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T Ott

Publications and source records attributed to T Ott.

At least 19 recordsLinked to original sources
PubMed2002

A star in a 15.2-year orbit around the supermassive black hole at the centre of the Milky Way.

Many galaxies are thought to have supermassive black holes at their centres-more than a million times the mass of the Sun. Measurements of stellar velocities and the discovery of variable X-ray emission have provided strong evidence in favour of such a black hole at the centre of the Milky Way, but have hitherto been unable to rule out conclusively the presence of alternative concentrations of mass. Here we report ten years of high-resolution astrometric imaging that allows us to trace two-thirds of the orbit of the star currently closest to the compact radio source (and massive black-hole candidate) Sagittarius A*. The observations, which include both pericentre and apocentre passages, show that the star is on a bound, highly elliptical keplerian orbit around Sgr A*, with an orbital period of 15.2 years and a pericentre distance of only 17 light hours. The orbit with the best fit to the observations requires a central point mass of (3.7 +/- 1.5) x 10(6) solar masses (M(*)). The data no longer allow for a central mass composed of a dense cluster of dark stellar objects or a ball of massive, degenerate fermions.

Journal Article↗
PubMed2001

Blocking caspase-activated apoptosis improves contractility in failing myocardium.

Cardiac myocyte apoptosis has been demonstrated in end-stage failing human hearts. The therapeutic utility of blocking apoptosis in congestive heart failure (CHF) has not been elucidated. This study investigated the role of caspase activation in cardiac contractility and sarcomere organization in the development of CHF. In a rabbit model of heart failure obtained by rapid ventricular pacing, we demonstrate, using in vivo transcoronary adenovirus-mediated gene delivery of the potent caspase inhibitor p35, that caspase activation is associated with a reduction in contractile force of failing myocytes by destroying sarcomeric structure. In this animal model gene transfer of p35 prevented the rise in caspase 3 activity and DNA-histone formation. Genetically manipulated hearts expressing p35 had a significant improvement in left ventricular pressure rise (+dp/dt), decreased end-diastolic chamber pressure (LVEDP), and the development of heart failure was delayed. To better understand this benefit, we examined the effects of caspase 3 on cardiomyocyte dysfunction in vitro. Microinjection of activated caspase 3 into the cytoplasm of intact myocytes induced sarcomeric disorganization and reduced contractility of the cells. These results demonstrate a direct impact of caspases on cardiac function and may lead to novel therapeutic strategies via antiapoptotic regimens.

Adenoviridae↗
PubMed2001

A novel mammalian receptor for the evolutionarily conserved type II GnRH.

Mammalian gonadotropin-releasing hormone (GnRH I: pGlu-His-Trp-Ser-Tyr-Gly-Leu-Arg-Pro-Gly-NH2) stimulates pituitary gonadotropin secretion, which in turn stimulates the gonads. Whereas a hypothalamic form of GnRH of variable structure (designated type I) had been shown to regulate reproduction through a cognate type I receptor, it has recently become evident that most vertebrates have one or two other forms of GnRH. One of these, designated type II GnRH (GnRH II: pGlu-His-Ser-His-Gly-Trp-Tyr-Pro-Gly-NH2), is conserved from fish to man and is widely distributed in the brain, suggesting important neuromodulatory functions such as regulating K+ channels and stimulating sexual arousal. We now report the cloning of a type II GnRH receptor from marmoset cDNA. The receptor has only 41% identity with the type I receptor and, unlike the type I receptor, has a carboxyl-terminal tail. The receptor is highly selective for GnRH II. As with the type I receptor, it couples to G(alpha)q/11 and also activates extracellular signal-regulated kinase (ERK1/2) but differs in activating p38 mitogen activated protein (MAP) kinase. The type II receptor is more widely distributed than the type I receptor and is expressed throughout the brain, including areas associated with sexual arousal, and in diverse non-neural and reproductive tissues, suggesting a variety of functions. Surprisingly, the type II receptor is expressed in the majority of gonadotropes. The presence of two GnRH receptors in gonadotropes, together with the differences in their signaling, suggests different roles in gonadotrope functioning.

Amino Acid Sequence↗
PubMed2001

Dilated bile canaliculi and attenuated decrease of nerve-dependent bile secretion in connexin32-deficient mouse liver.

Gap junction channels in the rodent liver are composed of connexin26 (Cx26) and connexin32 (Cx32) proteins. Gap junctional intercellular communication in the mouse liver enhances the effects of hormonal or sympathetic stimulation of glucose release from glycogen stores. To determine whether contraction of bile canaliculi and bile secretion are dependent on the function of gap junction channels, we compared wild-type and connexin32-deficient mice. Confocal laser scanning microscopy of the wild-type mouse liver confirmed the close association of connexin26 and -32 proteins with the zona occludens-1 protein and actin filaments of the bile canaliculi. The decrease of bile flow after electrical stimulation of sympathetic nerves in the perfused liver was attenuated in the Cx32-deficient liver compared with wild-type controls. The amount of secreted bile, however, was similar in wild-type and Cx32-deficient livers. Furthermore, Cx32-deficient mice exhibited dilated bile canaliculi, suggesting that the contraction of bile canaliculi could be impaired in these animals.

Alanine Transaminase↗
PubMed2001

A new member of the spalt like zinc finger protein family, Msal-3, is expressed in the CNS and sites of epithelial/mesenchymal interaction.

We have identified a new member of the spalt-like gene family in mice, msal-3. We compared the expression patterns of msal-3 and msal-1 during development and show that they exhibit overlapping yet exclusive patterns of expression in the developing forebrain, diencephalon, midbrain/hindbrain boundary and spinal cord. Both genes are expressed from E7 in opposite gradients in primitive streak mesoderm. Subsequently their transcripts are localized to regions of mesenchyme/epithelial interaction in the palate, heart, limbs, anal and urogenital region.

Animals↗
PubMed2000

Lack of phenobarbital-mediated promotion of hepatocarcinogenesis in connexin32-null mice.

Connexin32 (Cx32) is the major gap junction forming protein in liver. We have recently shown that hepatocarcinogenesis is strongly enhanced in mice deficient in Cx32, demonstrating that lack of functional Cx32 accelerates liver tumorigenesis. Many tumor-promoting agents, including phenobarbital, block gap junctional intercellular communication in vitro, and it has been suggested that this effect is relevant for clonal expansion of neoplastic cells in vivo. We have now tested this hypothesis by analyzing the potency of phenobarbital as a liver tumor promoter in male Cx32-wild-type (Cx32(Y/+)) and Cx32-null (Cx32(Y/-)) mice. Preneoplastic and neoplastic liver lesions were induced in 6-week-old male mice by a single injection of 90 microg/g body weight of N-nitrosodiethylamine, and groups of mice were subsequently kept on phenobarbital-containing (0.05%) or control diet for 39 weeks. Frozen liver sections were prepared, and (pre)neoplastic lesions were identified by their deficiency in glucose-6-phosphatase staining. In addition, the number and size of macroscopically visible tumors were monitored. Phenobarbital led to a approximately 5-fold increase in the volume fraction occupied by glucose-6-phosphatase-deficient liver lesions in Cx32(Y/+) mice, whereas there was no such increase in Cx32(Y/-) mice. Even more pronounced differences were observed with respect to tumor response. Whereas phenobarbital clearly promoted the occurrence of numerous large hepatomas in Cx32(Y/+) mice, no such effect was seen in Cx32(Y/-) mice. These results demonstrate, for the first time, that functional Cx32 protein is required for tumor promotion by phenobarbital.

Animals↗
PubMed2000

Acute-phase response and circadian expression of connexin26 are not altered in connexin32-deficient mouse liver.

In mouse hepatocytes, the gap junctional proteins connexin32 (Cx32) and connexin26 (Cx26) are expressed in the same gap junctional plaque. Expression of the major Cx32 protein is downregulated during liver regeneration and cholestasis. Here we have analyzed the acute-phase response (after experimental inflammation) and circadian connexin expression in Cx32-deficient and wild-type mouse liver. Acute-phase response was triggered by intraperitoneal injection of lipopolysaccharide (LPS). Injection of recombinant mouse interleukin-1beta (mIL-1beta), mIL-6 or tumor necrosis factor alpha (mTNF-alpha) had no inflammatory effect. Northern blot analysis of positive and negative acute-phase transcripts following stimulation with cytokine or LPS revealed no difference between Cx32-deficient livers and wild-type controls, suggesting that loss of the Cx32 gene had no effect on experimental liver inflammation. Actin, beta-fibrinogen and Cx26 transcripts were increased after endotoxin stimulation. Under conditions of hepatic acute-phase response, Cx32 transcripts were not detected in LPS-treated livers of wild-type mice. Immunoblot analysis of proteins from inflamed wild-type livers indicated a strongly diminished amount of Cx32 protein, whereas the level of Cx26 protein was increased. Although intraperitoneal injection of mIL-1, mIL-6 as well as mTNF-alpha did not induce an acute-phase response, Cx32 protein expression was diminished, suggesting that post-transcriptional downregulation of Cx32 preceded the acute-phase response. Northern blot hybridization of RNA from wild-type and Cx32-deficient mouse liver revealed a similar circadian regulation of Cx26 and GAPDH transcripts with maximal expression around 2 p.m. and a minimum after midnight.

Actins↗
PubMed2000

Disopyramide block of K(ATP) channels is mediated by the pore-forming subunit.

The class Ia antiarrhythmic agent disopyramide blocks native ATP-sensitive K+ (K(ATP)) channels at micromolar concentrations. The K(ATP) channel is a complex of a pore-forming inwardly rectifying K+ channel (Kir6.2) and a sulfonylurea receptor (SUR). The aim of the present study was to further localize the site of action of disopyramide. We have used a C-terminal truncated form of Kir6.2 (Kir6.2delta26), which--in contrast to Kir6.2--expresses independently of SUR. Kir6.2delta26 channels were expressed in African green monkey kidney COS-7 cells, and enhanced green fluorescent protein (EGFP) cDNA was used as a reporter gene. EGFP fluorescence was visualized by a laser scanning confocal microscope. Disopyramide applied to the cytoplasmic membrane surface of inside-out patches inhibited Kir6.2delta26 channels half-maximally at 7.1 microM (at pH 7.15). Lowering the intracellular pH to 6.5 potentiated the inhibition of Kir6.2delta26 channels by disopyramide. These observations suggest that disopyramide directly blocks the pore-forming Kir6.2 subunit, in particular at reduced intracellular pH values that occur under cardiac ischaemia.

Animals↗
PubMed2000

The extent of synchronous initiation and termination of DNA synthesis in regenerating mouse liver is dependent on connexin32 expressing gap junctions.

BACKGROUND/AIMS: It has previously been shown in rat liver that the gap junctional proteins connexin32 and connexin26 are downregulated when murine hepatocytes are in the S-phase of the cell cycle. Therefore, it has been hypothesized that loss of functional gap junctions could affect proliferation of hepatocytes. This study aimed to check this hypothesis. METHODS: We searched for differences in liver regeneration after two-thirds partial hepatectomy between connexin32-deficient and wild-type mice. RESULTS: The ratio of liver to body weight in regenerating liver was not affected by loss of the connexin32 gene. The peak of DNA synthesis occurred at the same time, i.e. 36 to 96 h after partial hepatectomy, in connexin32-deficient and wild-type liver. During this time, however, only about half as many nuclei of hepatocytes in connexin32-deficient liver incorporated bromodeoxyuridine, compared to wild-type liver. Furthermore, 1-2 weeks after full recovery of liver mass, we detected a higher level of bromodeoxyuridine incorporation into hepatocytes of connexin32-deficient than in wild-type liver. CONCLUSIONS: Loss of connexin32 protein and/or diminished expression of connexin26 did not promote G0/1-S transition of hepatocytes in two-thirds hepatectomized mouse livers. Instead, the extent of synchronous initiation and termination of DNA synthesis in regenerating liver was altered in connexin32-deficient mice.

Animals↗
PubMed2000

Mechanism of terfenadine block of ATP-sensitive K(+) channels.

The ATP-sensitive K(+) (K(ATP)) channel is a complex of a pore-forming inwardly rectifying K(+) channel (Kir6.2) and a sulphonylurea receptor (SUR). The aim of the present study was to gain further insight into the mechanism of block of K(ATP) channels by terfenadine. Channel activity was recorded both from native K(ATP) channels from the clonal insulinoma cell line RINm5F and from a C-terminal truncated form of Kir6.2 (Kir6.2Delta26), which - in contrast to Kir6.2 - expresses independently of SUR. Kir6.2Delta26 channels were expressed in COS-7 cells, and enhanced green fluorescent protein (EGFP) cDNA was used as a reporter gene. EGFP fluorescence was visualized by a laser scanning confocal microscope. Terfenadine applied to the cytoplasmic side of inside-out membrane patches concentration-dependently blocked both native K(ATP) channel and Kir6.2Delta26 channel activity, and the following values were calculated for IC(50) (the terfenadine concentration causing half-maximal inhibition) and n (the Hill coefficient): 1.2 microM and 0.7 for native K(ATP) channels, 3.0 microM and 1.0 for Kir6. 2Delta26 channels. Terfenadine had no effect on slope conductance of either native K(ATP) channels or Kir6.2Delta26 channels. Intraburst kinetics of Kir6.2Delta26 channels were not markedly affected by terfenadine and, therefore, terfenadine acts as a slow channel blocker on Kir6.2Delta26 channels. Terfenadine-induced block of Kir6. 2Delta26 channels demonstrated no marked voltage dependence, and lowering the intracellular pH to 6.5 potentiated the inhibition of Kir6.2Delta26 channels by terfenadine. These observations indicate that terfenadine blocks pancreatic B-cell K(ATP) channels via binding to the cytoplasmic side of the pore-forming subunit. The presence of the pancreatic SUR1 has a small, but significant enhancing effect on the potency of terfenadine.

ATP-Binding Cassette Transporters↗
PubMed1999

Regulation of the photosynthetic electron transport chain.

The regulation of electron transport between photosystems II and I was investigated in the plant Silene dioica L. by means of measurement of the kinetics of reduction of P(700) following a light-to-dark transition. It was found that, in this species, the rate constant for P(700) reduction is sensitive to light intensity and to the availability of CO(2). The results indicated that at 25 degrees C the rate of electron transport is down-regulated by approximately 40-50% relative to the maximum rate achievable in saturating CO(2) and that this down-regulation can be explained by regulation of the electron transport chain itself. Measurements of the temperature sensitivity of this rate constant indicated that there is a switch in the rate-limiting step that controls electron transport at around 20 degrees C: at higher temperatures, CO(2) availability is limiting; at lower temperatures some other process regulates electron transport, possibly a diffusion step within the electron transport chain itself. Regulation of electron transport also occurred in response to drought stress and sucrose feeding. Measurements of non-photochemical quenching of chlorophyll fluorescence did not support the idea that electron transport is regulated by the pH gradient across the thylakoid membrane, and the possibility is discussed that the redox potential of a stromal component may regulate electron transport.Keywords: DeltapH. Electron transport. Photosynthesis. Photosynthetic control. Redox regulation. Silene (photosynthesis)

Journal Article↗
PubMed1999

Biological functions of connexin genes revealed by human genetic defects, dominant negative approaches and targeted deletions in the mouse.

Gap junction channels in mammalian organs can be built up of at least 13 different connexin proteins, most of which are expressed in only few cell types, although many cells express more than one connexin protein. Recently, the consequences of missing or defective connexin proteins were studied in human patients with defects in connexin32 (Cx32; beta 1; X-linked Charcot-Marie-Tooth disease) or in Cx26 (beta 2; non-syndromic sensorineural deafness), and in mice with targeted deletions in the Cx26, Cx32, Cx37 (alpha 4), Cx43 (alpha 1), Cx46 (alpha 3) or Cx50 (alpha 8) genes. Some effects of dominant negative mutations in connexin genes have been characterized in Xenopus oocytes and transfected mammalian cells in culture. Here we review results of these different experimental approaches and report new findings regarding the characterization of Cx40 (alpha 5)- and Cx31 (beta 3)-deficient mice. The phenotypic alterations, caused by different defective connexin genes in mice or humans, are divergent, although in most known cases the viability is not affected. When more than one connexin gene, coexpressed in the same cell, is inactivated, development or maturation can be more severely affected at an earlier stage. Some connexin proteins, if present in the same cell, can partially replace each other in certain functions. Thus, the diversity of connexin proteins in mammalian cells may provide functional overlap and complementation.

Animals↗
PubMed1999

The effect of connexin32 null mutation on hepatocarcinogenesis in different mouse strains.

Connexin32 (Cx32) is the major gap junctional protein in mouse liver. We have shown recently that the formation of liver tumours in Cx32-deficient mice is strongly increased in comparison with control wild-type mice, demonstrating that the deficiency in gap junctional communication has an enhancing effect on hepatocarcinogenesis. We have now compared the effect of Cx32 deficiency on liver carcinogenesis in two strains of mice with differing susceptibility to hepatocarcinogenesis. Heterozygous Cx32(+/-) females were crossed with male Cx32 wild-type C57BL/6J (low susceptibility) or C3H/He (high susceptibility) mice. Since the Cx32 gene is located on the X-chromosome, the resulting F1 males segregated to the genotypes Cx32(Y/+) and Cx32(Y/-). Genotyping was performed by PCR-analysis using tail-tip DNA. Weanling male mice were i.p. injected with a single dose of N-nitrosodiethylamine and were killed 16, 21 or 26 weeks later. The number, volume fraction and size distribution of precancerous liver lesions characterized by a deficiency in the marker enzyme glucose-6-phosphatase were quantitated. The results demonstrate that Cx32 deficiency only slightly affects the number of enzyme-altered lesions, but strongly enhances their growth, both in the resistant and the susceptible mouse strain, suggesting that decreased intercellular communication results in tumour promoting activity irrespective of the genetic background of the mouse strain used. Since Cx32-deficient C3H/He hybrids were approximately 5-10 times more sensitive than C3H/He hybrids with an intact Cx32 gene, this mouse strain may prove very useful for toxicological screening purposes.

Animals↗
PubMed1999

Effects of P2 purinoceptor agonists on membrane potential and intracellular Ca2+ of human cardiac endothelial cells.

Vasoactive agonists like adenosine-5'-triphosphate (ATP) increase intracellular Ca2+ ([Ca2+]i) in vascular endothelial cells with an initial peak due to inositol 1,4,5-triphosphate-mediated Ca2+ release from intracellular stores followed by a sustained plateau that is dependent on the presence of extracellular Ca2+, thus leading to an increased synthesis and release of prostacyclin and nitric oxide. We studied the effects of nucleotides on membrane potential and [Ca2+]i in confluent human microvascular cardiac endothelial cells obtained from patients with dilated cardiomyopathy. The whole-cell configuration of the patch-clamp technique and a confocal laser scanning microscope employing fluo-3 as a Ca2+ indicator were used. Both uridine-5'-triphosphate (UTP) and 2-methylthioadenosine-5'-triphosphate (2MeSATP) induced depolarizations in human microvascular cardiac endothelial cells and increased [Ca2+]i with a rank order of potency 2MeSATP>ATP=UTP (EC50 values (in microM) were 0.084 2MeSATP, 0.67 ATP and 1.1 UTP). This suggests that both P2u and P2y purinoceptors are present on human microvascular cardiac endothelial cells. Maximal [Ca2+]i responses of confluent human microvascular cardiac endothelial cell monolayers to UTP were lower when compared to 2MeSATP. Nucleotide-induced increases in [Ca2+]i consisted of a transient peak, which was also observed in the absence of extracellular Ca2+, and a sustained [Ca2+]i plateau. This plateau, which was not observed in all monolayers studied, was not markedly influenced by increasing extracellular [K+]. Previous incubation with thapsigargin abolished ATP-induced increases of [Ca2+]i. It is concluded that human microvascular cardiac endothelial cells express both P2y and P2u purinoceptors. P2 purinoceptor agonists release Ca2+ from intracellular thapsigargin-sensitive stores and stimulate capacitative Ca2+ influx pathways. K+ efflux through Ca2+-dependent K+ (K(Ca)) channels does not play a major role in the regulation of nucleotide-induced Ca2+ influx in human microvascular cardiac endothelial cells, which might be related to an impaired function of the cells.

Adenosine Triphosphate↗
PubMed1999

Platelet-activating factor may act as an endogenous pulse generator for sheep of luteolytic PGF2alpha release.

Pulsatile release of uterine prostaglandin F2alpha (PGF2alpha) induces luteolysis in ruminants. However, the mechanism(s) that initiates and maintains luteolysis has not been defined. The present study tested the hypothesis that the endogenous PGF2alpha pulse generator is uterine-derived platelet-activating factor (PAF). Ovariectomized ewes were given exogenous progesterone (P), estradiol (E), or both (P+E, mimicking the normal luteal phase). Only ewes treated with steroids released PAF into the uterine lumen and had increased PAF:acetylhydrolase activity in the uterine lumen. Steroid treatment also influenced the capacity of the uterus to release PGF2alpha in response to exogenous PAF. PAF infusion did not affect plasma PGF2alpha metabolite (PGFM) levels in control (no steroid treatment) ewes but increased plasma PGFM levels in P+E ewes (P < 0.001) and ewes treated with P or E alone (P < 0.05). Infusion of PAF followed by or coincident with oxytocin (OT) acted in a synergistic manner to increase plasma PGFM levels. Repeated infusion of PAF into the uterus at 1-h intervals induced tachyphylaxis of the PGFM response to PAF; however, sensitivity of the uterus to PAF returned spontaneously by the 6th h. Interferon-tau (IFN-tau) inhibits pulsatile release of PGF2alpha during pregnancy to prevent luteolysis. Exogenous recombinant ovine IFN-tau (50 microgram) inhibited the uterine response to PAF alone or the combined effects of PAF and OT. These results indicate that uterine PAF fulfills many of the criteria for an endogenous PGF2alpha pulse-generator: steroid induction of PAF production and uterine responsiveness to PAF-induced release of PGF; synergistic stimulation of PAF-induced PGF release by OT; inhibition of PAF effects by IFN-tau; and PAF's ability to induce pulses of PGF with a periodicity during a period of chronic exposure of the uterus to PAF.

1-Alkyl-2-acetylglycerophosphocholine Esterase↗
PubMed1998

Connexin 32 gap junctions enhance stimulation of glucose output by glucagon and noradrenaline in mouse liver.

Gap junctions connect neighboring cells via intercellular channels composed of connexins (Cx). Connexin 32 (Cx32) is the main connexin in hepatocytes. Gap junctions propagate a signal from periportal to perivenous hepatocytes generated by electrical stimulation of sympathetic liver nerves. Therefore, it was the aim of this study to examine the involvement of hepatocellular gap junctions in hormonal regulation. In perfused livers from wild-type mice and Cx32-deficient mice, the stimulation of glucose release by varying noradrenaline and glucagon concentrations was investigated. At saturating hormone concentrations, glucose release was the same in wild-type and Cx32-deficient livers. However, glucose output was significantly smaller in Cx32-deficient than wild-type livers at half-maximally effective hormone concentrations. Because the two hormones circulate at less than half-saturating concentrations and because they are degraded during passage of blood through the liver, they lose efficiency from the periportal to the perivenous zone. In wild-type livers, this decrease in efficiency can be partially compensated by intercellular signal propagation through gap junctions, resulting in higher hormone actions than in Cx32-deficient livers. It is concluded that gap junctions are not only involved in intercellular propagation of nervous, but also of hormonal signals from periportal to perivenous hepatocytes.

Animals↗
PubMed1998

Maternal dietary protein deficiency decreases amino acid concentrations in fetal plasma and allantoic fluid of pigs.

This study was conducted to test the hypothesis that maternal dietary protein deficiency decreases amino acid availability to the fetus, thereby contributing to retarded fetal growth. Primiparous gilts selected genetically for low or high plasma total cholesterol concentrations (low line and high line, respectively) were mated, and then fed 1.8 kg/d of isocaloric diets containing 13% or 0.5% crude protein. At d 40 or 60 of gestation, they were hysterectomized, and maternal and fetal blood samples as well as amniotic and allantoic fluids were obtained for analyses of amino acids, ammonia and urea. Dietary protein restriction decreased (P < 0.05) the following: 1) maternal plasma concentrations of urea at d 40 and 60 of gestation; 2) fetal plasma concentrations of alanine, arginine, branched-chain amino acids (BCAA), glutamine, glycine, lysine, ornithine, proline, taurine, threonine and urea at d 60 of gestation; 3) amniotic and allantoic fluid concentrations of urea at d 40 and 60 of gestation; and 4) allantoic fluid concentrations of alanine, arginine, BCAA, citrulline, cystine, glycine, histidine, methionine, proline, serine, taurine, threonine and tyrosine at d 40 of gestation, in gilts of both genetic lines. At d 60 of gestation, protein deficiency decreased (P < 0.05) allantoic fluid concentrations of arginine, cystine, glycine, taurine and tyrosine in low line gilts and of cystine, glutamine, ornithine, serine, taurine and tyrosine in high line gilts. Low line and high line gilts also differed remarkably in allantoic fluid concentrations of arginine, glutamine, ornithine and ammonia at d 40 and 60 of gestation. Our results suggest the following: 1) protein-deficient gilts maintain maternal plasma concentrations of amino acids by mobilizing maternal protein stores and decreasing oxidation of amino acids during the first half of gestation; 2) protein deficiency may impair placental transport of amino acids from the maternal to the fetal blood; and 3) low line and high line gilts differ in fetal amino acid metabolism. Decreases in concentrations of the essential and nonessential amino acids in the fetus may be a mechanism whereby maternal dietary protein restriction results in fetal growth retardation.

Allantois↗