Choline Supplementation Research Articles

Beneficial effects of postnatal choline supplementation on long-Term neurocognitive deficit resulting from fetal-Neonatal iron deficiency

Early-life iron deficiency is a common nutrient condition worldwide and can result in cognitive impairment in adulthood despite iron treatment. In rodents, prenatal choline supplementation can diminish long-term hippocampal gene dysregulation and neurocognitive deficits caused by iron deficiency. Since fetal iron status is generally unknown in humans, we determined whether postnatal choline supplementation exerts similar beneficial effects. Male rat pups were made iron deficient (ID) by providing pregnant and nursing dams an ID diet (3–6ppm Fe) from gestational day (G) 3 through postnatal day (P) 7, and an iron-sufficient (IS) diet (200ppm Fe) thereafter. Control pups were provided IS diet throughout. Choline (5ppm) was given to half the nursing dams and weanlings in each group from P11-P30. P65 rat cognitive performance was assessed by novel object recognition (NOR). Real-time PCR was performed to validate expression levels of synaptic plasticity genes known to be dysregulated by early-life iron deficiency. Postnatal choline supplementation prevented impairment of NOR memory in formerly iron-deficient (FID) adult rats but impaired NOR memory in IS controls. Gene expression analysis revealed a recovery of 4 out of 10 dysregulated genes compared to 8 of the same 10 genes that we previously demonstrated to recover following prenatal choline supplementation. Recognition memory deficits induced by early-life iron deficiency can be prevented by postnatal choline supplementation and disrupted expression of a subset of synaptic plasticity genes can be ameliorated. The positive response to postnatal choline represents a potential adjunctive therapeutic supplement to treat iron-deficient anemic children in order to spare long-term neurodevelopmental deficits.

Choline prevents fetal overgrowth and normalizes placental fatty acid and glucose metabolism in a mouse model of maternal obesity

Maternal obesity increases placental transport of macronutrients, resulting in fetal overgrowth and obesity later in life. Choline participates in fatty acid metabolism, serves as a methyl donor and influences growth signaling, which may modify placental macronutrient homeostasis and affect fetal growth. Using a mouse model of maternal obesity, we assessed the effect of maternal choline supplementation on preventing fetal overgrowth and restoring placental macronutrient homeostasis. C57BL/6J mice were fed either a high-fat (HF, 60% kcal from fat) diet or a normal (NF, 10% kcal from fat) diet with a drinking supply of either 25 mM choline chloride or control purified water, respectively, beginning 4 weeks prior to mating until gestational day 12.5. Fetal and placental weight, metabolites and gene expression were measured. HF feeding significantly (P<.05) increased placental and fetal weight in the HF-control (HFCO) versus NF-control (NFCO) animals, whereas the HF choline-supplemented (HFCS) group effectively normalized placental and fetal weight to the levels of the NFCO group. Compared to HFCO, the HFCS group had lower (P<.05) glucose transporter 1 and fatty acid transport protein 1 expression as well as lower accumulation of glycogen in the placenta. The HFCS group also had lower (P<.05) placental 4E-binding protein 1 and ribosomal protein s6 phosphorylation, which are indicators of mechanistic target of rapamycin complex 1 activation favoring macronutrient anabolism. In summary, our results suggest that maternal choline supplementation prevented fetal overgrowth in obese mice at midgestation and improved biomarkers of placental macronutrient homeostasis.

Prenatal choline supplementation attenuates MK-801-induced deficits in memory, motor function, and hippocampal plasticity in adult male rats

Choline is essential to the development and function of the central nervous system and supplemental choline during development is neuroprotective against a variety of insults, including neurotoxins like dizocilpine (MK-801). MK-801 is an NMDA receptor antagonist that is frequently used in rodent models of psychological disorders, particularly schizophrenia. At low doses, it causes cognitive impairments, and at higher doses it induces motor deficits, anhedonia, and neuronal degeneration. The primary goals of the present study were to investigate whether prenatal choline supplementation protects against the cognitive impairments, motor deficits, and neuropathologies that are precipitated by MK-801 administration in adulthood. Adult male Sprague–Dawley rats were fed a standard or supplemented choline diet prenatally. Using the novelty preference test of object recognition, we found that only prenatal standard-fed rats displayed memory consolidation deficits induced by low-dose MK-801 administered immediately following study of sample objects; all other groups, including prenatal choline supplemented rats given MK-801, showed intact memory. Following high-dose MK-801, prenatal choline supplementation significantly alleviated rats’ motor response to MK-801, particularly ataxia. Using doublecortin and Ki67 to mark neurogenesis and cell division, respectively, in the hippocampus, we found that prenatal choline supplementation, in the face of MK-801 toxicity, protected against reduced hippocampal plasticity. Taken together, the current findings suggest that prenatal choline supplementation protects against a variety of behavioral and neural pathologies induced by the neurotoxin, MK-801. This research contributes to the growing body of evidence supporting the robust neuroprotective capacity of choline.

Dietary choline and phospholipid supplementation enhanced docosahexaenoic acid enrichment in egg yolk of laying hens fed a 2% Schizochytrium powder-added diet

The aim of this study was to evaluate the effect of dietary phospholipid supplementation on laying hen performance, egg quality, and the fatty acid profile of egg yolks from hens fed a 2% Schizochytrium powder diet. Three-hundred-sixty 28-wk-old Hy-line W-36 laying hens were randomly allocated to one of the 5 dietary treatments, each treatment with 6 replicates of 12 birds each. All diets included 2% Schizochytrium powder (docosahexaenoic acid [DHA], 137.09 mg/g). The control group was not supplemented with any additional phospholipids, whereas the other 4 experimental diets were supplemented with 1,000 mg/kg choline (CHO), 1,000 mg/kg monoethanolamine (MEA), 1,000 mg/kg lysophosphatidylcholine (LPC), or 500 mg/kg LPC + 500 mg/kg MEA (LPC + MEA). The experimental diets were isocaloric (metabolizable energy, 11.15 MJ/kg) and isonitrogenous (crude protein, 16.60%). The feeding trial lasted 28 days. Laying hen performance and egg quality were not affected (P>0.05) by the diets used. The monounsaturated fatty acid (MUFA) level was reduced in the LPC group at d 28 (P < 0.01), whereas the polyunsaturated fatty acid (PUFA) level was increased (P < 0.05). The omega-6 (n-6) PUFA level of the egg yolks in the LPC group had a trend to increase in comparison to the control (P = 0.07). The CHO and LPC groups had higher omega-3 (n-3) PUFA and DHA levels and lower n-6/n-3 ratios than the other groups at d 28 (P < 0.01). The DHA content in egg yolk reached a plateau after the laying hens consumed the experimental diets for 14 days, and higher yolk DHA contents were observed in the CHO and LPC groups as compared with the other groups at d 14. It was concluded that dietary choline supplementation for more than 14 d enhanced egg yolk enrichment with n-3 PUFA and DHA when laying hen diets were supplemented with 2% Schizochytrium powder. All the diets had no adverse effect on hen performance, egg quality, or egg components under the experimental condition.

Effects of supplementary choline on quail meat and fatty liver

ABSTRACT The objective of this study was to investigate the effects of supplementary choline on amount of choline passing to quail meat and reduction of fat deposition in liver. A hundred and thirty-six one-day-old Japanese quails were divided into eight equal groups of 17 quails each. The experiment was designed based on completely randomized design in two controls and six treatment groups: high stocking density, basal diet, control group (HSD; control 1); normal stocking density, basal diet, control group (NSD; [...]

Maternal Choline Supplementation Alters Fetal Growth Patterns in a Mouse Model of Placental Insufficiency

Impairments in placental development can adversely affect pregnancy outcomes. The bioactive nutrient choline may mitigate some of these impairments, as suggested by data in humans, animals, and human trophoblasts. Herein, we investigated the effects of maternal choline supplementation (MCS) on parameters of fetal growth in a Dlx3+/− (distal-less homeobox 3) mouse model of placental insufficiency. Dlx3+/− female mice were assigned to 1X (control), 2X, or 4X choline intake levels during gestation. Dams were sacrificed at embryonic days E10.5, 12.5, 15.5, and 18.5. At E10.5, placental weight, embryo weight, and placental efficiency were higher in 4X versus 1X choline. Higher concentrations of hepatic and placental betaine were detected in 4X versus 1X choline, and placental betaine was positively associated with embryo weight. Placental mRNA expression of Igf1 was downregulated by 4X (versus 1X) choline at E10.5. No differences in fetal growth parameters were detected at E12.5 and 15.5, whereas a small but significant reduction in fetal weight was detected at E18.5 in 4X versus 1X choline. MCS improved fetal growth during early pregnancy in the Dlx3+/− mice with the compensatory downregulation of Igf1 to slow growth as gestation progressed. Placental betaine may be responsible for the growth-promoting effects of choline.

Transport of long-chain polyunsaturated fatty acids in preterm infant plasma is dominated by phosphatidylcholine.

Docosahexaenoic (C22:6) and arachidonic (C20:4) acids are long-chain polyunsaturated fatty acids (LC-PUFA) essential to neonatal development, being present in the glycerophospholipids of all organs, particularly the brain. In plasma, LC-PUFAs are mainly present in lipoprotein lipids, which are neutral lipids (triglycerides and cholesterol esters) and glycerophospholipids, like choline containing phosphatidylcholine (PC). To guide future supplementation strategies of C22:6 and C20:4 in combination with choline, we determined the distribution of C20:4 and C22:6 between PC and neutral lipid. Preterm infant plasma (N=59, postmenstrual age [PMA] 33.9wk (32.4-36.0)) and cord plasma (N=34, PMA 34.0wk (30.86-38.4)) were investigated. PC and neutral lipids were extracted and analyzed using tandem mass spectrometry and gas chromatography, respectively. Data are reported as medians and 25th/75th percentiles. In cord blood, C20:4-PC and C22:6-PC comprised 36.1% (34.2-38.6) and 10.2% (8.8-12.8) of total PC, respectively. In preterm infant plasma, values were only 20.8% (19.2-23.1) and 5.7% (5.2-6.0), respectively (p<0.001 each). Nevertheless, in preterm infant plasma, 80.6% (77.6-83.0) of C20:4 and 86.0% (83.0-88.9) of C22:6 were found in PC. These values exceeded the proportions of C20:4 and C22:6 in PC of cord plasma [71.3% (67.8-72.9) and 79.2% (75.2-85.4), respectively] (p<0.0001 each). Irrespective of the low proportions of C20:4-PC and C22:6-PC in preterm infant plasma lipids, PC is the major transporter for C20:4 and C22:6. Our data support the hypotheses that choline deficiency may impair end-organ availability of these LC-PUFA in preterm infants. Therefore, supplementation of C20:4 and C22:6 might better be accompanied by choline supplementation.

Chronic choline supplementation improves cognitive and motor performance via modulating oxidative and neurochemical status in rats

Choline, an essential nutrient, accounts for multiple functions in the body and brain. While its beneficial effects on healthy adults are not clear, choline supplementation is important during pregnancy for brain development, in elderly patients for support of cognitive performance and in patients with neurological disorders to reduce memory deficits. Thus, the aim of this study is to investigate whether choline administration in healthy adult rats beneficially impacts cognitive and locomotor performance, and associated oxidative and neurochemical outcomes. Two groups, control and choline, received tap water and choline bitartrate, respectively at the dose equivalent to adequate intake for five weeks. Food intake and body weight were monitored daily. Behavioral analysis comprising assessment of cognitive performance (by novel object recognition, passive avoidance and Morris Water Maze test) and locomotor performance (by Open field, Kondziela's inverted screen and beam walking test) were performed. Following testing, rats were decapitated and brain samples were collected for estimation of acetylcholine, redox profile and monoamine measurements. The results showed that chronic choline administration significantly improves cognitive and locomotor performance accompanied by a reduction in oxidative stress, enhanced cholinergic neurotransmission and monoamine levels in the brain of healthy adult rats. Hence, chronic choline intake was found to improve behavioral, oxidative and neurochemical outcomes in the normal population, so it can be suggested that choline tablets can be used as a safe and effective supplement for improving the neurological health of normal individuals and that they might also be beneficial in preventing cognitive and motor disorders later in life.

The effects of rumen-protected choline and l-carnitine supplementation in the transition period on reproduction, production, and some metabolic diseases of dairy cattle

ABSTRACTThis experiment was designed to examine the effects of l-carnitine and choline on production parameters, reproduction indices, as well as ketosis and fatty liver indicators in pre- and post-partum Holstein cows. A number of 120 dairy cows were randomly allocated to four treatment groups: protected choline (60 gm/day per cow), l-carnitine (50 gm/day per cow), choline + l-carnitine (60 + 50 gm/day per cow), and control group (without supplement). Treatments were given from one week before calving to four weeks after calving. Milk and blood samples were collected at the time of calving till four successive weeks. Results showed that combined choline and l-carnitine supplementation increased milk fat % (3.93 ± 0.11), but decreased solids-non-fat % (8.04 ± 0.10) and lactose % (3.92 ± 0.05). Reproduction indices – including service/conception rate (1.24 ± 0.40), calving to first visible oestrus (53.36 ± 8.20), calving to first service (59.07 ± 4.20 days), and days open (63.36 ± 8.10 days) – were improved for combined choline and l-carnitine group. A significantly lower level of aspartate aminotransferase (50.16 ± 5.96) and a higher level of beta hydroxy butyrate acid (0.31 ± 0.10) were observed in blood serum when combined choline and l-carnitine was supplemented. In conclusion, concomitant administration of choline and l-carnitine improved reproduction indices as well as the liver health index in Holstein cows.

EFFECT OF CHOLINE AND LECITHIN ON GROWTH AND FEED EFFICIENCY OF JUVENILE HUMPBACK GROUPER, Cromileptes altivelis

This experiment was conducted to determine the effect of supplemental choline and lecithin in the diet of juvenile humpback grouper.

Differences in liver functionality indexes in peripartal dairy cows fed rumen-protected methionine or choline are associated with performance, oxidative stress status, and plasma amino acid profiles.

The liver functionality index (LFI) represents an assessment of transition cow metabolic health by measuring changes in biomarkers associated with liver plasma protein synthesis (albumin), lipoprotein synthesis (cholesterol), and heme catabolism (bilirubin). The present analysis was conducted to determine the role of peripartal rumen-protected Met or choline (CHOL) supplementation on LFI groupings, and to assess relationships with performance, inflammation, oxidative stress status, and plasma AA profiles. A cohort of 40 multiparous Holstein cows that were part of a randomized complete block design with 2 × 2 factorial arrangement of Met (Smartamine M, Adisseo NA, Alpharetta, GA) and CHOL (ReaShure, Balchem Inc., New Hampton, NY) level (with or without) were used. From -21 d to calving, cows received the same close-up diet and were assigned randomly to each treatment. From calving to 30 d, cows were on the same postpartal diet and continued to receive the same treatments until 30 d. Addition of Met was adjusted daily at 0.08% dry matter of diet and CHOL was fed at 60 g/cow per day. Liver (-10, 7, 20, and 30 d) and blood (-10, 4, 8, 20, and 30 d) samples were harvested for biomarker analyses. Cows were ranked retrospectively and assigned to low (LLFI, LFI <0) and high (HLFI, LFI >0) LFI groups regardless of Met or CHOL supplementation. Compared with cows in LLFI, close-up and lactation DMI, milk yield, milk fat yield, and milk protein yield were greater in HLFI cows. As expected, cows in LLFI had lower plasma cholesterol and albumin but greater bilirubin concentrations around parturition. Plasma haptoglobin concentration was also lower in HLFI cows, but plasma paraoxonase and hepatic total and reduced hepatic glutathione concentrations were greater. Although higher concentrations of His, Met, and Trp, as well as a tendency for greater Ile, were observed in HLFI cows, overall essential AA concentrations did not differ with LFI status. In contrast, overall concentrations of nonessential AA were greater in HLFI cows due to greater circulating concentrations of Ala, Asn, Gln, Pro, and Ser. Similarly, overall concentrations of total AA and total sulfur-containing compounds were greater in cows with HLFI. Feeding Met compared with CHOL led to a tendency for more cows classified as HLFI. Overall, results support the broader application of the LFI in the management of transition cows. In that context, the fact that precalving concentrations of compounds such as reduced glutathione, total sulfur-containing compounds, Met, Tau, and homocysteine differed between HLFI and LLFI independent of Met or CHOL feeding also underscores their potential for monitoring cows that might be at a greater risk of developing health problems after calving. Further studies on the applicability of these biomarkers to monitor transition success appears warranted.

Effects of rumen-protected methionine and choline supplementation on vaginal discharge and uterine cytology of Holstein cows

Methionine is one of the most limiting amino acids in dairy diets and low feed intake around the time of calving could lead to decreased synthesis of phosphatidylcholine. An alternative pathway for phosphatidylcholine is to have choline as a precursor. The objective of this study was to determine the effects of feeding rumen-protected methionine and choline pre – and postpartum on reproduction of Holstein cows. Seventy-two Holstein cows were randomly assigned to four treatments from 21days before calving to 30days in milk (DIM): supplementation with rumen-protected methionine (MET; n=20, received 0.08% of the dry matter (DM) of the diet/d as methionine, Smartamine M® to a Lys:Met=2.9:1), rumen-protected choline (CHO; n=17, received 60g/d choline, Reassure), both rumen protected methionine and choline (MIX; n=19, received 0.08% of the DM of the diet/d as methionine to a Lys:Met=2.9:1 and 60g/d choline), or no supplementation to serve as control (CON; n=16, fed total mixed ration with a Lys:Met=3.5:1). Cows were evaluated at 4, 7, 10, 13, 15, 17, and 30d after calving for the presence of secretion using the Metricheck® device. On 15, 30, and 72d after calving, the uterine endometrium of all cows was sampled using a cytological brush and streaked onto slides for analysis of the presence of polymorphonuclear neutrophils (PMN). We hypothesized that cows supplemented with methionine would have lower metricheck smell scores and lower rates of PMN than non-supplemented cows. On d 30, a treatment difference was detected using the metricheck score and smell (P<0.04), with treatment MIX (score=0.38) having a lower score than CHO (score=2.11). Supplementing cows with rumen-protected methionine may have a beneficial effect on cows’ uterine health.

Choline supplementation attenuates severity of hippocampal BDNF reductions caused by developmental alcohol exposure

Choline supplementation attenuates severity of hippocampal BDNF reductions caused by developmental alcohol exposure

B-vitamin and choline supplementation increases neuroplasticity and recovery after stroke

Folates are B-vitamins that play an important role in brain function. Dietary and genetic deficiencies in folate metabolism result in elevated levels of homocysteine which have been linked to increased risk of developing a stroke. Reducing levels of homocysteine before or after a stroke through B-vitamin supplementation has been a focus of many clinical studies, however, the results remain inconsistent. Animal model systems provide a powerful mechanism to study and understand functional impact and mechanisms through which supplementation affects stroke recovery. The aim of this study was to understand the role of B-vitamins in stroke pathology using in vivo and in vitro mouse models. The first objective assessed the impact of folate deficiency prior to ischemic damage followed by B-vitamins and choline supplementation. Ischemic damage targeted the sensorimotor cortex. C57Bl/6 wild-type mice were maintained on a folic acid deficient diet for 4weeks prior to ischemic damage to increased levels of plasma homocysteine, a risk factor for stroke. Post-operatively mice were placed on a B-vitamin and choline supplemented diet for a period of four weeks, after which motor function was assessed in mice using the rotarod, ladder beam and forepaw asymmetry tasks. The second objective was to determine how a genetic deficiency in methylenetetrahydrofolate reductase (MTHFR), an enzyme involved in folate metabolism, increases vulnerability to stroke. Primary cortical neurons were isolated from Mthfr+/+, Mthfr+/− and Mthfr−/− embryos and were exposed to in vitro models of stroke which include hypoxia or oxygen glucose deprivation. Cell viability was measured 24-h after exposure stroke like conditions in vitro. In supplemented diet mice, we report improved motor function after ischemic damage compared to mice fed a control diet after ischemic damage. Within the perilesional cortex, we show enhanced proliferation, neuroplasticity and anti-oxidant activity in mice fed the supplemented diet. A genetic MTHFR deficiency resulted in neurodegeneration after exposure to in vitro models of stroke, by activating apoptosis promoting p53-dependent mechanisms. These results suggest that one-carbon metabolism plays a significant role in recovery after stroke and MTHFR deficiency contributes to poor recovery from stroke.

A Genome‐Wide Analysis of Placental Epigenetic Markers in Response to Maternal Choline Supplementation

Choline is an essential micronutrient that provides methyl groups for cellular DNA methylation, an epigenetic modification with downstream effects on gene expression. Maternal choline supplementation (MCS) during pregnancy has many beneficial effects on placental and fetal development, which may be mediated in part by an altered placental methylation profile. In addition to DNA methylation, other epigenetic mechanisms such as genomic imprinting and microRNA (miRNA) regulation are also important to normal placental and fetal development, but whether these markers are modulated by choline remains largely unknown. We sought to investigate the impact of MCS on these epigenetic markers using a subset of placental samples collected at gestational day 15.5 from dams consuming 1× or 4× the recommended choline level. Placental mRNA and miRNA were extracted and sequenced, and the RNAs with differential expression were determined using the edgeR package developed in R. In response to MCS, three imprinted genes (Dcn, Qpct and Tnfrsf23) were downregulated in the male placentas (Padj≤0.01) whereas four imprinted genes (Ampd3, Tfpi2, Gatm, and Aqp1) were upregulated in the female placentas (Padj≤0.05). Furthermore, five miRNAs (miR‐712‐5p, miR‐3470a, miR‐6538, miR‐6240 and miR‐5126) were significantly downregulated in the female placentas from the 4× choline group (Padj≤0.033). Consistent with the downregulation of these miRNAs, some of their predicted mRNA targets showed a higher expression (P&lt;0.05). These target genes are involved in processes such as cell signaling, immune response and macronutrient transport, all of which are crucial to placental development and fetal health. In contrast, none of the miRNAs in the male placentas remained significant after correction for false discovery rate (Padj&gt;0.05). Overall, these data indicate that the placental imprintome and miRNA profile are responsive to MCS, but the effects may differ between the male and the female placentas.Support or Funding InformationUSDA, NIH, Graduate Women in Science, Egg Nutrition Center

Maternal choline supplementation during murine pregnancy modulates placental markers of inflammation, apoptosis and vascularization in a fetal sex-dependent manner

IntroductionNormal placental vascular development is influenced by inflammatory, angiogenic and apoptotic processes, which may be modulated by choline through its role in membrane biosynthesis, cellular signaling and gene expression regulation. The current study examined the effect of maternal choline supplementation (MCS) on placental inflammatory, angiogenic and apoptotic processes during murine pregnancy. MethodPregnant dams were randomized to receive 1, 2 or 4 times (X) the normal choline content of rodent diets, and tissues were harvested on embryonic day (E) 10.5, 12.5, 15.5 or 18.5 for gene expression, protein abundance and immunohistochemical analyses. ResultsThe choline-induced changes in the inflammatory and angiogenic markers were a function of fetal sex. Specifically, 4X (versus 1X) choline reduced the transcript (P ≤ 0.05) and protein (P ≤ 0.06) expression of TNF-a and IL-1β in the male placentas at E10.5 and E18.5, respectively. In the female placentas, 4X (versus 1X) choline modulated the transcript expression of Il1b in a biphasic pattern with reduced Il1b at E12.5 (P = 0.045) and E18.5 (P = 0.067) but increased Il1b at E15.5 (P = 0.031). MCS also induced an upregulation of Vegfa expression in the female placentas at E15.5 (P = 0.034; 4X versus 2X) and E18.5 (P = 0.026; 4X versus 1X). MCS decreased (P = 0.011; 4X versus 1X) placental apoptosis at E10.5. Additionally, the luminal area of the maternal spiral arteries was larger (P ≤ 0.05; 4X versus 1X) in response to extra choline throughout gestation. DiscussionMCS during murine pregnancy has fetal sex-specific effects on placental inflammation and angiogenesis, with possible consequences on placental vascular development.

Effects of rumen-protected methionine and choline supplementation on steroidogenic potential of the first postpartum dominant follicle and expression of immune mediators in Holstein cows

Multiparous Holstein cows were assigned in a randomized complete block design into four treatments from 21 d before calving to 30 d in milk (DIM). Treatments were: MET [n = 19, fed the basal diet + rumen-protected methionine at a rate of 0.08% (w/w) of the dry matter, Smartamine® M], CHO (n = 17, fed the basal diet + choline 60 g/d, Reashure®), MIX (n = 21, fed the basal diet + Smartamine® M at a rate of 0.08% (w/w) of the dry matter and 60 g/d Reashure®), and CON (n = 20, no supplementation, fed the close-up and fresh cow diets). Follicular development was monitored via ultrasound every 2 d starting at 7 DIM until ovulation (n = 37) or aspiration (n = 40) of the first postpartum dominant follicle (DF). Follicular fluid from 40 cows was aspirated and cells were retrieved immediately by centrifugation. Gene expression of TLR4, TNF, IL1-β, IL8, IL6, LHCGR, STAR, 3β-HSD, P450scc, CYP19A1, IRS1, IGF, MAT1A, and SAHH, was measured in the follicular cells of the first DF. Cows in CON had higher TNF, TLR4, and IL1-β mRNA expression (11.70 ± 4.6, 21.29 ± 10.4, 6.28 ± 1.4, respectively) than CHO (2.77 ± 0.9, 2.16 ± 0.9, 2.29 ± 0.7, respectively), and MIX (2.23 ± 0.7, 1.46 ± 0.6, 2.92 ± 0.8, respectively). Cows in CON had higher IL1-β expression (6.27 ± 1.4) than cows in MET (3.28 ± 0.6). Expression of IL8 mRNA was lower for cows in CHO (0.98 ± 0.3) than cows in CON (4.90 ± 0.7), MET (6.10 ± 1.7), or MIX (5.05 ± 1.8). Treatments did not affect mRNA expression of LHCGR, STAR, P450scc, CYP19A, SAHH, MAT1A, or IL6 however, 3β-HSD expression was higher for cows in MET (1.46 ± 0.3) and MIX (1.25 ± 0.3) than CON (0.17 ± 0.04) and CHO (0.26 ± 0.1). Supplementation of methionine, choline, and both methionine and choline during the transition period did not affect days to first ovulation or number of cows that ovulated the first follicular wave. Plasma and follicular fluid estradiol and progesterone concentrations were not different among treatments. Methionine concentrations in the follicular fluid of the first postpartum DF was higher for cows in MET (18.2 ± 0.1 μM) than cows in CON (11.1 ± 0.9 μM). In conclusion, supplementing choline and methionine during the transition period changed mRNA expression in follicular cells and dietary methionine supplementation increased plasma and follicular fluid concentrations of methionine of the first postpartum DF in Holstein cows.

138. Higher Maternal Serum Choline Levels Mitigate the Impact of Prenatal Infection on 4-Month-Old Behavior

Background: Prenatal maternal infection is associated with increased risk in the offspring for a variety of neuropsychiatric illnesses including schizophrenia, autism, and ADHD. Higher prenatal maternal serum choline levels have been shown in basic science experiments to mitigate the impact of prenatal infection. This report addresses whether higher prenatal maternal serum choline levels mitigates the impact of prenatal infection on 3-month-old human infant behavior. Methods: 153 initially healthy pregnant women reported at 16 weeks gestation whether they had experienced symptoms of an infection in the previous 6 weeks. Women who reported moderate–severe symptoms and/or who sought treatment were considered positive for an infection. Serum was drawn for choline levels at the same time. Infant behavior was assessed via a parent-report instrument, the Infant Behavior Questionnaire (IBQ), at 12 weeks of age (age adjusted for gestational age at birth). The IBQ produces three summary scores: Surgency/Extraversion, Negative Affectivity, and Orienting/Regulation. Results: For Orienting/Regulation, regression analysis demonstrated a trend towards an effect of maternal serum choline level (adjusted beta = .194, P = .059) with significant effects of maternal infection (adjusted beta = −.226, P = .016) and the interaction between maternal choline levels and maternal infection (adjusted beta = .360, P = .002). There was a significant main effect for maternal infection on Surgency/Extraversion (standardized beta = .214, P = .042). No other significant main or interaction effects were identified. Conclusion: Prenatal exposure to maternal infection in the late first trimester/early second trimester period has previously been associated with a lifelong increase in risk for a variety of psychiatric and behavioral problems. These results suggest that the relationship between prenatal infection and risk for behavioral problems can be identified as early as 3 months of age. Higher maternal serum choline levels mitigate this impact of maternal infection. Maternal prenatal choline supplementation emerges as a potential primary prevention strategy to mitigate risk for later severe mental disorder.

Choline supplementation increased total body lipid gain, while surplus methionine improved growth and amino acid retention in adult Atlantic salmon (Salmo salar)

Choline supplementation increased total body lipid gain, while surplus methionine improved growth and amino acid retention in adult Atlantic salmon (<i>Salmo salar</i>)

Supplemental methionine, choline, or taurine alter in vitro gene network expression of polymorphonuclear leukocytes from neonatal Holstein calves

Isolated PMNL from neonatal calves were used to evaluate the effect of Met, choline, and taurine supplementation on mRNA expression of genes related to the Met cycle and innate immunity. Five neonatal Holstein calves (3 wk old) were used for PMNL isolation and in vitro culture. The selected genes were related to the 1-carbon and Met cycles, cell signaling and cytokine mediators, inflammation, antimicrobial and killing mechanism associated genes, immune mediators, adhesion, and pathogen recognition. The results indicated that supplementation of Met, choline, and taurine increased homocysteine synthesis through upregulation of SAHH. Furthermore, the lower expression of CXCR1, IL10, IL6, IRAK1, NFKB1, NR3C1, SELL, TLR4, and TNFA indicated that all treatments mitigated the inflammatory activation of blood PMNL. As indicated by the modulation of GCLC and GPX1, choline and taurine supplementation also affected the antioxidant system. However, data indicate that oversupplementation could alter the inflammatory and oxidative status, suggesting the existence of cytotoxicity thresholds. Overall, multiple biological processes in calf PMNL related to inflammatory response and cytoprotection against oxidative stress were affected by Met, choline, and taurine supplementation. These data underscore an important role of these compounds in pre-weaning calf nutritional management.