Rate of Incorporation of CO2 Carbon into Glucose and Other Body Constituents in Vivo

1975 ◽  
Vol 53 (5) ◽  
pp. 895-902 ◽  
Author(s):  
R. A. Shipley ◽  
A. P. Gibbons
Keyword(s):  
Fasting Glucose ◽  
Specific Activity ◽  
Fold Increase ◽  
Whole Body ◽  
Appreciable Amount ◽  
Hepatic Glycogen ◽  
Total Lipids ◽  
Fourfold Increase ◽  
Glucose Carbon

Specific activity curves of respired CO2 and of body glucose after intravenous NaH14CO3 as tracer and, in separate experiments, after [U-14C]glucose as tracer were employed to assess rate of interchange of carbon between HCO3 and glucose, and to calculate other rates of input and output for each of these substances. Solution for six rates attending the model was by integrals rather than by curve analysis. Fasting caused a twofold increase in rate of transport of CO2 carbon to glucose. Whereas in fed animals this rate was only 7% of the forward flow from glucose to CO2, it rose to 31% during fasting. Glucose carbon derived from CO2 rose from 3.7 to 20%. As expected, the rates of entry of new glucose to blood, and the conversion rate of glucose to products in body depots and to CO2 were reduced by fasting, whereas, the non-glucose input to CO2 was increased. Fasting was attended by a 20-fold increase in rate of conversion of CO2-derived carbon to hepatic glycogen and a fourfold increase to non-hepatic glycogen. Protein exceeded all whole-body depots for rate of acceptance of such carbon, and total lipids received an appreciable amount, but fasting caused no overall increase for either.

Degradation Rate of Aircraft Deicing Fluid in a Sequential Biological Reactor

1992 ◽  
Vol 26 (9-11) ◽  
pp. 2061-2064 ◽  
Author(s):  
Y. Sabeh ◽  
K. S. Narasiah
Keyword(s):  
Reaction Rate ◽  
Rate Coefficient ◽  
Fold Increase ◽  
Organic Load ◽  
Appreciable Amount ◽  
Biological Degradation ◽  
Order Model ◽  
Fourfold Increase ◽  
First Order ◽  
Deicing Fluid

Glycol-based fluids are used at northern airports during the winter to deice aircraft prior to takeoff. As a result of these operations, an appreciable amount of deicing fluid mixes with runoff and finds its way into nearby streams and lakes. The research described herein focuses on establishing the reaction rate coefficient (k) for the biological degradation of UCAR ADF-D in a sequential biological reactor under different conditions of temperature and organic bad. The rate of removal of the deicing chemical follows a first-order model. It was found that, at 22°C with a food-to-micrcorganisms ratio (F/M) of less than or equal to 2.8, a fourfold increase in F/M reduces k values by a factor of eight. The organic load is less sensitive when F/M is equal to or greater than 2.8: a seven-fold increase in F/M decreases k by only a fector of three. Temperature is very important since, when F/M ≈ 2, Jc returned values of 1.03, 0.29, and 0.05, respectively, for temperatures of 22°C, 10°C, and 4°C. This study clearly demonstrates that UCAR ADF-D can be treated biologically and that the rate of removal can be significantly affected by organic load and temperature.

Influence of C-ANF receptor and neutral endopeptidase on pharmacokinetics of ANF in rats

1991 ◽  
Vol 260 (1) ◽  
pp. R208-R216 ◽  
Author(s):  
P. J. Chiu ◽  
G. Tetzloff ◽  
M. T. Romano ◽  
C. J. Foster ◽  
E. J. Sybertz
Keyword(s):  
High Performance ◽  
Fold Increase ◽  
Neutral Endopeptidase ◽  
Volume Of Distribution ◽  
Fourfold Increase ◽  
Control Value ◽  
Enzymatic Pathways ◽  
Hydrolysis Of

The role of C-atrial natriuretic factor (ANF) receptors and neutral endopeptidase (NEP) in the pharmacokinetics and hydrolysis of 125I-labeled ANF was evaluated in rats by using C-ANF and SCH 39370 to block the nonenzymatic and enzymatic pathways, respectively. After a bolus injection of 125I-ANF, the resulting area under the plasma concentration curve (AUC) with C-ANF treatment was seven times the control value with regard to trichloroacetic acid-precipitable (TCA-ppt) radioactivity (intact ANF). SCH 39370 tended to increase AUC, but the changes were not significant. Nevertheless, SCH 39370 suppressed the appearance of TCA-soluble radioactivity (hydrolytic products), indicating that in vivo inhibition of ANF degradation had occurred. SCH 39370 plus C-ANF produced a 15-fold increase in AUC for TCA-ppt radioactivity and a reduction in plasma TCA-soluble radioactivity. High-performance liquid chromatography (HPLC) analysis confirmed that combination treatment increased intact ANF and reduced hydrolytic products in the plasma. SCH 39370 reduced clearance (C) without altering volume of distribution in steady state (Vss) and half-life (t1/2). C-ANF decreased both C and Vss leading to a fourfold increase in t1/2, which was further prolonged by SCH 39370 (7.5 times control). Bilateral nephrectomy caused a proportionally similar decrease in Vss and C without changing t1/2, suggesting significant extrarenal metabolism of ANF. SCH 39370 systemically inhibits ANF hydrolysis; the resulting increase in ANF, however, is masked by the great capacity of ANF clearance receptors but can be revealed with excess C-ANF, suggesting that the plasma ANF concentrations are determined by the interplay of the C-ANF receptor and NEP systems.

Copper transport in rats involving a new plasma protein

1985 ◽  
Vol 249 (1) ◽  
pp. E77-E88 ◽  
Author(s):  
K. C. Weiss ◽  
M. C. Linder
Keyword(s):  
Time Course ◽  
Specific Activity ◽  
High Specific Activity ◽  
Apparent Molecular Weight ◽  
Female Rats ◽  
Whole Body ◽  
Peripheral Tissues ◽  
Chelex 100

The time course of distribution of high-specific activity 67CuCl2 to tissues and plasma components was followed in adult, female rats. Immediately after intubation or injection, tracer 67Cu associated with two components of the blood plasma separable on columns of Sephadex G-150: albumin and another (larger) component, which was not ceruloplasmin. The latter, tentatively named transcuprein, had an apparent molecular weight of 270,000 and a high affinity for Cu2+, as judged by processing through Chelex-100, dilution, and exchange with albumin copper, in vitro and in vivo. It was capable of donating copper to tumor cells in serum-free medium. Analysis of "cold" plasma by furnace atomic absorption confirmed the presence of 10-15% of plasma copper in this peak. Plots of percent dose and 67Cu specific activity against time showed that copper followed a very specific pathway after binding to albumin and transcuprein, entering mainly the liver, then reappearing in the plasma on ceruloplasmin, and then achieving peak distribution in peripheral tissues (muscles, brain, etc.). 67Cu disappeared from liver and kidney with an apparent half-life of 4.5 days, the same exponential rate found for whole body turnover. Apparent turnover of ceruloplasmin copper was more rapid. Even after 7-12 days, tracer copper in plasma was still found exclusively with ceruloplasmin. The results indicate that copper follows a carefully prescribed path, on entering the blood and binding to a new transport protein.

scholarly journals The phospholipid-dependence of uridine diphosphate glucuronyltransferase. Effect of protein deficiency on the phospholipid composition and enzyme activity of rat liver microsomal fraction

1974 ◽  
Vol 137 (3) ◽  
pp. 567-574 ◽  
Author(s):  
A. B. Graham ◽  
B. G. Woodcock ◽  
G. C. Wood
Keyword(s):  
Specific Activity ◽  
Phospholipid Composition ◽  
Fold Increase ◽  
Protein Deficiency ◽  
Male Rats ◽  
Striking Difference ◽  
Uridine Diphosphate ◽  
Microsomal Membranes ◽  
Microsomal Phospholipid

After force-feeding a protein-free diet to male rats for 5–7 days a substantial (2.4-fold) increase in the specific activity of the liver microsomal enzyme UDP-glucuronyltransferase (EC 2.4.1.17) was observed. A similar activation of the enzyme occurred when rats were fed on a low-protein (5%, w/w, casein) diet for 60 days. Although both the short- and long-term protein-deficient diets decreased the contents of microsomal protein and phospholipid in liver tissue they did not significantly alter the ratio of these major membrane components. Protein deficiency profoundly altered the phospholipid composition of microsomal membranes. The most striking difference in microsomal phospholipid composition between control and protein-deficient rats was their content of lysophosphatides. Whereas microsomal membranes from protein-deficient rats contained significant proportions of lysophosphatidylcholine and lysophosphatidylethanolamine very little or no lysophosphatides were detected in control preparations. Pretreatment of microsomal fractions from normal rats with phospholipase A markedly increased their UDP-glucuronyltransferase activity as did their pretreatment with lysophosphatidylcholine. It is concluded that the quantities of lysophosphatides present in microsomal membranes from protein-deficient rats were sufficient to have caused the increased UDP-glucuronyltransferase activities of these preparations. Evidence is presented suggesting that these changes in microsomal phospholipid composition and UDP-glucuronyltransferase activity caused by protein deficiency reflect changes that occur in vivo. The possible physiological significance of these findings is discussed.

scholarly journals Stimulation of cell proliferation in skeletal tissues of the rat by defined parathyroid hormone fragments

1991 ◽  
Vol 277 (3) ◽  
pp. 863-868 ◽  
Author(s):  
D Sömjen ◽  
K D Schlüter ◽  
E Wingender ◽  
H Mayer ◽  
A M Kaye
Keyword(s):  
Parathyroid Hormone ◽  
Bone Resorption ◽  
Thymidine Incorporation ◽  
Specific Activity ◽  
Fold Increase ◽  
Dependent Manner ◽  
Equimolar Concentration ◽  
Dose Dependent

We have found, in previous studies in vitro using skeletal derived cell cultures, that mid-region fragments of human parathyroid hormone (hPTH) stimulate [3H]thymidine incorporation into DNA and increase the specific activity of the brain-type isoenzyme of creatine kinase (CK). These changes occurred without an increase in cyclic AMP formation which is linked to bone resorption. In this study, we found that the mid-region fragment hPTH-(28-48) stimulated CK activity in diaphysis, epiphysis and kidney in a time- and dose-dependent manner, parallel to the effects of the whole molecule bovine (b)PTH-(1-84) and the fully active fragment hPTH-(1-34). The increase caused by hPTH-(28-48) at a dose of 1.25 micrograms/rat was not less than the 2-fold increase caused by a roughly equimolar concentration bPTH-(1-84). A significant increase was reached at 1 h after intraperitoneal injection in all cases. All three sequences of PTH caused an increase in [3H]thymidine incorporation into DNA in diaphysis and epiphysis, but not in kidney, 24 h after injection. A fragment further towards the C-terminal, hPTH-(34-47), was inactive compared with an equimolar concentration of the fragment hPTH-(25-39), which stimulated both CK activity and DNA synthesis. These results in vivo are in line with previous findings in vitro; they provide further support for the suggestion that mid-region fragments of the PTH molecule could be used to induce bone formation without incurring the deleterious effect of bone resorption.

scholarly journals Effects of fasting on hepatic and peripheral glucose metabolism in conscious rats with near-total fat depletion

1995 ◽  
Vol 310 (3) ◽  
pp. 819-826 ◽  
Author(s):  
N Barzilai ◽  
D Massillon ◽  
L Rossetti
Keyword(s):  
Glucose Metabolism ◽  
Experimental Diabetes ◽  
Hepatic Glucose Production ◽  
Glycogen Synthesis ◽  
Fold Increase ◽  
Whole Body ◽  
Conscious Rats ◽  
Hepatic Glucose ◽  
Total Fat

Experimental diabetes and fasting are both associated with hypoinsulinaemia and share several other metabolic features. We investigated hepatic and peripheral glucose metabolism in young rats after near-total depletion of their fat mass. Conscious rats were fasted for 72 h (n = 13), while 6 h-fasted animals (n = 14) served as controls. Rats were studied either during saline infusion or insulin (18 m-units/kg per min)-clamp studies. In fasting, despite a 2-fold increase in hepatic glucose-6-phosphatase (Glc-6-Pase) Vmax. (from 16 +/- 2 mumol/g of liver per min in control; P < 0.001), the basal hepatic glucose production (HGP) decreased by 47% [from 88 +/- 3 mumol/kg lean body mass (LBM) per min in control; P < 0.01]. The decreased HGP in fasting was associated with a 70% decrease in the hepatic levels of glucose 6-phosphate (Glc-6-P) (from 366 +/- 53 nmol/g wet wt. in control; P < 0.01). Thus Glc-6-Pase activity assayed in the presence of the Glc-6-P levels found in vivo was decreased by 44%. During hyperinsulinaemia, peripheral glucose uptake was decreased by 15% with 3 days of fasting (from 272 +/- 17 mumol/kg LBM per min in control; P < 0.01). This was completely accounted for by a 42% decrease in whole-body glycolysis (P < 0.01), while the rate of glycogen synthesis was unchanged. Thus fasting (after near-total fat depletion) differs from experimental diabetes because: (1) despite markedly increased Glc-6-Pase, HGP is decreased in fasting, due to a marked decrease in the substrate level (Glc-6-P) in vivo; and (2) the impairment in peripheral insulin sensitivity in fasting is due to a decrease in the glycolytic, and not the glycogen-synthetic, pathway.

Fever-range hyperthermia dynamically regulates lymphocyte delivery to high endothelial venules

Blood ◽  
2001 ◽  
Vol 97 (9) ◽  
pp. 2727-2733 ◽  
Author(s):  
Sharon S. Evans ◽  
Wan-Chao Wang ◽  
Mark D. Bain ◽  
Randy Burd ◽  
Julie R. Ostberg ◽  
...  
Keyword(s):  
Lymph Node ◽  
Acute Infection ◽  
Fold Increase ◽  
Whole Body ◽  
Lymphoid Tissues ◽  
Hyperthermia Treatment ◽  
High Endothelial Venules ◽  
Adhesive Interactions

Abstract Fever is associated with increased survival during acute infection, although its mechanism of action is largely unknown. This study found evidence of an unexpectedly integrated mechanism by which fever-range temperatures stimulate lymphocyte homing to secondary lymphoid tissues by increasing L-selectin and α4β7 integrin–dependent adhesive interactions between circulating lymphocytes and specialized high endothelial venules (HEV). Exposure of splenic lymphocytes in vivo to fever-like whole-body hyperthermia (WBH; 39.8 ± 0.2°C for 6 hours) stimulated both L-selectin and α4β7 integrin–dependent adhesion of lymphocytes to HEV under shear conditions in lymph nodes and Peyer patches. The adhesiveness of HEV ligands for L-selectin and α4β7 integrin (ie, peripheral lymph node addressin and mucosal addressin cell adhesion molecule-1) also increased during WBH or febrile responses associated with lipopolysaccharide-induced or turpentine-induced inflammation. Similar increases in HEV adhesion occurred during hyperthermia treatment of lymph node and Peyer patch organ cultures in vitro, indicating that the local lymphoid tissue microenvironment is sufficient for the hyperthermia response. In contrast, WBH did not augment adhesion in squamous endothelium of nonlymphoid tissues. Analysis of homing of α4β7hi L-selectinlo murine TK1 cells and L-selectinhi α4β7 integrin-negative 300.19/L-selectin transfectant cells showed that fever-range temperatures caused a 3- to 4-fold increase in L-selectin and α4β7 integrin–dependent trafficking to secondary lymphoid tissues. Thus, enhanced lymphocyte delivery to HEV by febrile temperatures through bimodal regulation of lymphocyte and endothelial adhesion provides a novel mechanism to promote immune surveillance.

scholarly journals Genetic and Functional Analysis of the Soluble Oxaloacetate Decarboxylase from Corynebacterium glutamicum

2010 ◽  
Vol 192 (10) ◽  
pp. 2604-2612 ◽  
Author(s):  
Simon Klaffl ◽  
Bernhard J. Eikmanns
Keyword(s):  
Specific Activity ◽  
Fold Increase ◽  
Peptide Mass Fingerprinting ◽  
Transcriptional Analysis ◽  
Lysine Production ◽  
Ionization Time ◽  
Peptide Mass ◽  
Methyltransferase Gene ◽  
High Level

ABSTRACT Soluble, divalent cation-dependent oxaloacetate decarboxylases (ODx) catalyze the irreversible decarboxylation of oxaloacetate to pyruvate and CO2. Although these enzymes have been characterized in different microorganisms, the genes that encode them have not been identified, and their functions have been only poorly analyzed so far. In this study, we purified a soluble ODx from wild-type C. glutamicum about 65-fold and used matrix-assisted laser desorption ionization-time of flight (MALDI-TOF) analysis and peptide mass fingerprinting for identification of the corresponding odx gene. Inactivation and overexpression of odx led to an absence of ODx activity and to a 30-fold increase in ODx specific activity, respectively; these findings unequivocally confirmed that this gene encodes a soluble ODx. Transcriptional analysis of odx indicated that there is a leaderless transcript that is organized in an operon together with a putative S-adenosylmethionine-dependent methyltransferase gene. Biochemical analysis of ODx revealed that the molecular mass of the native enzyme is about 62 ± 1 kDa and that the enzyme is composed of two ∼29-kDa homodimeric subunits and has a Km for oxaloacetate of 1.4 mM and a V max of 201 μmol of oxaloacetate converted per min per mg of protein, resulting in a k cat of 104 s−1. Introduction of plasmid-borne odx into a pyruvate kinase-deficient C. glutamicum strain restored growth of this mutant on acetate, indicating that a high level of ODx activity redirects the carbon flux from oxaloacetate to pyruvate in vivo. Consistently, overexpression of the odx gene in an l-lysine-producing strain of C. glutamicum led to accumulation of less l-lysine. However, inactivation of the odx gene did not improve l-lysine production under the conditions tested.

In Vivo Disposal Kinetics of Blood Glucose Carbon to Hepatic and Non-hepatic Products in Normal and Diabetic Rats

1974 ◽  
Vol 52 (4) ◽  
pp. 797-807 ◽  
Author(s):  
R. A. Shipley ◽  
A. P. Gibbons ◽  
E. B. Chudzik
Keyword(s):  
Glycogen Content ◽  
No Reduction ◽  
Neutral Lipids ◽  
Diabetic Rats ◽  
High Rate ◽  
Hepatic Tissue ◽  
Hepatic Glycogen ◽  
Glucose Carbon ◽  
Kinetics Of

Individual rates of conversion of glucose (carbon) to a variety of products were determined separately for hepatic and non-hepatic tissue in fasted normal and diabetic rats. Because the method requires a sustained sojourn of 14C tracer in a conversion product, curves of accumulation of 14C during 6–8 h were obtained for each product. For non-hepatic tissue a satisfactory rise to a sustained level was observed for all products in normals and diabetics, but in the case of liver such behavior was observed only for glycogen in diabetics, neutral lipids in normals, and protein and phospholipids in both groups. For all measurable rates to products in both liver and non-hepatic tissue diabetes caused no reduction, but the associated rate constants and clearance constants were invariably impaired. Rates to non-hepatic products exceeded those to hepatic, save for glycogen in diabetics, however as ratios to recipient mass the hepatic rates were higher. An observed high rate to hepatic glycogen in diabetics accompanying a high glycogen content points to a relative depression of phosphorylase and/or activation of synthetase by hyperglycemia. It also argues against the presence of an on–off mechanism which would direct movement either to synthesis alone or degradation alone.

scholarly journals Cyclic AMP-modulated phosphorylation of intermediate filament proteins in cultured avian myogenic cells

1982 ◽  
Vol 2 (9) ◽  
pp. 1104-1114
Author(s):  
D L Gard ◽  
E Lazarides
Keyword(s):  
Cyclic Amp ◽  
Intermediate Filament ◽  
Specific Activity ◽  
Fold Increase ◽  
Major Protein ◽  
Myogenic Cells ◽  
Intermediate Filament Proteins ◽  
Dependent Protein

The intermediate filament proteins desmin and vimentin and the muscle tropomyosins were the major protein phosphate acceptors in 8-day-old myotubes incubated for 4 h in medium containing radiolabeled phosphate. The addition of isoproterenol or 8-bromo-cyclic AMP (BrcAMP) resulted in a two- to threefold increase in incorporation of 32PO4 into both desmin and vimentin, whereas no changes in the incorporation of 32PO4 into tropomyosin or other cellular proteins were observed. The BrcAMP- or hormonally induced increase in 32PO4 incorporation into desmin and vimentin was independent of protein synthesis and was not caused by stimulation of protein phosphate turnover. In addition, BrcAMP did not induce significant changes in the specific activity of the cellular ATP pool. These data suggest that the observed increase in 32PO4 incorporation represented an actual increase in phosphorylation of the intermediate filament proteins desmin and vimentin. Two-dimensional tryptic analysis of desmin from 8-day-old myotubes revealed five phosphopeptides of which two showed a 7- to 10-fold increase in 32PO4 incorporation in BrcAMP-treated myotubes. Four of the phosphopeptides identified in desmin labeled in vivo were also observed in desmin phosphorylated in vitro by bovine heart cAMP-dependent protein kinase. Although phosphorylation of desmin and vimentin was apparent in myogenic cells at all stages of differentiation, BrcAMP- and isoproterenol-induced increases in phosphorylation of these proteins were restricted to mature myotubes. These data strongly suggest that in vivo phosphorylation of the intermediate filament proteins desmin and vimentin is catalyzed by the cAMP-dependent protein kinases and that such phosphorylation may be regulated during muscle differentiation.

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