-choline PET is not hampered by urinary radioactivity; however, variable background activity in the intestine may interfere with the interpretation.

Adenocarcinoma↗
PubMed1975

[A spectrophotometric method for the determination of serum cholinesterase variants with succinyl choline as substrate (author's transl)].

A simple and rapid method for the estimation of the hydrolysis of succinyl choline by serum cholinesterase variants is described. Succinyl choline, as substrate for the enzyme assay, has many advantages over other substrates (acetyl choline, benzoyl choline and butyryl choline) which have no clinical application. Choline, the hydrolytic product of succinyl choline, is oxidized to betaine aldehyde by choline oxidase (EC 1.1.99.1), a rat liver mitochondrial preparation; this is coupled to the reduction of cytochrome c which is measured at 550 nm. Fifty normal sera (UU), 17 heterozygous (UA) and 8 atypical (AA) were tested with this method, and on the basis of resistance to dibucaine (Cinchocain; Kalow, W. & Genest, K. (1957) Canad. J. Biochem. Physiol. 35, 339-346) inhibition, three distinct groups could be established using succinyl choline as substrate. These results are comparable with the standard optical method of Kalow & Genest (cf. above) using benzoyl choline as substrate.

Anesthesia↗
PubMed1991

Choline incorporation into phospholipids in brain areas from spontaneously hypertensive rats: effect of oxiracetam treatment.

It has been demonstrated that spontaneously hypertensive rats (SHR) develop severe hypertension and cerebrovascular lesions on drinking 1% NaCl from weaning. These animals present a learning and memory impairment as well as impairment of both energy metabolism and membrane phospholipid turnover. We tested both choline uptake into the cells and incorporation into choline phosphoglyceride (CPG) by incubating slices from hippocampus and cortex. After 5 min of incubation, a noticeable decrease in free labelled choline content inside the cells as well as its incorporation into phospho-choline (PC) and CPG were found in the brain of SHR, as compared to Wistar-Kyoto (WK) rats. This may indicate that in the SHRs with cerebrovascular lesions there is a reduction in choline uptake which in turn causes a decline in CPG biosynthesis through de novo pathway. Oxiracetam treatment is able to restore the labeled choline content in the cells from SH rats, as well as the incorporation of choline into its derivatives PC and CPG, to the levels found in the WK or more. Tests performed in the presence of such a high affinity choline uptake as hemicholinium (HC) confirmed the capacity of oxiracetam to stimulate choline uptake into the cells even if the results obtained up to now are not sufficient to hypothesize a direct effect of oxiracetam on acetylcholine metabolism. In conclusion, from the results obtained it would seem reasonable to hypothesize that the effects of the drug above mentioned on the cholinergic system may be secondary to its effect on choline phosphoglycerides biosynthesis.

Animals↗
PubMed1987

Phosphatidylcholine as a precursor of choline for acetylcholine synthesis.

It has been hypothesized that the selective vulnerability of certain brain cholinergic neurons in Alzheimer's disease may reflect the unique way that choline is utilized by these neurons, i.e. not only as a component of major membrane phospholipids, e.g. phosphatidylcholine (PC), but also as a precursor of their neurotransmitter, acetylcholine (ACh). A prolonged utilization of choline liberated from PC, for ACh production, without adequate resynthesis of this lipid, might result in a net loss of the phosphatide followed by an impairment of membrane function and loss of cellular viability. Studies described in this paper, performed on electrically stimulated striatal slices and on cholinergic cell lines, test this hypothesis. 1) Electrically-stimulated striatal slices continue to release ACh, and sustain their free choline and ACh levels, even when perfused with a choline-free medium. Striatal levels of PC decline under these circumstances, and this decline can be blocked by adding tetrodotoxin (which blocks neuronal depolarization) or choline to the medium. The other major membrane phospholipids, phosphatidylserine and phosphatidylethanolamine, also decline proportionately to PC when slices are stimulated in the absence of choline. 2) In a population of purely cholinergic cells (human neuroblastoma, LA-N-2), ACh can be synthesized from choline derived from degradation of endogenous PC formed de novo by methylation of phosphatidylethanolamine. 3) PC content of cells in culture (neuroblastoma X glioma hybrid, NG 108-15) can be altered by adding various amounts of choline to the growth media. The proportion of PC in the cells apparently affects cellular survival and rate of growth. Taken together these data demonstrate that cholinergic neurons utilize the choline stored in PC to synthesize ACh; that this process may lead to a depletion in membrane phospholipids (when choline supply is inadequate); and that the resulting changes in neuronal membrane composition might adversely affect cellular viability.

Acetylcholine↗
PubMedDate not supplied

Effect of ethanol on the renal excretion and metabolism of choline in the isolated perfused rat kidney.

The isolated perfused rat kidney was used to investigate the effect of ethanol on the renal excretion and metabolism of choline. Choline at an initial perfusate concentration of 2.8 mM, with tracer amounts of [methyl-14C]choline, was recirculated through kidneys and radioactivity measured in perfusate, urine, and kidney. 14C-Choline and its metabolites were identified by chromatographic and electrophoretic procedures. Tubular excretion of choline was demonstrated and a transport maximum (Tm) of 1.6 mumol/kidney/min was reached at a choline perfusate concentration of 1.2 mM. Addition of 50 mM ethanol resulted in a 56% increase in the choline Tm and 100 mM ethanol decreased the choline Tm by 25%. The rate of loss of 14C-choline from the perfusate was increased by the lower ethanol concentration and decreased by the higher ethanol concentration. Ethanol at both concentrations diminished the amount of 14C remaining in the kidney. 14C-Betaine was the major choline metabolite and the only 14C-metabolite present in perfusate or urine. Addition of either 50 or 100 mM ethanol increased both glomerular filtration rate and urine volume.

Animals↗
PubMed1983

Relationships between choline uptake, acetylcholine synthesis and acetylcholine release in isolated rat atria.

Isolated rat atria take up [3H]choline and synthesize [3H]acetylcholine (ACh). The uptake of [3H]choline has a high-affinity component with a Km of approximately 0.2 microM and a Vmax of approximately 6 fmol/min/mg wet wt. This high-affinity component of choline uptake is difficult to measure directly because it represents only a small portion of total [3H]choline uptake. However, the rate of synthesis of [3H] ACh from [3H]choline appears to reflect the activity of the high-affinity choline uptake system. Thus, [3H]ACh synthesis is most efficient at low choline concentrations and is inhibited in the presence of hemicholinium-3 and low NaCl medium. The neuronal localization of the [3H]Ach synthesized from [3H]choline is demonstrated by the finding that [3H]ACh is released from the atria by depolarization with 57 mM K+ medium. The release is Ca++ -dependent and there is a compensatory increase in the synthesis of [3H]ACh after depolarization-induced ACh release. These data suggest that [3H]choline can be specifically incorporated into a releasable pool of [3H]ACh localized in cardiac parasympathetic neurons. The synthesis of [3H]ACh is inhibited by blockade of high-affinity choline uptake and is regulated in response to neuronal activity. The application of these methods will provide a means for directly examining the physiological and pharmacological control of ACh synthesis and release from cardiac parasympathetic neurons.

Acetylcholine↗
PubMed1982

The activation of presynaptic choline uptake by acetylcholine release.

1. Acetylcholine release evoked from nerve terminals in vivo or in vitro results in a subsequent activation of choline uptake. 2. The activation of choline transport is not due to any obligatory coupling with acetylcholine synthesis because incoming choline is diluted with endogenous choline. 3. The choline carrier demonstrates trans-activation, i.e. influx stimulates efflux and vice versa. Acetylcholine is a weak competitor for the choline binding site and is hardly transported. 4. The binding of acetylcholine without concomitant transport has the effect of immobilizing the carrier on the side of the high acetylcholine concentration inside the terminal so that it is not available for the transport of choline from the outside. When intraterminal acetylcholine concentration is reduced by the release process the immobilization of the carrier is relieved thus enabling it to return to the outside of the membrane and activate choline uptake. 5. The choline carrier has been solubilized and incorporated into an artificial membrane system (liposomes). In liposomes the carrier demonstrates saturability, inhibition by hemicholinium-3 and trans-activation. The choline transported is not acetylated nor does S-acetyl-CoA increase the rate. Influx is stimulated by Na+ on the outside and K+ on the inside.

Acetylcholine↗
PubMed1995

Effect of choline supplementation on fatigue in trained cyclists.

The availability of choline, the precurser of the neurotransmitter, acetylcholine, in the diet is sufficient to provide the body's requirements under normal conditions. However, preliminary evidence indicates that depletion of choline may limit performance, while oral supplementation may delay fatigue during prolonged efforts. A double-blind cross-over design was used to determine the relationship between plasma choline and fatigue during supramaximal brief and submaximal prolonged activities. Twenty male cyclists (ages 23-29) with maximal aerobic power (VO2max) between 58 and 81 ml.min-1.kg-1 were randomly divided into BRIEF (N = 10) and PROLONGED (N = 10) groups. One hour after drinking a beverage with or without choline bitartrate (2.43 g), cyclists began riding at a power output equivalent to approximately 150% (BRIEF) and 70% (PROLONGED) of VO2max at a cadence of 80-90 rpm. Time to exhaustion, indirect calorimetry and serum choline, lactate, and glucose were measured. Increases in choline levels of 37 and 52% were seen within one hour of ingestion for BRIEF and PROLONGED groups, respectively. Neither group depleted choline during exercise under the choline or placebo conditions. Fatigue times and work performed under either test condition for the BRIEF or PROLONGED groups were similar. Consequently, trained cyclists do not deplete choline during supramaximal brief or prolonged submaximal exercise, nor do they benefit from choline supplementation to delay fatigue under these conditions.

Administration, Oral↗
PubMed1994

Brain mapping activity and mental performance after chronic treatment with CDP-choline in Alzheimer's disease.

CDP-choline participates in brain phospholipid metabolism and acts as an endogenous intermediate in a biosynthetic pathway incorporating free choline into phosphatidylcholine and choline plasmalogens in several tissues, including the central nervous system (CNS). In patients with chronic cerebrovascular disorders, CDP-choline reduces the slow delta frequencies and increases alpha activity in spectral electroencephalogram analysis. We have studied the effect of CDP-choline (cytidine-S-diphosphate-choline; 1000 mg/day x 30 days, p.o.) on brain electrical activity mapping and mental performance in 19 Alzheimer's disease (AD) patients (10 males/9 females; age: 66.21 +/- 1.48 years; Mini-Mental State Examination (MMSE): 26.55 +/- 1.22, Spanish version max. score 35). EEG was registered from 19 electrodes placed according to the 10-20 system and digitalized online. Artefact-free 2-s periods were visually selected, submitted to a frequency analysis and averaged across periods. CDP-choline significantly decreased spectral amplitude in the theta band in F4, F8, and T4 electrodes, and did not modify relative power parameters in any of the frequency bands (delta, theta, alpha, beta) as compared to basal recordings. In patients with late-onset AD (LOAD; N = 6; age: 73.5 +/- 1.34 years; MMSE: 28.75 +/- 2.33), CDP-choline tended to increase relative alpha power in O1 and O2 electrodes. No changes were found in early-onset AD patients (EOAD; N = 13; age: 62.85 +/- 1.21 years; MMSE: 25.54 +/- 1.4). We detected a significant improvement in mental performance after 1 month of treatment with CDP-choline in patients with early-onset AD in whom brain electrical activity data correlated with cognitive parameters. It is likely that the bioelectrical changes induced by CDP-choline in AD are the result of its immunogenic and/or neurotrophic activity in the vicinity of the vascular microenvironment.

Aged↗
PubMed1999

Choline deficiency-induced apoptosis in PC12 cells is associated with diminished membrane phosphatidylcholine and sphingomyelin, accumulation of ceramide and diacylglycerol, and activation of a caspase.

It is not well appreciated that nutritional status can modulate apoptosis, a process that eliminates unwanted or damaged cells. Choline is an essential nutrient, and its absence induces apoptosis. When PC12 cells were cultivated in a choline-free medium, apoptosis was induced (27.4% of cells apoptotic at 72 h as compared to 4.4% in control medium). In choline-free medium at 72 h, there was a 49% decrease in phosphatidylcholine concentration (P<0.01) and a 34% decrease in sphingomyelin concentration (P<0.01); however, there was no change in phosphatidylethanolamine concentration. Before detecting increased apoptosis in choline-deficient cells, we measured a significant increase in ceramide (218% control) and diacyglycerol (155% control) concentrations. The addition of a cell-permeable ceramide to cells in control medium induced apoptosis; however, adding a cell-permeable diacyglycerol did not induce apoptosis. Caspase is a common mediator of apoptosis, and choline deficiency-induced apoptosis was prevented completely by replacing choline or adding a caspase inhibitor into the medium within 48 h of initial choline deprivation. In those cells rescued by replacing choline at 36 h, the concentrations of phosphatidylcholine, sphingomyelin, ceramide, and diacyglycerol returned to levels of control cells. In those cells rescued by adding a caspase inhibitor at 36 h, the concentrations of sphingomyelin and ceramide returned to control levels, but the concentrations of phosphatidylcholine and diacyglycerol did not return to normal. We propose that availability of dietary factors (choline in this model) can modulate apoptosis. Mechanisms that we identify using this model may help us to explain why dietary choline influences brain development.

Amino Acid Chloromethyl Ketones↗
PubMed1990

Choline deficiency causes translocation of CTP:phosphocholine cytidylyltransferase from cytosol to endoplasmic reticulum in rat liver.

The choline-deficient rat liver has been chosen as a physiologically relevant model system in which to study the regulation of phosphatidylcholine biosynthesis. When 50-g rats were placed on a choline-deficient diet for 3 days, the activity of CTP:phosphocholine cytidylyltransferase (CT) was increased 2-fold in the microsomes and decreased proportionately in the cytosol. A low titer antibody to CT was obtained from chickens and used to identify the amount of CT protein in cytosol from rat liver. The amount of CT recovered from the choline-deficient cytosol was significantly less than in cytosol from choline-supplemented rats. When hepatocytes were prepared from choline-deficient livers, supplementation of the medium of the cells with choline caused CT to move from the membranes to cytosol within 1-2 h. The activity of another translocatable enzyme of glycerolipid metabolism, phosphatidate phosphohydrolase, was unchanged in cytosol from choline-deficient rat livers, and the microsomal activity of this enzyme was only minimally increased. When the livers were fractionated into endoplasmic reticulum and Golgi, there was a 2-fold increase in the activity on the endoplasmic reticulum from choline-deficient livers but no change in activity associated with Golgi. Thus, the increased association of CT with endoplasmic reticulum in choline-deficient livers appears to be specific to that subcellular fraction, and the subcellular location of other enzymes may not be affected.

Animals↗
PubMed1991

Comparative Physiological Evidence that beta-Alanine Betaine and Choline-O-Sulfate Act as Compatible Osmolytes in Halophytic Limonium Species.

The quaternary ammonium compounds accumulated in saline conditions by five salt-tolerant species of Limonium (Plumbaginaceae) were analyzed by fast atom bombardment mass spectrometry. Three species accumulated beta-alanine betaine and choline-O-sulfate; the others accumulated glycine betaine and choline-O-sulfate. Three lines of evidence indicated that beta-alanine betaine and choline-O-sulfate replace glycine betaine as osmo-regulatory solutes. First, tests with bacteria showed that beta-alanine betaine and choline-O-sulfate have osmoprotective properties comparable to glycine betaine. Second, when beta-alanine betaine and glycine betaine accumulators were salinized, the levels of their respective betaines, plus that of choline-O-sulfate, were closely correlated with leaf solute potential. Third, substitution of sulfate for chloride salinity caused an increase in the level of choline-O-sulfate and a matching decrease in glycine betaine level. Experiments with (14)C-labeled precursors established that beta-alanine betaine accumulators did not synthesize glycine betaine and vice versa. These experiments also showed that beta-alanine betaine synthesis occurs in roots as well as leaves of beta-alanine betaine accumulators and that choline-O-sulfate and glycine betaine share choline as a precursor. Unlike glycine betaine, beta-alanine betaine synthesis cannot interfere with conjugation of sulfate to choline by competing for choline and does not require oxygen. These features of beta-alanine betaine may be advantageous in sulfate-rich salt marsh environments.

Journal Article↗
PubMed1998

Uptake of choline and its conversion to glycine betaine by bacteria in estuarine waters.

The uptake and degradation of nanomolar levels of [methyl-C]choline in estuarine water samples and in seawater filtrate cultures composed mainly of natural free-living bacteria was studied. Uptake of [C]choline exhibited Michaelis-Menten kinetics, with K(t) + S(n) values of 1.7 to 2.9 nM in filtrate cultures and 1.7 to 4.1 nM in estuarine-water samples. V(max) values ranged from 0.5 to 3.3 nM . h. The uptake system for choline in natural microbial assemblages therefore displays very high affinity and appears able to scavenge this compound at the concentrations expected in seawater. Uptake of choline was inhibited by some natural structural analogs and p-chloromercuribenzoate, indicating that the transporter may be multifunctional and may involve a thiol binding site. When 11 nM [C]choline was added to water samples, a significant fraction (>50%) of the methyl carbon was respired to CO(2) in incubations lasting 10 to 53 h. Cells taking up [C]choline produced [C]glycine betaine ([C]GBT), and up to 80% of the radioactivity retained by cells was in the form of GBT, a well-known osmolyte. Alteration of the salinity in filtrate cultures affected the relative proportion of [C]choline degraded or converted to [C]GBT, without substantially affecting the total metabolism of choline. Increasing the salinity from 14 to 25 or 35 ppt caused more [C]GBT to be produced from choline but less CO(2) to be produced than in the controls. Lowering the salinity to 7 ppt decreased [C]GBT production and increased CO(2) production slightly. Intracellular accumulations of [C]GBT in the salt-stressed cultures were osmotically significant (34 mM). Choline may be used as an energy substrate by estuarine bacteria and may also serve as a precursor of the osmoprotectant GBT, particularly as bacteria are mixed into higher-salinity waters.

Journal Article↗
PubMed1995

Incorporation of a phosphonium analogue of choline into the rat brain as measured by magnetic resonance spectroscopy.

A clear understanding of choline metabolism is important in our goal to modify demyelination and remyelination in multiple sclerosis. To develop a technique capable of measuring metabolic changes in the brain, we have studied the incorporation of a phosphonium analogue of choline (P-choline) in tissue extracts of rats. After feeding adult rats a choline-deficient diet supplemented with P-choline, the analogue was not detectable by in vivo volume-localized 1H spectroscopy. However, in vitro 31P measurements of brain extracts revealed an 11% incorporation of P-choline into phosphatidylcholine. We report that P-choline incorporates preferentially into the lipid pool over the lipid precursor pool and we provide evidence that the choline peak resolved by in vivo 1H spectroscopy is only composed of small molecular weight choline-containing compounds.

Animals↗
PubMed1995

Staphylococcal enterotoxin-B (SEB) alters [14C]-choline transport and phosphatidylcholine metabolism in cultured human kidney proximal tubular cells.

We studied the effects of SEB on [14C]-choline transport and metabolism of choline containing phospholipids in cultured human kidney proximal tubular (PT) cells. SEB increased the uptake of [14C]-choline in PT cells as a function of toxin concentration, incubation time, and pH. The maximum increase in uptake (3.5-5-fold compared to control) was observed at a toxin concentration of 10 micrograms/10(4) cells, at 4 h and at pH 7.4. Two toxins structurally related to SEB, Staphylococcal enterotoxin-A and toxic shock toxin (TST-1) failed to alter [14C]-choline uptake in PT cells, a finding which indicates that SEB-mediated alteration in choline uptake in PT cells has high specificity. We found that SEB markedly and significantly increased the incorporation of [14C]-choline into phosphatidylcholine, Iysophosphatidylcholine and sphingomyelin, but not into phosphatidylethanolamine. Maximum increase in the incorporation of [14C]-choline into phosphatidylcholine (3-fold compared to control) was observed at 4 h after incubation with toxin. In contrast, SEB did not alter the incorporation of [14C]-choline in phosphatidylethanolamine. The cellular level of phosphatidylcholine was also increased (2-fold compared to control) in PT cells incubated with SEB. This was accompanied by a 3-to-4-fold increase in CTP; phosphocholine, cytidyltransferase activity. In sum, SEB specifically stimulates phosphatidylcholine synthesis in PT cells by increasing choline uptake or by activating CTP: phosphocholine, cytidyltransferase, or both. We believe this is the first-ever report indicating that a toxin can increase phosphatidylcholine synthesis.(ABSTRACT TRUNCATED AT 250 WORDS)

Biological Transport, Active↗
PubMed1992

Vitamin B12 improves cognitive disturbance in rodents fed a choline-deficient diet.

The effect of vitamin B12 on learning disturbance was tested in rats. Rats were fed a choline-enriched, choline-deficient, and choline-deficient diet with vitamin B12. Concentrations of acetylcholine in the brain were significantly lower in rats fed a choline-deficient diet than rats fed a choline-enriched diet. Passive avoidance learning shows that rats on a choline-deficient diet showed significantly impaired learning compared to rats on a choline-enriched diet. However, there was no significant difference of acetylcholine in the brain or in the passive avoidance learning between rats fed a choline-enriched and a choline-deficient with vitamin B12 diet. We, therefore, suggest that vitamin B12 potentiates learning in an acetylcholine-deprived brain.

Acetylcholine↗
PubMed2026

Source- and Solubility-specific Choline, Gut Microbiota, and Dyslipidemia Risk: Trimethylamine N-oxide-associated and Non-trimethylamine N-oxide-Associated Patterns in a Prospective Cohort Study.

BACKGROUND: Dietary choline, a major precursor of the gut microbial metabolite trimethylamine N-oxide (TMAO), is implicated in dyslipidemia risk; however, source- and form-specific associations and interactions with gut microbiota remain unclear. OBJECTIVES: The aim of this study was to examine longitudinal associations of source- and form-specific dietary choline with plasma TMAO and dyslipidemia and to identify gut microbiota interactions. METHODS: Using data from the China Health and Nutrition Survey (2018-2023), dietary intake was assessed via 3 consecutive 24-h recalls in this prospective cohort study. Two-level generalized linear mixed-effects models were applied in 4828 adults (mean age: 55.9 &#xb1; 12.6 y, 56.6% females) to assess choline-dyslipidemia associations. Choline-TMAO and TMAO-dyslipidemia analyses were conducted in 1091 participants free of dyslipidemia at baseline. Among 7169 adults with gut microbiome data, Least Absolute Selection and Shrinkage Operator and logistic regression identified lipid-associated gut genera; TMAO relationships were examined in a subset of 693 participants. RESULTS: Higher intakes of total [Q4 compared with Q1: odds ratio (OR) = 1.261; 95% confidence interval (CI): 1.007, 1.580], red meat-derived (OR: 1.753; 95% CI: 1.196, 2.568), and lipid-soluble choline (OR: 1.304; 95% CI: 1.047, 1.624) were associated with higher risk of elevated low-density lipoprotein cholesterol (LDL cholesterol), whereas vegetable-derived choline was inversely associated. Egg-derived and lipid-soluble choline were positively associated with plasma TMAO, which was prospectively associated with 5-y incident dyslipidemia (Q4 compared with Q1-OR: 1.620; 95% CI: 1.047, 2.509), elevated LDL cholesterol (Q3 compared with Q1-OR: 2.478; 95% CI: 1.187, 5.174), and hypertriglyceridemia (Q4 compared with Q1-OR: 1.829; 95% CI: 1.028, 3.225). Three TMAO-associated genera were identified: Lachnospiraceae and Phascolarctobacterium as pro-risk taxa and Turicibacter as protective. The adverse LDLcholesterol association of egg-derived choline was observed exclusively in Phascolarctobacterium-enriched individuals. CONCLUSIONS: Dietary choline source and solubility differentially associated with dyslipidemia risk through TMAO-associated and non-TMAO-associated patterns, with gut microbiota as key modulators.

Humans↗
PubMed2001

Plasma choline in normal newborns, infants, toddlers, and in very-low-birth-weight neonates requiring total parenteral nutrition.

Choline deficiency is associated with hepatic abnormalities in adult volunteers and patients administered total parenteral nutrition (TPN). Preliminary investigation has suggested that plasma-free choline concentration (PFCh) is greater in neonatal animals, including humans, than in adults. The aims of this study were to determine the normal PFCh and phospholipid-bound choline concentration (PPLBCh) for newborns, infants, and toddlers and to determine the change during TPN. We also sought to determine the degree of fetal choline extraction, the relation between maternal and newborn plasma choline concentrations, and the relation between plasma choline status and normal newborn length, weight, and gestational age. Blood samples were obtained from 104 full-term newborns in two centers (Ben Taub and Maimonides), 25 mothers, 21 normal infants aged 20.3 +/- 11.8 wk, 12 normal infants aged 62.4 +/- 3.9 wk, and 14 preterm infants (gestational age = 28.9 +/- 2.2 wk) who required TPN. The vein PFChs were 28.1 +/- 13.0 nmol/mL (Ben Taub) and 68.1 +/- 16.9 nmol/mL (Maimonides). The artery PFChs were 27.1 +/- 13.0 nmol/mL (Ben Taub) and 57.9 +/- 11.6 nmol/mL (Maimonides). The vein PPLChs were 1004.7 +/- 246.6 nmol/mL (Ben Taub) and 1121.2 +/- 289.6 nmol/mL (Maimonides). The artery PPLChs were 1065.7 +/- 469.3 nmol/mL (Ben Taub) and 1106.9 +/- 285.8 nmol/mL (Maimonides). The vein-minus-artery differences for PFCh were 1.0 +/- 9.7 nmol/mL (Ben Taub) and 10.2 +/- 10.9 nmol/mL (Maimonides). The vein-minus-artery differences for PPLCh were -51.9 +/- 398.2 nmol/mL (Ben Taub General Hospital, Houston, Texas) and 14.4 +/- 254.3 nmol/mL (Maimonides, New York, New York). Maternal venous PFCh was 8.4 +/- 3.1 nmol/mL. Maternal venous PPLCh was 2592.1 +/- 584.0 nmol/mL (range = 1227.8-3729.0). Maternal venous PFCh correlated with newborn arterial PFCh (r = 0.53, P < 0.05) but not with newborn venous PFCh. No correlation was seen between maternal venous and newborn PPLCh. No significant differences were seen in PPLCh or choline extraction in Ben Taub versus Maimonides patients, although PFCh was significantly greater in the newborns from Maimonides (P < 0.05). The mean venous PFCh and PPLCh in the preterm infants before beginning TPN was 21.2 +/- 6.3 and 1366.8 +/- 339.1 nmol/mL, respectively. Just before initiation of tube feeding (4.0 +/- 2.7 d after TPN had been started), mean venous PFCh and PPLCh was 18.4 +/- 5.3 and 2251.8 +/- 686.9 nmol/mL, respectively. When TPN was discontinued and tube feeding increased to goal, after 10.8 +/- 10.4 d, venous PFCh and PPLCh was 22.6 +/- 8.7 and 2072.5 +/- 540.6 nmol/mL, respectively. Venous PFCh and PPLCh was 13.4 +/- 2.5 and 1827.5 +/- 327.0 nmol/mL, respectively in the older infant group. In conclusion, newborn PFCh is significantly greater than PFCh in adults but falls to adult levels within the first year of life. Low maternal PFCh may be associated with low newborn PFCh. Normal newborn plasma choline status has no bearing on intrauterine growth, although the role of maternal choline deficiency in underweight newborns is unknown. Newborn PPLCh is substantially below that of adults, which suggests its use in membrane synthesis during growth.

Adult↗