scholarly journals Histidine metabolism in experimental protein malnutrition in rats

1965 ◽  
Vol 97 (1) ◽  
pp. 311-317 ◽  
Author(s):  
DR Rao ◽  
AD Deodhar ◽  
K Hariharan
Keyword(s):  
Urinary Excretion ◽  
Metabolic Control ◽  
Dietary Protein ◽  
Protein Malnutrition ◽  
Reversible Nature

1. The activities of the enzymes histidase, urocanase and histidine-pyruvate transaminase were studied in rats under conditions of protein malnutrition. Urocanase and histidase activities in liver were markedly lowered in experimental protein malnutrition, but the activity of histidine-pyruvate transaminase was unaffected. There is a metabolic control in vivo of the enzymes involved in the catabolism of histidine. 2. Significant changes in the urinary excretion of histidine, composition of liver and serum were apparent in the protein-malnourished rat. 3. The changes in the activities of the enzymes and other parameters were of a reversible nature and dependent on the nature of the dietary protein. 4. The significance of these findings is discussed in relation to abnormal histidine metabolism in kwashiorkor.

scholarly journals Dietary protein deprivation decreases the serine phosphorylation of insulin receptor substrate-1 in rat skeletal muscle

2004 ◽  
Vol 32 (2) ◽  
pp. 519-531 ◽  
Author(s):  
Y Toyoshima ◽  
Y Ohne ◽  
SI Takahashi ◽  
T Noguchi ◽  
H Kato
Keyword(s):  
Skeletal Muscle ◽  
Insulin Receptor ◽  
Tyrosine Phosphorylation ◽  
Dietary Protein ◽  
Cultured Cells ◽  
Insulin Injection ◽  
The State ◽  
Protein Malnutrition ◽  
Serine Phosphorylation

Evidence has shown that protein malnutrition tends to increase peripheral insulin sensitivity, but the molecular mechanism underlying this increase is not yet clear. Here we show that, in rat muscle, the state of insulin receptor (IR) substrate-1 (IRS-1), a pivotal component of the signaling pathway of the IR, changes drastically according to protein supply. After rats were fed a protein-free diet (PF) or a 12% casein diet for 1 week, their IR and IRS-1 states were analyzed by immunoblotting using various antibodies. PF slightly increased the amount of IR without affecting the state of IR tyrosine phosphorylation. In contrast, PF decreased the amount of IRS-1 and markedly increased phosphorylation of IRS-1 tyrosine residues after insulin injection. Moreover, IRS-1 in PF rats exhibited faster mobility in SDS-PAGE as well as far less phosphorylation of Ser612 and Ser307, indicating hypophosphorylation on its serine residues. Results of additional experiments using energy-restricted (pair-fed) rats and streptozotocin-induced diabetic rats suggest that dietary protein deficiency by itself alters serine phosphorylation of IRS-1, while the up-regulation of tyrosine phosphorylation requires other factors, such as a reduction in basal plasma insulin. The serine dephosphorylation followed by up-regulation of insulin-dependent IRS-1 tyrosine phosphorylation in skeletal muscle of PF rats in vivo is similar to a phenomenon observed in cultured cells under restriction of amino acids in the medium. With these findings, it could be inferred that the reduction of serine phosphorylation contributes to the sensitization of IRS-1 to IR tyrosine kinase under protein malnutrition.

ÉTUDES IN VIVO SUR LE MÉTABOLISME DES ANDROGÉNES APRES ADMINISTRATION DE STÉROÏDES INHIBITEURS DE L'OVULATION

1965 ◽  
Vol 50 (1) ◽  
pp. 131-144 ◽  
Author(s):  
P. Mauvais-Jarvis ◽  
M. F. Jayle ◽  
J. Decourt ◽  
J. Louchart ◽  
J. Truffert
Keyword(s):  
Luteinizing Hormone ◽  
Urinary Excretion ◽  
Normal Subjects ◽  
Hormone Activity ◽  
Testosterone Production ◽  
Normal Men ◽  
Ethinyl Oestradiol

ABSTRACT Normal subjects and hirsute women with micropolycystic ovaries were treated with ethinyl-oestrenol + 3-methoxy-ethinyl-oestradiol (Lyndiol®), in view of studying the action of this compound on the production of androgens and on the urinary excretion of their metabolites. In normal men, the production of testosterone and the excretion of androsterone and aetiocholanolone are suppressed, whereas the excretion of other 17-ketosteroids and the production of dehydroepiandrosterone sulphate are unchanged. Moreover, the luteinizing hormone activity (LH) in plasma is depressed. It seems that the preparation inhibits specifically the testicular androgen production, by suppressing the hypothalamo-hypophyseal control of LH. Testosterone production and urinary 17-ketosteroid excretion are modified in the same way in women with Stein-Leventhal's syndrome. Physiopathological and therapeutical implications which come from these results are discussed.

ATYPICAL ADRENAL HYPERFUNCTION: IN VIVO STUDIES AND INCUBATIONS OF ADRENAL TISSUE WITH 4-14C PROGESTERONE

1968 ◽  
Vol 58 (3_Suppl) ◽  
pp. S5-S34
Author(s):  
Joseph W. Goldzieher ◽  
Leonard R. Axelrod ◽  
Arthur S. Weissbein
Keyword(s):  
Urinary Excretion ◽  
Clinical Features ◽  
In Vivo Studies ◽  
Acth Stimulation ◽  
Adrenal Tissue ◽  
Adrenal Hyperfunction

ABSTRACT Six women with atypical forms of adrenal cortical hyperfunction were studied by means of urinary excretion of 17-ketosteroids and 17-hydroxycorticoids and their response to ACTH stimulation and corticosteroid suppression. Unusual responses were observed, particularly with respect to the independence of 17-KS and 17-OHCS excretion. The adrenals of 3 patients were anatomically normal whereas the others showed hyperplasia. Minced adrenal tissue was incubated with 4-14C progesterone and the metabolites isolated and definitively identified. The pattern of biosynthesized corticosteroids showed great variation, and in some instances clarified certain clinical features. The pattern of certain C19-metabolites could not be studied adequately because of the use of a Δ4 rather than a Δ5 substrate.

scholarly journals Comprehensive assessment of post-prandial protein handling by the application of intrinsically labelled protein in vivo in human subjects

2021 ◽  
pp. 1-9
Author(s):  
Jorn Trommelen ◽  
Andrew M. Holwerda ◽  
Philippe J. M. Pinckaers ◽  
Luc J. C. van Loon
Keyword(s):  
Protein Synthesis ◽  
Amino Acid ◽  
Stable Isotope ◽  
Dietary Protein ◽  
Protein Metabolism ◽  
Muscle Protein ◽  
Human Subjects ◽  
Whole Body ◽  
Body Protein

All human tissues are in a constant state of remodelling, regulated by the balance between tissue protein synthesis and breakdown rates. It has been well-established that protein ingestion stimulates skeletal muscle and whole-body protein synthesis. Stable isotope-labelled amino acid methodologies are commonly applied to assess the various aspects of protein metabolism in vivo in human subjects. However, to achieve a more comprehensive assessment of post-prandial protein handling in vivo in human subjects, intravenous stable isotope-labelled amino acid infusions can be combined with the ingestion of intrinsically labelled protein and the collection of blood and muscle tissue samples. The combined application of ingesting intrinsically labelled protein with continuous intravenous stable isotope-labelled amino acid infusion allows the simultaneous assessment of protein digestion and amino acid absorption kinetics (e.g. release of dietary protein-derived amino acids into the circulation), whole-body protein metabolism (whole-body protein synthesis, breakdown and oxidation rates and net protein balance) and skeletal muscle metabolism (muscle protein fractional synthesis rates and dietary protein-derived amino acid incorporation into muscle protein). The purpose of this review is to provide an overview of the various aspects of post-prandial protein handling and metabolism with a focus on insights obtained from studies that have applied intrinsically labelled protein under a variety of conditions in different populations.

scholarly journals Procyanidins are not bioavailable in rats fed a single meal containing a grapeseed extract or the procyanidin dimer B3

2002 ◽  
Vol 87 (4) ◽  
pp. 299-306 ◽  
Author(s):  
Jennifer L. Donovan ◽  
Adam Lee ◽  
Claudine Manach ◽  
Laurent Rios ◽  
Christine Morand ◽  
...  
Keyword(s):  
Gastrointestinal Tract ◽  
Urinary Excretion ◽  
Ring Structure ◽  
Future Research ◽  
Human Gastrointestinal Tract ◽  
Human Diet ◽  
Single Meal ◽  
Nutritional Effects ◽  
Grapeseed Extract

Flavanols are the most abundant flavonoids in the human diet where they exist as monomers, oligomers and polymers. In the present study, catechin, the procyanidin dimer B3 and a grapeseed extract containing catechin, epicatechin and a mixture of procyanidins were fed to rats in a single meal. After the meals, catechin and epicatechin were present in conjugated forms in both plasma and urine. In contrast, no procyanidins or conjugates were detected in the plasma or urine of any rats. Procyanidins were not cleaved into bioavailable monomers and had no significant effects on the plasma levels or urinary excretion of the monomers when supplied together in the grapeseed extract. We conclude that the nutritional effects of dietary procyanidins are unlikely to be due to procyanidins themselves or monomeric metabolites with the intact flavonoid-ring structure, as they do not exist at detectable concentrations in vivo. Future research should focus on other procyanidin metabolites such as phenolic acids and on the effects of the unabsorbed oligomers and polymers on the human gastrointestinal tract.

scholarly journals Simultaneous Assessment of Endothelial Function, Nitric Oxide Synthase Activity, Nitric Oxide–Mediated Signaling, and Oxidative Stress in Individuals with and without Hypercholesterolemia

2008 ◽  
Vol 54 (2) ◽  
pp. 292-300 ◽  
Author(s):  
Renke Maas ◽  
Edzard Schwedhelm ◽  
Lydia Kahl ◽  
Huige Li ◽  
Ralf Benndorf ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Endothelial Function ◽  
Urinary Excretion ◽  
Indirect Evidence ◽  
No Oxidation ◽  
Whole Body ◽  
Gas Chromatography Mass Spectrometry ◽  
Synthesis Rate ◽  
No Production

Abstract Background: Endothelial function is impaired in hypercholesterolemia and atherosclerosis. Based on mostly indirect evidence, this impairment is attributed to reduced synthesis or impaired biological activity of endothelium-derived nitric oxide (NO). It was the aim of this study to directly estimate and compare whole-body NO production in normo- and hypercholesterolemia by applying a nonradioactive stable isotope dilution technique in vivo. Methods: We enrolled 12 normocholesterolemic and 24 hypercholesterolemic volunteers who were all clinically healthy. To assess whole-body NO synthesis, we intravenously administered l-[guanidino-(15N2)]-arginine and determined the urinary excretion of 15N-labeled nitrate, the specific end product of NO oxidation in humans, by use of gas chromatography-mass spectrometry. In addition, we measured flow-mediated vasodilation (FMD) of the brachial artery, expression of endothelial NOS (eNOS) in platelets, plasma concentration of the endogenous NOS inhibitor asymmetric dimethylarginine (ADMA), and urinary excretion of 8-isoprostaglandin F2α (8-iso-PGF2α). Results: After infusion of l-[guanidino-(15N2)]-arginine, cumulative excretion of 15N-labeled-nitrate during 48 h was 40% [95% CI 15%–66%] lower in hypercholesterolemic than normocholesterolemic volunteers [mean 9.2 (SE 0.8) μmol vs 15.4 (2.3) μmol/l, P = 0.003]. FMD was on average 36% [4%–67%] lower in hypercholesterolemic than normocholesterolemic volunteers [6.3 (4.0)% vs 9.4 (4.6)%, P = 0.027]. Normalized expression of NOS protein in platelets was also significantly lower in hypercholesterolemic volunteers, whereas there were no significant differences in plasma ADMA concentration or urinary excretion of 8-iso-PGF2α between the 2 groups. Conclusions: This study provides direct evidence for a decreased whole body NO synthesis rate in healthy people with hypercholesterolemia.

ANDROGEN METABOLISM IN CONGENITAL ADRENAL HYPERPLASIA DUE TO 11 β-HYDROXYLASE DEFICIENCY

PEDIATRICS ◽  
1969 ◽  
Vol 44 (2) ◽  
pp. 201-208
Author(s):  
S. Douglas Frasier ◽  
Richard Horton ◽  
Robert A. Ulstrom
Keyword(s):  
Plasma Concentration ◽  
Urinary Excretion ◽  
Congenital Adrenal Hyperplasia ◽  
Conversion Ratio ◽  
Metabolic Clearance ◽  
Adrenal Hyperplasia ◽  
Metabolic Clearance Rate ◽  
Hydroxylase Deficiency ◽  
Glucocorticoid Administration

The plasma concentration of androstenedione and testosterone, metabolic clearance rate of androstenedione, and in vivo conversion ratio of androstenedione to testosterone have been studied in a normotensive 5-year-old female with congenital adrenal hyperplasia due to a deficiency of 11 β-hydroxylase. Prior to glucocorticoid administration, the urinary excretion of 17-ketosteroids varied from 2.2 to 4.9 mg/24 hours, urinary excretion of pregnanetriol varied from 0.7 to 2.2 mg/24 hours, and total 17-hydroxysteroid excretion varied from 1.2 to 7.5 mg/24 hours. Urinary tetrahydro-11-deoxy cortisol (TSH) was detected at a concentration of 550 µg/24 hours. The plasma concentration of androstenedione varied from 100 to 530 mµg/100 ml and the plasma concentration of testosterone varied from 40 to 90 mµg/100 ml. These values are significantly elevated when compared to those obtained in normal prepubertal females. Urinary steroid excretion and plasma androgen concentrations fell to normal in response to glucocorticoid administration. The metabolic clearance rate of androstenedione was 890 liters per day per M2 and the in vivo conversion ratio of androstenedione to testosterone was 11%. The calculated production rate of androstenedione was 4.7 mg per day per M2. Virilization in congenital adrenal hyperplasia due to 11 β-hydroxylase deficiency can be explained by an elevated plasma concentration of testosterone, which can be accounted for on the basis of conversion from androstenedione.

ASC deglutathionylation is a checkpoint for NLRP3 inflammasome activation

2021 ◽  
Vol 218 (9) ◽  
Author(s):  
Shuhang Li ◽  
Linlin Wang ◽  
Zhihao Xu ◽  
Yuanyuan Huang ◽  
Rufeng Xue ◽  
...  
Keyword(s):  
Metabolic Control ◽  
Nlrp3 Inflammasome ◽  
Inflammasome Activation ◽  
Mitochondrial Ros ◽  
Nlrp3 Inflammasome Activation ◽  
Multiple Molecules ◽  
Excessive Activation

Activation of NLRP3 inflammasome is precisely controlled to avoid excessive activation. Although multiple molecules regulating NLRP3 inflammasome activation have been revealed, the checkpoints governing NLRP3 inflammasome activation remain elusive. Here, we show that activation of NLRP3 inflammasome is governed by GSTO1-promoted ASC deglutathionylation in macrophages. Glutathionylation of ASC inhibits ASC oligomerization and thus represses activation of NLRP3 inflammasome in macrophages, unless GSTO1 binds ASC and deglutathionylates ASC at ER, under control of mitochondrial ROS and triacylglyceride synthesis. In macrophages expressing ASCC171A, a mutant ASC without glutathionylation site, activation of NLRP3 inflammasome is GSTO1 independent, ROS independent, and signal 2 less dependent. Moreover, AscC171A mice exhibit NLRP3-dependent hyperinflammation in vivo. Our results demonstrate that glutathionylation of ASC represses NLRP3 inflammasome activation, and GSTO1-promoted ASC deglutathionylation at ER, under metabolic control, is a checkpoint for activating NLRP3 inflammasome.

Comparison of the feedback effect of magnesium and calcium on parathyroid hormone secretion in man

1987 ◽  
Vol 113 (1) ◽  
pp. 117-122 ◽  
Author(s):  
O. Ferment ◽  
P. E. Garnier ◽  
Y. Touitou
Keyword(s):  
Parathyroid Hormone ◽  
Urinary Excretion ◽  
Hormone Secretion ◽  
Plasma Concentrations ◽  
Magnesium Salt ◽  
Saline Injection ◽  
Molar Basis ◽  
Magnesium Salts ◽  
High Doses

ABSTRACT Administration of high doses of magnesium is known to produce a decrease in parathyroid hormone (PTH) secretion in human patients but the effect of magnesium on the secretion of PTH in healthy man is not known. We have looked at the effect of a relatively moderate i.v. dose of magnesium (7·08 mmol) in seven healthy men. In addition and for comparison the effect of calcium (4·25 mmol) was studied. Two magnesium salts were considered, magnesium sulphate (MgSO4) and magnesium pyrrolidone carboxylate (MgPC). Four i.v. injections were given at 08.00 h (MgPC, NaCl (control), MgSO4 and Ca gluconate), with an interval of 1 week between each injection. Whatever the magnesium salt the variations in plasma concentrations of magnesium were the same whereas no change in erythrocyte magnesium was observed. Plasma concentration of C-terminal PTH did not show significant variations after MgPC or saline injection. Both MgSO4 and Ca gluconate produced a statistically significant 30% decrease in plasma PTH levels 45 min after the injection. The effect was more sustained with calcium (2 h) than with magnesium (45 min). The urinary excretion of magnesium was significantly higher after injection of MgSO4 than after MgPC. These results suggest (1) that magnesium was, on a molar basis, less potent than calcium in regulating PTH secretion in vivo, (2) that the nature of the magnesium salt used must be kept in mind for the interpretation of the effect of magnesium on PTH secretion in vivo and (3) that the decrease in plasma PTH can partly explain the larger urinary excretion of magnesium after MgSO4 than after MgPC. J. Endocr. (1987) 113, 117–122

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