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1.
Delwing D Tagliari B Chiarani F Wannmacher CM Wajner M Wyse AT 《Cellular and molecular neurobiology》2006,26(2):177-189
Summary 1 We have previously demonstrated that arginine administration induces oxidative stress and compromises energy metabolism in rat hippocampus. In the present study we initially investigated the influence of pretreatment with α-tocopherol and ascorbic acid on the effects produced by arginine on hippocampus energy metabolism. We also tested the effect of acute administration of arginine on various parameters of energy metabolism, namely glucose uptake, lactate release and on the activities of succinate dehydrogenase, complex II and cytochrome c oxidase in rat cerebellum, as well as the influence of pretreatment with α-tocopherol and ascorbic acid on the effects elicited by arginine on this structure.2. Sixty-day-old female Wistar rats were treated with a single i.p. injection of saline (control) or arginine (0.8 g/kg) and were killed 1 h later. In another set of experiments, the animals were pretreated for 1 week with daily i.p. administration of saline (control) or α-tocopherol (40 mg/kg) and ascorbic acid (100 mg/kg). Twelve hours after the last injection of the antioxidants the rats received one i.p. injection of arginine (0.8 g/kg) or saline and were killed 1 h later.3. Results showed that arginine administration significantly increased lactate release and diminished glucose uptake and the activities of succinate dehydrogenase and complex II in rat cerebellum. In contrast, complex IV (cytochrome c oxidase) activity was not changed by this amino acid. Furthermore, pretreatment with α-tocopherol and ascorbic acid prevented the impairment of energy metabolism caused by hyperargininemia in cerebellum and hippocampus of rats. 相似文献
2.
Kyu-Bong Kim Myeon Woo Chung So Young Um Ji Seon Oh Seon Hwa Kim Mi Ae Na Hye Young Oh Wan-Seob Cho Ki Hwan Choi 《Metabolomics : Official journal of the Metabolomic Society》2008,4(4):377-392
The primary objective of this study was to discover biomarkers which are correlated with hepatotoxicity induced by chemicals
using 1H NMR spectral data of urine. A procedure of nuclear magnetic resonance (NMR) urinalysis using pattern recognition was proposed
for early screening of the hepatotoxicity of CCl4, acetaminophen (AAP), and d-galactosamine (GalN) in rats. The hepatotoxic compounds were expected to induce necrosis in hepatocytes. This was confirmed
through blood biochemistry and histopathology. CCl4 (1 ml/kg, po) or GalN (0.8 g/kg, ip) was single administered to Sprague–Dawley (S–D) rats and urine was collected every 24 h.
Animals were sacrificed 24 h or 48 h post-dosing. AAP (2 g/kg, po) was administered for 2 days and then the animals were sacrificed
24 h after the last treatment. NMR spectroscopy revealed evidently different clustering between control groups and hepatotoxicant
treatment groups in global metabolic profilings as indicated by partial least square (PLS)-discrimination analysis (DA). In
targeted profilings, endogenous metabolites of allantoin, citrate, taurine, 2-oxoglutarate, acetate, lactate, phenylacetyl
glycine, succinate, phenylacetate, 1-methylnicotinamide, hippurate, and benzoate were selected as putative biomarkers for
hepatoxicity by CCl4, AAP, and GalN. Comparison of our rat 1H NMR PLS-DA data with histopathological changes suggests that 1H NMR urinalysis can be used to predict hepatotoxicity induced by CCl4, AAP, and GalN. 相似文献
3.
M. H. M. N. Senden A. J. G. M. van der Meer T. G. Verburg H. Th. Wolterbeek 《Plant and Soil》1995,171(2):333-339
Experiments were carried out to investigate the effects of root citric acid on uptake and initial distribution of cadmium
(Cd) in tomato plants (Lycopersicon esculentum, cv. Tiny Tim). Cd was measured by γ-spectrometry, using 115Cd spikes. Citric acid was measured by UV-detection, and, after spiking with 14C-citric acid, by β-spectrometry. Cd was applied for 48 h periods, in control experiments, in the presence of citric acid,
and after 24 h plant pre-incubation with citric acid.
Pre-incubation resulted in two-fold increases in fast-exchangeable amounts of root citric acid, as measured by the presence
of citric acid in xylem exudates of decapitated and pressurized roots.
Simultaneous application of Cd and citric acid did not change Cd accumulation in total plants and in the roots, nor did any
significant change occur with respect to Cd root-to-shoot transport, and Cd concentrations in shoot tissues and xylem fluid.
After citric acid pre-incubation, total plant uptake of Cd increased twofold, without any significant change in Cd accumulation
in the roots. Cd root-to-shoot transport was increased 5–6 fold, and Cd concentrations in shoot tissues and xylem fluid were
increased 6–8 fold. Speciation calculations indicated that, under the conditions applied, xylem Cd may be, at least partly,
complexed in citric acid. A C Borstlap Section editor 相似文献
4.
Metabolomic analysis of amino acid and energy metabolism in rats supplemented with chlorogenic acid 总被引:1,自引:0,他引:1
Zheng Ruan Yuhui Yang Yan Zhou Yanmei Wen Sheng Ding Gang Liu Xin Wu Peng Liao Zeyuan Deng Houssein Assaad Guoyao Wu Yulong Yin 《Amino acids》2014,46(9):2219-2229
This study was conducted to investigate effects of chlorogenic acid (CGA) supplementation on serum and hepatic metabolomes in rats. Rats received daily intragastric administration of either CGA (60 mg/kg body weight) or distilled water (control) for 4 weeks. Growth performance, serum biochemical profiles, and hepatic morphology were measured. Additionally, serum and liver tissue extracts were analyzed for metabolomes by high-resolution 1H nuclear magnetic resonance-based metabolomics and multivariate statistics. CGA did not affect rat growth performance, serum biochemical profiles, or hepatic morphology. However, supplementation with CGA decreased serum concentrations of lactate, pyruvate, succinate, citrate, β-hydroxybutyrate and acetoacetate, while increasing serum concentrations of glycine and hepatic concentrations of glutathione. These results suggest that CGA supplementation results in perturbation of energy and amino acid metabolism in rats. We suggest that glycine and glutathione in serum may be useful biomarkers for biological properties of CGA on nitrogen metabolism in vivo. 相似文献
5.
S. Canpolat N. Tug A. D. Seyran S. Kumru B. Yilmaz 《Journal of physiology and biochemistry》2010,66(1):23-28
This study was designed to investigate effects of raloxifene (RLX) and estradiol on bone formation and resorption in intact
and ovariectomized (ovx) rat models. In the intact model, a total of 24 adult female rats were divided into three groups:
Controls subcutaneously received saline alone. RLX (2 mg/kg) and estradiol (30 μg/kg) were injected to two groups of animals
for a period of 6 weeks at two daily intervals. In the second model, rats (n = 24) were ovx and allowed to recover for a period of at least 3 weeks. Control group received vehicle alone. Remaining rats
were divided into two groups and injected with RLX (2 mg/kg) and estradiol (30 μg/kg) for 6 weeks. Urine samples were collected
from all animals 24 h after the last drug administration. Urinary deoxypyridinoline (DPD) was measured by ELISA. Serum parathyroid
hormone (PTH), calcitonin, and osteocalcin levels were measured by immunoradiometric method. Serum concentrations of alkaline
phosphatase (ALP), Ca, and inorganic phosphate were determined by enzymatic–colorimetric method. Lumbar vertebrae (L2) of
all animals were dissected out and processed for histopathological evaluation. Removal of ovaries significantly elevated urinary
DPD levels (p < 0.01) compared with intact controls. Treatment of both intact and ovx rats with estradiol resulted in significant decreases
(p < 0.01) in DPD values. RLX administration had no significant effect in the intact rats, but it remarkably reduced bone turnover
in the ovx animals (p < 0.001). Both estradiol and RLX produced conflicting effects on serum ALP, osteocalcin, and PTH levels in both animal models.
These findings suggest that RLX exerts its protective effects by reducing bone resorption, similar to that of estradiol, in
ovx rats. 相似文献
6.
Seminotti B Fernandes CG Leipnitz G Amaral AU Zanatta A Wajner M 《Neurochemical research》2011,36(2):205-214
Lysine (Lys) accumulation in tissues and biological fluids is the biochemical hallmark of patients affected by familial hyperlysinemia
(FH) and other inherited metabolic disorders. In the present study we investigated the effects of acute administration of
Lys on relevant parameters of energy metabolism and oxidative stress in striatum of young rats. We verified that Lys in vivo
intrastriatal injection did not change the citric acid cycle function and creatine kinase activity, but, in contrast, significantly
inhibited synaptic Na+,K+-ATPase activity in striatum prepared 2 and 12 h after injection. Moreover, Lys induced lipid peroxidation and diminished
the concentrations of glutathione 2 h after injection. These effects were prevented by the antioxidant scavengers melatonin
and the combination of α-tocopherol and ascorbic acid. Lys also inhibited glutathione peroxidase activity 12 h after injection.
Therefore it is assumed that inhibition of synaptic Na+,K+-ATPase and oxidative damage caused by brain Lys accumulation may possibly contribute to the neurological manifestations of
FH and other neurometabolic conditions with high concentrations of this amino acid. 相似文献
7.
Paula B.M. Luís Cátia C.P. Aires Isabel Tavares de Almeida Ronald J.A. Wanders 《BBA》2007,1767(9):1126-1133
The effect of the antiepileptic drug valproic acid (VPA) on mitochondrial oxidative phosphorylation (OXPHOS) was investigated in vitro. Two experimental approaches were used, in the presence of selected respiratory-chain substrates: (1) formation of ATP in digitonin permeabilized rat hepatocytes and (2) measurement of the rate of oxygen consumption by polarography in rat liver mitochondria. VPA (0.1-1.0 mM) was found to inhibit oxygen consumption and ATP synthesis under state 3 conditions with glutamate and 2-oxoglutarate as respiratory substrates. No inhibitory effect on OXPHOS was observed when succinate (plus rotenone) was used as substrate. We tested the hypothesis that dihydrolipoyl dehydrogenase (DLDH) might be a direct target of VPA, especially its acyl-CoA intermediates. Valproyl-CoA (0.5-1.0 mM) and valproyl-dephosphoCoA (0.5-1.0 mM) both inhibited the DLDH activity, acting apparently by different mechanisms. The decreased activity of DLDH induced by VPA metabolites may, at least in part, account for the impaired rate of oxygen consumption and ATP synthesis in mitochondria if 2-oxoglutarate or glutamate were used as respiratory substrates, thus limiting the flux of these substrates through the citric acid cycle. 相似文献
8.
TLQP-21, a vgf-derived peptide modulates gastric emptying and prevents ethanol-induced gastric lesions in rats. However, it remains to be
studied whether or not TLQP-21 affects gastric acid secretion. In this study, we evaluated the effects of central (0.8–8 nmol/rat)
or peripheral (48–240 nmol/kg, intraperitoneally) TLQP-21 administration on gastric acid secretion in pylorus-ligated rats.
The mechanisms involved in such activity were also examined. Central TLQP-21 injection significantly reduced gastric acid
volume and dose-dependently inhibited total acid output (ED50 = 2.71 nmol), while peripheral TLQP-21 administration had no effect. The TLQP-21 antisecretory activity was prevented by
cysteamine (300 mg/kg, subcutaneously), a depletor of somatostatin, by indomethacin (0.25 mg/rat, intracerebroventricularly),
a non-selective cyclooxygenase inhibitor, and by functional ablation of sensory nerves by capsaicin. We conclude that TLQP-21
could be considered a new member of the large group of regulatory peptides affecting gastric acid secretion. The central inhibitory
effect of TLQP-21 on gastric acid secretion is mediated by endogenous somatostatin and prostaglandins and requires the integrity
of sensory nerve fibres. 相似文献
9.
The effect of the administration of chitosan (CS) and chitooligosaccharides (COS) on rat fecal microbiota was analyzed in this study. The profile of total bacterial population was monitored during 3 weeks of CS or COS application using denaturing gradient gel electrophoresis (DGGE) analysis of 16S rRNA gene amplicons. Quantitative PCR was used for monitoring possible changes in the levels of total bacteria and the levels of individual bacterial groups: Bifidobacteria, Clostridium leptum, Enterobacteriaceae, Lactobacillus–Streptococcus–Enterobacter, and Bacteroides–Prevotella. The DGGE profiles revealed a high complexity and individuality of each tested subject, and variations in the composition of band pattern were observed. CS or COS per os administration changed the profile and structure of the microbial ecosystem of the gastrointestinal tract of healthy rats. COS have, in most cases, an opposite effect compared with CS; only the Bacteroides–Prevotella bacterial group and Enterobacteriaceae were influenced in the same way. The Bifidobacteria group was not influenced by the administration CS and COS. 相似文献
10.
Zheng Ruan Yinfei Lv Xiaofang Fu Qinghua He Zeyuan Deng Wenqun Liu Yu Yingli Xiaosong Wu Guoyao Wu Xin Wu Yulong Yin 《Amino acids》2013,45(4):877-887
Intestinal inflammation causes metabolic disorders. The purpose of this study was to determine the effect of dietary supplementation with lactosucrose (LS) on the serum metabolome and intestinal luminal content of fatty acids in colitic rats. Colitis was induced in rats using trinitrobenzene sulfonic acid. Subsequently, rats received intragastric administration of either 250 mg LS/kg body weight or saline (the control group) every day for 5 weeks. Short-chain fatty acids in the intestinal lumen, blood profile, and metabolites in serum were measured, respectively, using gas chromatography, biochemistry analyzer, and nuclear magnetic resonance-based metabolomics combined with multivariate statistics. Metabolic effects of LS included: (1) decreases in concentrations of branched-chain amino acids (isoleucine and valine), alanine, citric acid, trimethylamine oxide and taurine, and the abundance of aspartate aminotransferase in serum; (2) increases in concentrations of glucose metabolites (including succinate) in serum; and (3) altered concentrations of butyrate in the cecal content and of butyrate and acetate in the colon content. The results indicate that LS supplementation to colitic rats affects whole-body metabolism of amino acids and release of aspartate aminotransferase and alkaline phosphatase from tissues into the blood circulation, and enhances the production of short-chain fatty acids in the intestinal lumen. 相似文献
11.
12.
Tu XK Yang WZ Liang RS Shi SS Chen JP Chen CM Wang CH Xie HS Chen Y Ouyang LQ 《Neurochemical research》2011,36(11):2022-2028
Focal cerebral ischemia results in an increased expression of matrix metalloproteinase-9 (MMP-9), which induces vasogenic
brain edema via disrupting the blood–brain barrier (BBB) integrity. Recent studies from our laboratory showed that baicalin
reduces ischemic brain damage by inhibiting inflammatory reaction and neuronal apoptosis in a rat model of focal cerebral
ischemia. In the present study, we first explored the effect of baicalin on the neuronal damage, brain edema and BBB permeability,
then further investigated its potential mechanisms. Sprague–Dawley rats underwent permanent middle cerebral artery occlusion
(MCAO). Baicalin was administrated by intraperitoneally injected twice at 2 and 12 h after the onset of MCAO. Neuronal damage,
brain edema and BBB permeability were measured 24 h following MCAO. Expression of MMP-9 protein and mRNA were determined by
western blot and RT–PCR, respectively. Expression of tight junction protein (TJP) occludin was detected by western blot. Neuronal
damage, brain edema and BBB permeability were significantly reduced by baicalin administration following focal cerebral ischemia.
Elevated expression of MMP-9 protein and mRNA were significantly down-regulated by baicalin administration. In addition, MCAO
caused the decreased expression of occludin, which was significantly up-regulated by baicalin administration. Our study suggested
that baicalin reduces MCAO-induced neuronal damage, brain edema and BBB permeability, which might be associated with the inhibition
of MMP-9 expression and MMP-9-mediated occludin degradation. 相似文献
13.
The influence of zinc (Zn) on the serum levels of triiodothyronine (T3), thyroxine (T4), thyroid-stimulating hormone (TSH) and sodium (Na), potassium (K), and calcium (Ca) was evaluated following ethanol toxicity
to the rats. To achieve this, male Wistar rats (150–195 g) were given 3 ml of 30% ethanol orally, and zinc was given in the
form of zinc sulfate (227 mg/l) in their drinking water daily for 8 weeks. Ethanol feeding resulted in a slight decrease in T3 and T4 levels and a significant increase in thyroid-stimulating hormone concentration, which may be due to the direct stimulatory
effect of ethanol on thyroid. Interestingly, when zinc was given to these rats, all the above levels were brought quite close
to their normal levels, thus indicating the positive role of zinc in thyroid hormone metabolism. Serum Zn and Ca levels were
found to be reduced, but Na levels were raised upon ethanol feeding. Restoration of normal levels of these metals upon zinc
supplementation to ethanol fed rats confirms that zinc has potential in alleviating some of the altered thyroid functions
following ethanol administration. 相似文献
14.
Glutaric Acid Administration Impairs Energy Metabolism
in Midbrain and Skeletal Muscle of Young Rats
Ferreira Gda C Viegas CM Schuck PF Tonin A Ribeiro CA Coelho Dde M Dalla-Costa T Latini A Wyse AT Wannmacher CM Vargas CR Wajner M 《Neurochemical research》2005,30(9):1123-1131
A genetic mice model of glutaric acidemia type I (GAI) has recently been developed, however affected animals do not develop
the striatal damage characteristic of patients with this disorder. Therefore, the initial aim of the present work was to induce
high glutaric acid (GA) concentrations in rat brain similar to those found in GAI patients through subcutaneous injection
of GA. High brain GA concentrations (up to 0.60 μmol/g ≅ 0.60mM) were achieved by a single subcutaneous injection of saline-buffered
GA (5 μmol/g body weight) to Wistar rats of 7–22 days of life. GA brain levels were about 10-fold lower than in plasma and
5-fold lower than in skeletal and cardiac muscles, indicating that the permeability of the blood brain barrier to GA is low.
We also aimed to use this model to investigate neurochemical parameters in the animals. Thus, we evaluated the effect of this
model on energy metabolism parameters in midbrain, in which the striatum is localized, as well as in peripheral tissues (skeletal
and cardiac muscles) of 22-day-old rats. Control rats were treated with saline in the same volumes. We verified that CO2 production from glucose was not altered in midbrain of rats treated with GA, indicating a normal functioning of the tricarboxylic
acid cycle. Creatine kinase activity was also not changed in midbrain, skeletal and cardiac muscles. In contrast, complex
I–III activity of the respiratory chain was inhibited in midbrain (25%), while complexes I–III (25%) and II–III (15%) activities
were reduced in skeletal muscle, with no alterations found in cardiac muscle. These data indicate that GA administration moderately
impairs cellular energy metabolism in midbrain and skeletal muscle of young rats. 相似文献
15.
Carol J. Lang Michelle Hansen Eugene Roscioli Jessica Jones Chiara Murgia Margaret Leigh Ackland Peter Zalewski Gary Anderson Richard Ruffin 《Biometals》2011,24(1):23-39
In mouse asthma models, inflammation can be modulated by zinc (Zn). Given that appetite loss, muscle wasting and poor nutrition
are features of chronic obstructive pulmonary disease (COPD) and that poor dietary Zn intake is in itself accompanied by growth
retardation and appetite loss, we hypothesised that dietary Zn limitation would not only worsen airway inflammation but also
exaggerate metabolic effects of cigarette smoke (CS) exposure in mice. Conversely, Zn supplementation would lessen inflammation.
Mice were exposed to CS [2× 2RF, 3×/day; 15 min/cigarette] and fed diets containing 2, 20 or 140 mg/kg Zn ad libitum. Airway
cells were collected by bronchoalveolar lavage (BAL). Plasma Zn was measured by fluorometric assay. Inflammatory, metabolic
and Zn transport markers were measured by real-time RT-PCR. Mice fed low Zn diets had less plasma labile zinc (0–0.18 μM)
than mice fed moderate (0.61–0.98 μM) or high (0.77–1.1 μM) Zn diets (SDs 0.1–0.4, n = 8–10). Smoke exposure increased plasma
and BAL labile Zn (1.5–2.5 fold, P < 0.001), bronchoalveolar macrophages (2.0 fold, P < 0.0001) and MT-1 (1.5 fold), MIP-2 (2.3 fold) and MMP-12 (3.5 fold) mRNA. Zn supplementation reduced alveolar macrophage
numbers by 62 and 52% in sham and smoke-exposed mice, respectively (Zn effect: P = 0.011). Gastrocnemius, soleus and tibialis anterior muscle mass were affected by both smoke and dietary Zn in the order
of 3–7%. The 50–60% reduction in alveolar macrophages in Zn-supplemented mice supports our evolving hypothesis that Zn is
an important anti-inflammatory mediator of airway inflammation. Restoring airway Zn levels through dietary supplementation
may lessen the severity of lung inflammation when Zn intake is low. 相似文献
16.
Penicillium simplicissimum excreted citrate, isocitrate, and succinate when grown in a strongly buffered medium [1 M Mes (pH 6) or 1 M Hepes (pH 7.3)].
Growth in a weakly buffered medium did not lead to citrate excretion despite a similar intracellular citrate concentration.
When nongrowing, citrate-excreting hyphae were aerated in a glucose solution, the following steady-state intracellular concentrations
of organic acids were measured: succinate (25 mM); citrate, isocitrate, malate, and fumarate (all less than 5 mM). After 2
h of incubation, the extracellular concentrations of these acids were [μmol (g dry wt.)–1]: isocitrate [100], citrate [60], succinate [30], and malate, fumarate, and α-ketoglutarate [<5]. The excretion of citrate
was due neither to an unspecific change in the permeability of the plasma membrane nor to simple diffusion of undissociated
citric acid. The involvement of a transport protein in citrate excretion was indicated because N-ethylmaleimide and sodium azide inhibited citrate excretion strongly despite an unchanged outward-directed citrate gradient.
Arguments are given why efflux via a citrate uptake carrier is not considered probable. These results indicate that citrate
is excreted by P. simplicissimum via a transport protein that probably specifically mediates the efflux of citrate.
Received: 28 July 1997 / Accepted: 19 November 1997 相似文献
17.
The effect of clofibrate [ethyl 2-(4-chlorophenoxy)-2-methylpropionate] administered subcutaneously to rats (600 mg/kg per day for 7 days) on the hepatic concentrations of the citric acid cycle intermediates and malonyl-CoA was studied. The concentration of isocitrate increased by 40%, whereas that of oxaloacetate, succinyl-CoA and malate tended to decrease. No significant changes were found in the concentrations of 2-oxoglutarate, fumarate, succinate and citrate. A significant decrease in hepatic malonyl-CoA content was found. This reduction of malonyl-CoA may be the reason for the reported increase in hepatic fatty acid oxidation during clofibrate treatment. 相似文献
18.
Pathways of glutamine metabolism in resting and proliferating rat thymocytes were evaluated by in vitro incubations of freshly prepared or 60-h cultured cells for 1-2 h with [U14C]glutamine. Complete recovery of glutamine carbons utilized in products allowed quantification of the pathways of glutamine metabolism under the experimental conditions. Partial oxidation of glutamine via 2-oxoglutarate in a truncated citric acid cycle to CO2 and oxaloacetate, which then was converted to aspartate, accounted for 76 and 69%, respectively, of the glutamine metabolized beyond the stage of glutamate by resting and proliferating thymocytes. Complete oxidation to CO2 in the citric acid cycle via 2-oxoglutarate dehydrogenase and isocitrate dehydrogenase accounted for 25 and 7%, respectively. In proliferating cells a substantial amount of glutamine carbons was also recovered in pyruvate, alanine, and especially lactate. The main route of glutamine and glutamate entrance into the citric acid cycle via 2-oxoglutarate in both cells is transamination by aspartate aminotransferase rather than oxidative deamination by glutamate dehydrogenase. In the presence of glucose as second substrate, glutamine utilization and aspartate formation markedly decreased, but complete oxidation of glutamine carbons to CO2 increased to 37 and 23%, respectively, in resting and proliferating cells. The dipeptide, glycyl-L-glutamine, which is more stable than free glutamine, can substitute for glutamine in thymocyte cultures at higher concentrations. 相似文献
19.
Mehta K 《Amino acids》2009,37(4):709-716
Cholesterol and docosahexaenoic acid (DHA) are important nutrients for neural development of infants. However, little is known
about the effect of cholesterol or DHA on concentrations of amino acids (AA) in neonatal tissues. This study was conducted
with the piglet (an established model for studying human infant nutrition) to test the hypothesis that dietary supplementation
with the lipids may modulate AA availability in tissues. Sixteen newborn pigs were nursed by sows for 24 h and then assigned
to one of four treatment groups, representing supplementation with 0.0% (control), 0.2% cholesterol, 0.2% DHA, or cholesterol
plus DHA to the basal milk-formula. All piglets were euthanized at 49 days of age. In brain, cholesterol supplementation reduced
(P < 0.05) concentrations of glutamate, serine, glutamine, threonine, β-alanine, alanine, methionine, isoleucine, leucine, and
γ-aminobutyrate but increased (P < 0.05) concentrations of glycine and lysine, whereas DHA supplementation similarly affected (P < 0.05) concentrations of the same AA (except for isoleucine and lysine) and taurine. In addition, concentrations of most
AA in liver, muscle and plasma were substantially altered by dietary supplementation of cholesterol and DHA in a tissue-dependent
manner. Further, DHA reduced concentrations of carnosine in skeletal muscle, as well as ammonia in both plasma and brain.
The results reveal that cholesterol and DHA can regulate AA metabolism and availability in various tissues of piglets. These
novel findings have important implications for designing the next generation of infant formula to optimize neonatal growth
and development. 相似文献
20.
Changes in brain tryptophan concentrations may affect the synthesis of brain serotonin (5-hydroxytryptamine, 5-HT). Concentrations
of tryptophan are regulated more than those of any other amino acid. Such stimuli as acute stress, carbohydrate ingestion,
and treatment with various drugs increase the brain content of tryptophan. Treatment of rats and mice with interleukin-1 (IL-1),
interleukin-6 (IL-6), lipopolysaccharide (LPS), and β-adrenoceptor agonists, as well as a variety of stressors, such as footshock
and restraint, all increase brain concentrations of tryptophan. The peak effect following both acute stress and β-adrenoceptor
agonist administration occurs within 30–60 min, whereas the peak effect following LPS and the cytokines occurs much later
at around 4–8 h. Experiments using the ganglionic blocker chlorisondamine, and β-adrenoceptor antagonists suggest that the
sympathetic nervous system plays an important role in the modulation of brain tryptophan concentrations. The mechanisms involved
in the increases observed in brain tryptophan are discussed, as well as their possible biological significance.
Special issue dedicated to Dr. Simo S. Oja 相似文献