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At least 919 records · Page 51Linked to original sources
PubMed1989

CSF choline levels in neurologically disturbed children.

Choline levels in cerebrospinal fluid (CSF) were measured in a large group of neurologically disturbed children (n = 114) and in a control group (n = 15). Only 5 children showed CSF choline levels that differed more than 2 standard deviations from the mean of the total investigated group, suggesting that CSF choline levels are extremely stable. Of the 5 children showing extreme values, 3 suffered primarily from psychomotor retardation. Further analysis showed that the CSF choline levels in the medication-free patient group suffering from psychomotor retardation (n = 18) were significantly elevated in comparison with the control group. CSF choline levels of children were found to fit excellently in the regression line showing the increase of CSF choline levels with age as calculated earlier for adults. Therefore, CSF choline levels appear to increase linearly with age during the whole life span. From direct measurements and from measurements in consecutive fractions of lumbar CSF it is concluded that choline levels in intracranial CSF are 2-3 fold as high as those in lumbar CSF.

Adolescent↗
PubMed2007

Inhibition of pneumococcal choline-binding proteins and cell growth by esters of bicyclic amines.

Streptococcus pneumoniae is one of the major pathogens worldwide. The use of currently available antibiotics to treat pneumococcal diseases is hampered by increasing resistance levels; also, capsular polysaccharide-based vaccination is of limited efficacy. Therefore, it is desirable to find targets for the development of new antimicrobial drugs specifically designed to fight pneumococcal infections. Choline-binding proteins are a family of polypeptides, found in all S. pneumoniae strains, that take part in important physiologic processes of this bacterium. Among them are several murein hydrolases whose enzymatic activity is usually inhibited by an excess of choline. Using a simple chromatographic procedure, we have identified several choline analogs able to strongly interact with the choline-binding module (C-LytA) of the major autolysin of S. pneumoniae. Two of these compounds (atropine and ipratropium) display a higher binding affinity to C-LytA than choline, and also increase the stability of the protein. CD and fluorescence spectroscopy analyses revealed that the conformational changes of C-LytA upon binding of these alkaloids are different to those induced by choline, suggesting a different mode of binding. In vitro inhibition assays of three pneumococcal, choline-dependent cell wall lytic enzymes also demonstrated a greater inhibitory efficiency of those molecules. Moreover, atropine and ipratropium strongly inhibited in vitro pneumococcal growth, altering cell morphology and reducing cell viability, a very different response than that observed upon addition of an excess of choline. These results may open up the possibility of the development of bicyclic amines as new antimicrobials for use against pneumococcal pathologies.

Amines↗
PubMed1994

Carbachol-induced phosphatidylcholine hydrolysis and choline efflux in rat submandibular gland involves phospholipase D activation and is modulated by protein kinase C and calcium.

The role of calcium and protein kinase C activation in carbachol-induced choline efflux from submandibular glands was investigated. The participation of phospholipase D in this signal transduction pathway was demonstrated by the formation of [14C]phosphatidylethanol in [14C]lysophosphatidylcholine-labelled submandibular gland cells treated with carbachol or noradrenaline in the presence of ethanol. Chelation of the intracellular calcium with BAPTA/AM reduced the carbachol stimulated outflow of [3H]choline. The calcium ionophore A23187 in a high concentration (10 microM) increased the basal [3H]choline outflow, but decreased the carbachol-induced outflow. Removal of the extracellular calcium enhanced the carbachol-stimulated outflow, which returned to control when calcium was re-added to the medium. Activation of protein kinase C by phorbol-12,13-dibutyrate (100 nM) or 1-oleyl-2-acetyl-sn-glycerol (20 microM) was without effect per se, but enhanced the carbachol-mediated outflow of [3H]choline. Phorbol-12,13-dibutyrate in combination with 1 microM A23187 induced a small efflux of [3H]choline. A 2 h treatment with phorbol-12,13-dibutyrate (1 microM), causing down-regulation of protein kinase C, significantly decreased the carbachol-stimulated [3H]choline outflow. In conclusion, elevation of intracellular calcium levels and protein kinase C activation are of importance for the carbachol-stimulated outflow of [3H]choline. Inflow of calcium, if anything, reduces the carbachol-stimulated outflow of [3H]choline. Since phosphatidylcholine breakdown generates diacylglycerol and this could lead to activation of protein kinase C, activation of this signal transduction pathway may be important for the protein content of the saliva and for the known trophic effects of parasympathetic innervation.

Animals↗
PubMed2004

Role of alpha7 nicotinic acetylcholine receptors in the pressor response to intracerebroventricular injection of choline: blockade by amyloid peptide Abeta1-42.

Systemic blood pressure and cardiac function have long been known to be under the control of central autonomic and hormonal pathways that, in part, use cholinergic neural systems. Recently choline, a precursor and product of acetylcholine metabolism, has been shown to serve as a selective endogenous agonist for the alpha7 subtype of the nicotinic acetylcholine receptor (alpha7nAChR). This receptor subtype mediates several responses to nicotine in animals, most notably, neuroprotection and enhanced cognition. The purpose of this study was to determine whether the cardiovascular changes induced by central injection of choline in rats also were mediated by alpha7nAChRs. Moreover, we sought to determine whether these cardiovascular changes to choline could be blocked by central pretreatment with amyloid beta peptide (1-42) (Abeta1-42), a neurotoxic component of cerebral amyloid that is known to bind with high affinity to alpha7nAChRs. Central, i.c.v. injection of choline (50, 100, or 150 microg) produced dose-dependent (10-15-min duration) pressor response of up to about 20 mm Hg. The most consistent change in heart rate included a brief increase (up to 40 beats/min) that lasted 2 to 3 min, followed by a prolonged decrease averaging 50 beats/min that lasted up to 30 min. Pretreatment (i.c.v.) with the selective alpha7nAChR antagonists alpha-bungarotoxin and methyllycaconitine significantly inhibited the pressor and heart rate responses to subsequent injection of choline. Pretreatment with the non-alpha7-preferring antagonist dihydro-beta-erythroidin was not effective. These findings suggested that the cardiovascular response to i.c.v. injection of choline was mediated at least in part through alpha7nAChRs. Pretreatment (30 min) with low doses (1-100 pmol) of amyloid peptide Abeta1-42 (but not with Abeta40-1) administered by the i.c.v. route significantly inhibited the choline-induced blood pressure increase as well as the choline-induced decrease in heart rate.

Amyloid beta-Peptides↗
PubMed2005

Allelic variation of polymorphic locus lytB, encoding a choline-binding protein, from streptococci of the mitis group.

The choline-binding protein LytB, an N-acetylglucosaminidase of Streptococcus pneumoniae, is the key enzyme for daughter cell separation and is believed to play a critical pathogenic role, facilitating bacterial spreading during infection. Because of these peculiarities LytB is a putative vaccine target. To determine the extent of LytB polymorphism, the lytB alleles from seven typical, clinical pneumococcal isolates of various serotypes and from 13 additional streptococci of the mitis group (12 atypical pneumococci and the Streptococcus mitis type strain) were sequenced. Sequence alignment showed that the main differences among alleles were differences in the number of repeats (range, 12 to 18) characteristic of choline-binding proteins. These differences were located in the region corresponding to repeats 11 to 17. Typical pneumococcal strains contained either 14, 16, or 18 repeats, whereas all of the atypical isolates except strains 1283 and 782 (which had 14 and 16 repeats, respectively) and the S. mitis type strain had only 12 repeats; atypical isolate 10546 turned out to be a DeltalytB mutant. We also found that there are two major types of alternating repeats in lytB, which encode 21 and 23 amino acids. Choline-binding proteins are linked to the choline-containing cell wall substrate through choline residues at the interface of two consecutive choline-binding repeats that create a choline-binding site. The observation that all strains contained an even number of repeats suggests that the duplication events that gave rise to the choline-binding repeats of LytB involved two repeats simultaneously, an observation that is in keeping with previous crystallographic data. Typical pneumococcal isolates usually grew as diplococci, indicating that an active LytB enzyme was present. In contrast, most atypical isolates formed long chains of cells that did not disperse after addition of purified LytB, suggesting that in these strains chains were produced through mechanisms unrelated to LytB.

Alleles↗
PubMed1996

Osmoprotectants in Halomonas elongata: high-affinity betaine transport system and choline-betaine pathway.

The osmoregulatory pathways of the moderately halophilic bacterium Halomonas elongata DSM 3043 have been investigated. This strain grew optimally at 1.5 to 2 M NaCl in M63 glucose-defined medium. It required at least 0.5 M NaCl for growth, which is a higher concentration than that exhibited by the H. elongata type strain ATCC 33173. Externally provided betaine, choline, or choline-O-sulfate (but not proline, ectoine, or proline betaine) enhanced the growth of H. elongata on 3 M NaCl-glucose-M63 plates, demonstrating the utilization of these compounds as osmoprotectants. Moreover, betaine and choline stimulated the growth of H. elongata DSM 3043 over the entire range of salinity, although betaine was more effective than choline at salinities below and above the optimum. We found that H. elongata DSM 3043 has at least one high-affinity transport system for betaine (K(m) = 3.06 microM and Vmax = 9.96 nmol of betaine min(-1) mg of protein(-1)). Competition assays demonstrated that proline betaine and ectoine, but not proline, choline, or choline-O-sulfate, are also transported by the betaine permease. Finally, thin-layer chromatography and 13C-nuclear magnetic resonance analysis showed that exogenous choline was taken up and transformed to betaine by H. elongata, demonstrating the existence of a choline-glycine betaine pathway in this moderately halophilic bacterium.

Betaine↗
PubMed2004

Adenovirus stimulates choline efflux by increasing expression of organic cation transporter-2.

We examined the effect of wild-type human adenovirus (Ad5) on choline transport in murine lung epithelia (MLE) and in rodent primary alveolar type II cells. Cells were active in pH-sensitive, reversible transport of choline, a process blocked pharmacologically with phenoxybenzamine, an inhibitor of organic cation transporters (OCT). PCR products for the choline transporters, OCT-1 and OCT-2, were detected, but only OCT-2 protein was robustly expressed within MLE and primary alveolar epithelial cells. Ad5 produced a two- to threefold increase in choline efflux from cells, resulting in a significant reduction in intracellular choline content and its major product, phosphatidylcholine. Effects of Ad5 on choline efflux were inhibited with phenoxybenzamine, and choline efflux was attenuated by OCT-2 small interfering RNA. Adenovirus also produced a dose-dependent increase in immunoreactive OCT-2 levels concomitant with increased cellular OCT-2 steady-state mRNA. These results indicate that adenoviruses can significantly disrupt choline trafficking in lung epithelia by upregulating expression of an alveolar protein involved in organic cation transport.

Adenoviridae↗
PubMed2005

Choline kinase is a novel oncogene that potentiates RhoA-induced carcinogenesis.

Choline kinase is overexpressed in human breast, lung, colorectal, and prostate tumors, a finding that suggests the involvement of this enzyme in carcinogenesis. Here we show that overexpression of choline kinase induce oncogenic transformation of human embryo kidney fibroblasts and canine epithelial Madin-Darby canine kidney cells. Choline kinase lays downstream of RhoA signaling and is activated through ROCK kinase, one of the best-characterized RhoA effectors. In keeping with this, coexpression of RhoA and choline kinase potentiates both anchorage independent growth and tumorigenesis. Finally, choline kinase-mediated transformation is sensitive to MN58b, a well-characterized specific choline kinase inhibitor. These results provide the definitive evidence that choline kinase has oncogenic properties and that choline kinase inhibition constitutes a novel valid antitumor strategy.

Animals↗
PubMed2006

Noninvasive magnetic resonance spectroscopic pharmacodynamic markers of the choline kinase inhibitor MN58b in human carcinoma models.

MN58b is a novel anticancer drug that inhibits choline kinase, resulting in inhibition of phosphocholine synthesis. The aim of this work was to develop a noninvasive and robust pharmacodynamic biomarker for target inhibition and, potentially, tumor response following MN58b treatment. Human HT29 (colon) and MDA-MB-231 (breast) carcinoma cells were examined by proton (1H) and phosphorus (31P) magnetic resonance spectroscopy (MRS) before and after treatment with MN58b both in culture and in xenografts. An in vitro time course study of MN58b treatment was also carried out in MDA-MB-231 cells. In addition, enzymatic assays of choline kinase activity in cells were done. A decrease in phosphocholine and total choline levels (P < 0.05) was observed in vitro in both cell lines after MN58b treatment, whereas the inactive analogue ACG20b had no effect. In MDA-MB-231 cells, phosphocholine fell significantly as early as 4 hours following MN58b treatment, whereas a drop in cell number was observed at 48 hours. Significant correlation was also found between phosphocholine levels (measured by MRS) and choline kinase activities (r2 = 0.95, P = 0.0008) following MN58b treatment. Phosphomonoesters also decreased significantly (P < 0.05) in both HT29 and MDA-MB-231 xenografts with no significant changes in controls. 31P-MRS and 1H-MRS of tumor extracts showed a significant decrease in phosphocholine (P < or = 0.05). Inhibition of choline kinase by MN58b resulted in altered phospholipid metabolism both in cultured tumor cells and in vivo. Phosphocholine levels were found to correlate with choline kinase activities. The decrease in phosphocholine, total choline, and phosphomonoesters may have potential as noninvasive pharmacodynamic biomarkers for determining tumor response following treatment with choline kinase inhibitors.

Animals↗
PubMed1983

Conversion of choline to phosphatidylcholine in the isolated-ventilated-perfused neonatal rabbit lung.

The isolated-ventilated-perfused neonatal rabbit lung model was used to study pulse dosed 14C-choline incorporation into 14C-phosphatidylcholine (PC) and 14C-disaturated phosphatidylcholine (DSPC). 14C-PC and 14C-DSPC synthesis were linearly dependent upon perfusion time to 30 min and upon the pulse dose of 14C-choline of 20-250 nmol at both 10 and 30 min of perfusion. 2-3% of the pulse-dosed choline was taken up by the lung. The water-soluble metabolites of choline found in lung after 10-30 min of perfusion were: choline, 50-60%; betaine 2.4-3.0%; phosphorylcholine, 26-41%, and CDP-choline, trace-10%. 1-day-old perfused lungs incorporated pulse-dosed 14C-choline into 14C-PC and 14C-DSPC at slightly higher rates than at 10 days old. Newborn rabbits receiving an intraperitoneal injection of 0.1 mg dexamethasone/100 g body weight 16 and 22 h prior to perfusion incorporated significantly more 14C-choline into 14C-PC and 14C-DSPC than saline-injected controls.

Animals↗
PubMed1991

Time-dependent changes in cerebral choline and acetylcholine induced by transient global ischemia in rats.

We occluded the carotid and vertebral arteries of 12 rats for 15 minutes to measure the brain concentrations of choline and acetylcholine and cerebral blood flow at the end of the ischemic period or 15, 30, or 150 minutes after circulation was reestablished. The animals were sacrificed with microwave radiation focused to the head immediately after a brief infusion of [14C]iodoantipyrine with rapid sampling of arterial blood. Brain tissue samples were extracted with ether to separate the tracer, which was subsequently measured by liquid scintillation counting and used to calculate local cerebral blood flow. The aqueous phase was then processed for the measurement of choline and acetylcholine concentrations by gas chromatography/mass spectrometry. The results showed a large increase in tissue choline content and a decrease in tissue acetylcholine content during ischemia. During recirculation, choline levels progressively declined, reaching levels lower than those in four control rats after 150 minutes of recirculation for most brain regions. A reciprocal relation between the brain choline concentration and local cerebral blood flow was found. Acetylcholine levels showed an initial rebound to greater than control during recirculation, with subsequent normalization. Brain acetylcholine concentration was positively correlated with brain choline concentration, provided that cerebral blood flow was greater than 0.3 ml x g-1 x min-1. Because tissue free choline was depleted in most brain regions 150 minutes after transient ischemia, we speculate that prolonged ischemia may produce a greater depletion of tissue free choline with a resulting decline in tissue acetylcholine. This could play an important role in the cognitive deficit associated with vascular dementia.

Acetylcholine↗
PubMed1989

Choline transport by lung epithelium.

The uptake of [3H]choline was investigated using isolated perfused rat lungs and primary cultures of granular pneumocytes isolated by tryptic digestion of rat lungs. Metabolic products were separated from free choline by chloroform:methanol extraction and column chromatography. Tissue-associated [3H]choline increased progressively in the perfused lung, and estimated mean intracellular concentration at 2 h was 12 times the extracellular concentration (5 microM). Choline uptake was inhibited by ventilation with CO and by perfusion with the choline analog, hemicholinium-3 (HC-3). Isolated granular pneumocytes also accumulated choline against a concentration gradient by an energy-dependent process. The concentration for half-maximal uptake, after correction for the diffusion component, was estimated at 18 +/- 4 microM (mean +/- SE; n = 3), and the estimated maximal rate of uptake was 213 +/- 44 pmol/min/microliter cell water. HC-3 inhibited uptake by approximately 50% at a concentration of 10(-4) M. There was no effect on uptake when Na+ in the medium was replaced by Li+ or N-methylglucamine+. These results indicate that granular pneumocytes possess a transport system that results in accumulation of choline against a concentration gradient. The characteristics of uptake indicate that this system is similar to the low affinity choline transport system of other organs.

Animals↗
PubMed1999

Choline uptake by mouse brain capillary endothelial cells in culture.

Choline, a precursor of the neurotransmitter acetylcholine, is synthesized in only small amounts in the brain, so the choline concentration in the brain may vary depending on the plasma concentration and the transport rate across the blood-brain barrier. To elucidate the transport mechanism of choline, we carried out uptake experiments with mouse brain capillary endothelial cells in culture (MBEC4). [3H]Choline uptake was linear for up to 5 min. An examination of the concentration dependence of [3H]choline uptake revealed the operation of both saturable (Jmax = 423+/-27 pmol min(-1) (mg protein)(-1) and Kt = 20.0+/-3.1 microM) and non-saturable (kd = 1.23+/-0.045 microL min(-1)(mgprotein)-1) processes. The saturable process was independent of Na+ and pH, but was dependent on membrane potential as a driving force. Various basic drugs and endogenous substances, including substrates and inhibitors of the organic cation transporter, significantly inhibited the [3H]choline uptake. These data suggest that choline was taken up into the endothelial cells via two routes and that a membrane potential-dependent carrier-mediated transport system may participate in choline transport across the blood-brain barrier.

Adenosine Triphosphate↗
PubMed2006

Elevation of serum cerebral injury markers correlates with serum choline decline after coronary artery bypass grafting surgery.

The aims of this study were to determine circulating choline status and its relationship to circulating levels of S-100beta protein and neuron-specific enolase, biochemical markers of cerebral injury and cognitive decline, after coronary artery bypass grafting (CABG) surgery. Preoperatively, patients scheduled for off-pump or on-pump CABG surgery had serum concentrations of 12.0+/-0.2 and 11.7+/-0.4 micromol/L free choline and 2640+/-65 and 2675+/-115 micromol/L phospholipid-bound choline, respectively. Serum free and bound choline levels decreased by 22-37% or 34-47% and 16-36% or 31-38% at 48 h after off-pump or on-pump surgery, respectively. Serum S-100beta and neuron-specific enolase increased from preoperative values of 0.083+/-0.009 and 6.3+/-0.2 microg/L to 0.405+/-0.022 and 11.4+/-0.8 microg/L, respectively, at 0 h postoperatively and remained elevated for 48 h after off-pump surgery. Serum free and bound choline concentrations were inversely correlated with the concentrations of S-100beta (r=-0.798; p<0.001 and r=-0.734; p<0.001) and neuron-specific enolase (r=-0.840; p<0.001 and r=-0.728; p<0.001). In conclusion, CABG surgery induces a decline in serum free and phospholipid-bound choline concentrations. The decreased serum choline concentrations were inversely correlated with the elevated levels of circulating cerebral injury markers. Thus, a decline in circulating choline may be involved in postoperative cognitive decline.

Adult↗
PubMed2006

A choline-deficient diet exacerbates fatty liver but attenuates insulin resistance and glucose intolerance in mice fed a high-fat diet.

Liver fat accumulation is proposed to link obesity and insulin resistance. To dissect the role of liver fat in the insulin resistance of diet-induced obesity, we altered liver fat using a choline-deficient diet. C57Bl/6 mice were fed a low-fat (10% of calories) or high-fat (45% of calories) diet for 8 weeks; during the final 4 weeks, diets were either choline deficient or choline supplemented. In choline replete animals, high-fat feeding induced weight gain, elevated liver triglycerides (171%), hyperinsulinemia, and glucose intolerance. Choline deficiency did not affect body or adipose depot weights but amplified liver fat accumulation with high-fat diet (281%, P < 0.01). However, choline deficiency lowered fasting plasma insulin (from 983 +/- 175 to 433 +/- 36 pmol/l, P < 0.01) and improved glucose tolerance on a high-fat diet. In mice on 30% fat diet, choline deficiency increased liver mRNA levels of the rate-limiting enzyme in phosphatidylcholine synthesis and of enzymes involved in free fatty acid esterification, without affecting those of de novo lipogenesis or fatty acid oxidation. We conclude that liver fat accumulation per se does not cause insulin resistance during high-fat feeding and that choline deficiency may shunt potentially toxic free fatty acids toward innocuous storage triglyceride in the liver.

Animals↗
PubMed1986

Methionine, choline and sulfate interrelationships in the diet of weanling swine.

Experiments were conducted to examine the interrelationships between methionine, choline and inorganic sulfate in the diet of weanling pigs, and to evaluate the selenium (Se) status of pigs fed diets with or without supplemental sulfate. Two trials utilized 288 weanling (3-wk-old) pigs allotted to dietary treatment based on weight, sex and litter origin. There were six pigs/pen and three replicate pens/treatment in each trial. The basal corn-soybean meal diet was formulated to supply .55% sulfur amino acids and contained a choline and sulfur-free vitamin and mineral premix. Lysine was added to provide a total of 1.13% lysine. Seven additional treatments were formulated by substituting for corn .17% DL-methionine, .29% choline dihydrogen citrate or .25% Na2SO4 to create a 2(3) factorial arrangement of treatments. There were methionine X choline X sulfate interactions for average daily gain (P less than .001) and feed-to-gain ratio (F:G; P less than .05). Adding choline, methionine, Na2SO4 or choline plus methionine to the basal diet did not improve gains. However, when Na2SO4 plus methionine or Na2SO4 plus choline were added, daily gains were increased (P less than .05) and F:G was improved (P less than .1). Addition of all three supplements did not result in a further increase in gain. Pigs fed choline-supplemented diets had higher (P less than .01) hematocrit and tended (P = .07) to have increased hemoglobin concentration. There was no effect on serum triglycerides or alkaline phosphatase activity due to dietary treatment. The concentration of Se in muscle, liver, kidney and blood was not influenced by sulfate content of the diet.

Animals↗
PubMed1987

Effect of level of protein and supplemental choline on reproductive performance of gilts fed sorghum diets.

A total of 214 gilts was used (two trials) to determine the effect of protein level and choline supplementation during gestation on weight gain, conception rate and subsequent reproductive performance. The gilts were fed either a 12 or 16% crude protein sorghum-soybean meal diet containing either a high supplemental choline level or no supplemental choline in a 2 X 2 factorial arrangement of treatments. Conception rate was not influenced by either protein or choline level. Choline supplementation increased pig weight at 42 d of age (P less than .14) and litter weight at 21 (P less than .12) and 42 d (P less than .1). Gilts fed the 16% protein diet produced larger pigs at 42 d (P less than .13) and heavier litters at birth, (P less than .1) 21 d (P less than .14) and 42 d (P less than .05) than gilts fed the 12% protein diet. A larger choline effect on litter size and pig and litter weight was observed for gilts fed the 12% protein diet than for those fed the 16% gestation diet, although the protein-choline interaction was not significant for any traits measured. The incidence of spraddle leg condition was low and was not affected by level of dietary protein or supplemental choline.

Animal Feed↗
PubMed1984

Kinetics of methionine and choline and their incorporation into plasma lipids and milk components in lactating goats.

Rates of entry of L-methionine and choline and their incorporations into lipids of blood plasma and milk components were studied in lactating goats fed a concentrate-roughage ration with primed constant infusion of L-[methyl-carbon-14] methionine and [methyl-carbon-14] choline. Entry rates of methionine and choline were 30 and 47 mumol/h/kg body weight. Of the methionine pool, 10 and 28% were recovered in carbon dioxide and choline of blood plasma, but the contribution of methionine to the total carbon dioxide production was negligible. Two percent of serine was derived from methionine. Six percent of the choline pool was derived from methionine, whereas labeled choline was not recovered in methionine. Methionine and choline contributed to at least 4 and 19% of the phospholipid pool. Of the methionine dose, .2 and 3.7% appeared in milk lactose and protein. Little (.3%) labeled choline was recovered in milk; however, its contribution to milk fat was 10 times as high as that of methionine. The lipogenic effect of methionine in the liver is proposed as one mechanism among others stimulating production of milk and milk fat.

Animals↗