Hymenolepis diminuta: uptake of 5-hydroxytryptamine (serotonin), glucose, and changes in worm glycogen levels

1983 ◽  
Vol 61 (7) ◽  
pp. 1469-1474 ◽  
Author(s):  
Denis Cyr ◽  
S. Gruner ◽  
D. F. Mettrick
Keyword(s):  
Glucose Uptake ◽  
Regional Differences ◽  
Anterior Segment ◽  
Hymenolepis Diminuta ◽  
Stimulatory Action ◽  
Specific Antagonist ◽  
5 Ht Uptake ◽  
Stimulation Of

The effects of 5-hydroxytryptamine (5-HT) and its specific antagonist, methylsergide hydrogenmaleinate, on in vitro glucose uptake by Hymenolepis diminuta were followed for up to 60 min. Maximum stimulation of glucose uptake occurred with 0.5 mM 5-HT. With the addition of 10 mM methysergide (MET) glucose uptake decreased by 68%. Glucose uptake was greatest in the anterior, immature region of the worm strobila, and diminished through the middle to the posterior gravid portion of the strobila. 5-HT significantly increased glucose uptake in all three regions. The addition of 3 mM MET eliminated the stimulatory action of 5-HT on glucose uptake in the anterior and middle regions of the strobila; 10 mM MET significantly reduced glucose uptake in all three regions of the worm. The presence of 0.5 mM 5-HT both stimulated glucose uptake and decreased worm glycogen levels in all three regions of the strobila. The further addition of 0.5 mM MET did not affect the reduced glycogen levels. 5-HT uptake by H. diminuta was over 60% higher in the anterior segment of the strobila compared with uptake in the middle and posterior segments. The addition of 3 mM MET significantly decreased 5-HT uptake in the anterior and middle regions of the strobila; 10 mM MET decreased 5-HT uptake in all three regions. The regional differences in 5-HT and glucose uptake by H. diminuta suggest that the tryptaminergic receptors in the strobila are not equally distributed along the length of the worm. The effects of MET on glucose and 5-HT uptake are in part accountable through its action in blocking 5-HT receptors.

Characterization in vitro of H+ secretion and H+:Na+ exchange by an organism normally inhabiting a CO2-rich environment: Hymenolepis diminuta (Cestoda) in the rat intestine

1978 ◽  
Vol 56 (11) ◽  
pp. 2344-2354 ◽  
Author(s):  
R. B. Podesta
Keyword(s):  
Metabolic Pathways ◽  
Intestinal Parasite ◽  
Hymenolepis Diminuta ◽  
Ambient Fluid ◽  
Rat Intestine ◽  
Ion Concentrations ◽  
Intracellular Ion Concentrations ◽  
Metabolic Reactions ◽  
Stimulation Of

H+ and Na+ transport by the intestinal parasite Hymenolepis diminuta were studied in vitro. The flatworms acidified the ambient fluid by secreting H+ and the acidification could not be correlated with organic acid excretion. Ambient CO2-independent H+ secretion was attributed to protons of metabolic origin: dephosphorylation reactions and ionization of organic acids within the tissues. Ambient CO2-dependent H+ secretion was attributed to protons produced as a result of the hydration of CO2 within the tissue and to the stimulation of anaerobic metabolic pathways by CO2 acting as a cosubstrate in energy metabolism. Studies in which Na+ uptake was stimulated by CO2 or glucose and inhibited by ouabain, amiloride, or Na+ replacement suggested a partial direct coupling of Na+ absorption and H+ secretion but the different activation energies and the effect of buffer anions other than HCO3− suggested an indirect interaction. Various interactions were considered, including the effect of CO2 and intracellular ion concentrations on metabolic reactions leading to the supply of protons for H+ secretion and energy for ion transport.

THE EFFECT OF GROWTH HORMONE AND OF CORTISOL ON THE RESPONSE OF ISOLATED RAT DIAPHRAGM TO THE STIMULATING EFFECT OF INSULIN ON GLUCOSE UPTAKE AND ON INCORPORATION OF AMINO ACIDS INTO PROTEIN

1959 ◽  
Vol 18 (4) ◽  
pp. 395-408 ◽  
Author(s):  
K. L. MANCHESTER ◽  
P. J. RANDLE ◽  
F. G. YOUNG
Keyword(s):  
Amino Acids ◽  
Growth Hormone ◽  
Protein Synthesis ◽  
Glucose Uptake ◽  
Carbohydrate Metabolism ◽  
Rat Diaphragm ◽  
Pituitary Growth Hormone ◽  
Isolated Rat ◽  
Stimulation Of

SUMMARY 1. The effect of hypophysectomy, or of adrenalectomy, and injection of pituitary growth hormone (GH) or of cortisol, on the uptake of glucose and the incorporation of glycine into protein by isolated rat diaphragm, and the effect of the addition of insulin in vitro on these processes, has been studied. 2. Both hypophysectomy and adrenalectomy raised the uptake of glucose by isolated diaphragm, while treatment of the intact or of the hypophysectomized rat with GH, or of the intact or of the adrenalectomized rat with cortisol, depressed it. Although hypophysectomy and adrenalectomy did not influence the additional glucose uptake induced by 200 mu./ml. of insulin in vitro, both these operations enhanced the effect of 0·1–1·0 mu./ml. of insulin on glucose uptake by diaphragm in vitro. Treatment of the rat with GH or cortisol diminished the rise in glucose uptake of diaphragm induced by 0·1–1·0 mu./ml. insulin. 3. Hypophysectomy depressed, and administration of GH to the intact or hypophysectomized rat raised, the incorporation of glycine into protein of the isolated diaphragm, but neither of these operations altered the magnitude of the stimulation of incorporation induced by 1·0 mu./ml. insulin. 4. Adrenalectomy raised, and administration of cortisol to the intact or adrenalectomized rat depressed, the incorporation of glycine into protein of the isolated diaphragm; adrenalectomy enhanced, the injection of cortisol diminished, the effect of 1·0 mu./ml. insulin on these processes. 5. The possibility that GH directs insulin towards the stimulation of protein synthesis, in part by restraining the action of insulin on carbohydrate metabolism, is discussed.

Noradrenergic stimulation of serotonin release from rat pineal glands in vitro

1987 ◽  
Vol 114 (1) ◽  
pp. 3-9 ◽  
Author(s):  
V. J. Aloyo ◽  
R. F. Walker
Keyword(s):  
Serotonin Release ◽  
Time Interval ◽  
Intracellular Accumulation ◽  
Differential Distribution ◽  
Intracellular Compartments ◽  
5 Ht Uptake ◽  
Layer Chromatography ◽  
Adrenergic Terminals ◽  
Stimulation Of

ABSTRACT The pharmacodynamics of serotonin (5-hydroxytryptamine; 5-HT) uptake and release were studied in rat pineal glands. Initially, uptake was tested by incubating pineals with several concentrations of [3H]5-HT. The incubation media also contained [14C]mannitol to which cells are impermeable. Since [14C]mannitol accumulates only in extracellular spaces, the radio-labelled sugar was used to determine the differential distribution of [3H]5-HT in pineal compartments. Intracellular accumulation of 3H in pineal glands increased linearly as a function of time for [3H]5-HT concentrations ranging from 1 to 10 μmol/l. The ratio of 3H to 14C also increased for the same time-interval, indicating that the glands accumulated [3H]5-HT preferentially in non-extracellular spaces. [3H]5-HT accumulated in pineal glands which were denervated for more than 7 days before testing, suggesting that uptake is not restricted to adrenergic terminals but also occurs in pinealocytes. In addition to uptake, spontaneous and noradrenaline-stimulated release of [3H]5-HT was tested in perifusion and/or step-transfer systems. Spontaneous release of [3H]5-HT was biphasic consisting of rapid and slower efflux phases. In contrast, release of [14C]mannitol was monophasic, characterized exclusively by rapid efflux. Since [14C]mannitol does not enter cells, the rapid and slower phases of [3H]5-HT efflux may represent release from pineal extracellular and intracellular compartments respectively. The identity of [3H]5-HT in pineal glands and perifusion media was confirmed by thin-layer chromatography. When l-noradrenaline was added to the perifusion media, [3H]5-HT efflux during the slower phase of release was significantly increased above the non-stimulated state. In contrast, d-noradrenaline was significantly less effective than l-noradrenaline in releasing [3H]5-HT. Noradrenaline also stimulated [3H]5-HT release from denervated glands, suggesting that pinealocytes secrete 5-HT in response to noradrenergic signals. Since the pineal is innervated by fibres of the sympathetic division of the autonomic nervous system, differential release of 5-HT may occur in response to changing levels of glandular noradrenaline. J. Endocr. (1987) 114, 3–9

GLUT4 translocation precedes the stimulation of glucose uptake by insulin in muscle cells: potential activation of GLUT4 via p38 mitogen-activated protein kinase

2001 ◽  
Vol 359 (3) ◽  
pp. 639-649 ◽  
Author(s):  
Romel SOMWAR ◽  
David Y. KIM ◽  
Gary SWEENEY ◽  
Carol HUANG ◽  
Wenyan NIU ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Glucose Uptake ◽  
P38 Mapk ◽  
Mitogen Activated Protein Kinase ◽  
Kinase Assay ◽  
Glut4 Translocation ◽  
L6 Myotubes ◽  
Mitogen Activated Protein ◽  
Stimulation Of

We previously reported that SB203580, an inhibitor of p38 mitogen-activated protein kinase (p38 MAPK), attenuates insulin-stimulated glucose uptake without altering GLUT4 translocation. These results suggested that insulin might activate GLUT4 via a p38 MAPK-dependent pathway. Here we explore this hypothesis by temporal and kinetic analyses of the stimulation of GLUT4 translocation, glucose uptake and activation of p38 MAPK isoforms by insulin. In L6 myotubes stably expressing GLUT4 with an exofacial Myc epitope, we found that GLUT4 translocation (t1/2 = 2.5min) preceded the stimulation of 2-deoxyglucose uptake (t1/2 = 6min). This segregation of glucose uptake from GLUT4 translocation became more apparent when the two parameters were measured at 22°C. Preincubation with the p38 MAPK inhibitors SB202190 and SB203580 reduced insulin-stimulated transport of either 2-deoxyglucose or 3-O-methylglucose by 40–60%. Pretreatment with SB203580 lowered the apparent transport Vmax of insulin-mediated 2-deoxyglucose and 3-O-methylglucose without any significant change in the apparent Km for either hexose. The IC50 values for the partial inhibition of 2-deoxyglucose uptake by SB202190 and SB203580 were 1 and 2μM respectively, and correlated with the IC50 for full inhibition of p38 MAPK by the two inhibitors in myotubes (2 and 1.4μM, respectively). Insulin caused a dose- (EC50 = 15nM) and time- (t1/2 = 3min) dependent increase in p38 MAPK phosphorylation, which peaked at 10min (2.3±0.3-fold). In vitro kinase assay of immunoprecipitates from insulin-stimulated myotubes showed activation of p38α (2.6±0.3-fold) and p38β (2.3±0.2-fold) MAPK. These results suggest that activation of GLUT4 follows GLUT4 translocation and that both mechanisms contribute to the full stimulation of glucose uptake by insulin. Furthermore, activation of GLUT4 may occur via an SB203580-sensitive pathway, possibly involving p38 MAPK.

scholarly journals EFFECT OF GROWTH HORMONE ON THE METABOLISM OF THYMUS AND ON THE IMMUNE RESPONSE AGAINST SHEEP ERYTHROCYTES

1971 ◽  
Vol 134 (5) ◽  
pp. 1095-1113 ◽  
Author(s):  
M. R. Pandian ◽  
G. P. Talwar
Keyword(s):  
Growth Hormone ◽  
Immune Response ◽  
Dna Synthesis ◽  
Rna Synthesis ◽  
Calf Serum ◽  
Lymphoid Organs ◽  
Stimulatory Action ◽  
Early Action ◽  
Stimulation Of

The effect of pituitary growth hormone on the biosynthesis of DNA in the thymus and other lymphoid organs, as well as the ability of the rat to respond immunologically to sheep red blood cells, has been evaluated. There is a marked reduction in plaque-forming cells, hemagglutination titers, and DNA synthesis in animals when examined at 15 wk after hypophysectomy. Administration of bovine growth hormone (BGH) leads to the enhancement of DNA synthesis in lymphoid organs and recovery of the immune response. Similar effects of the hormone are observed in plateaued rats. Injection of rabbit anti-BGH globulins, in contrast to normal rabbit globulins, over 5 days causes a drop in the weight of the thymus and in the rate of DNA synthesis in this organ. The thymus is also the organ in which stimulation of DNA synthesis is observed at a time period earlier than the spleen and lymph nodes after a single injection of BGH. The hormone stimulates not only the incorporation of thymidine-3H into DNA in the cortical cells, but also the incorporation of sodium sulfate-35S into TCA-insoluble biopolymers reported to be elaborated in the medullary area of the thymus. An in vitro system for the action of BGH on the thymus has been described. There is an obligatory requirement for calcium, but not for fetal calf serum in the medium for the hormone effect. An early action of the hormone is the enhanced incorporation of uridine-G-3H into RNA in thymocytes which is followed by a stimulation of the synthesis of proteins and DNA. The stimulatory action of growth hormone on RNA synthesis is not because of a facilitated uptake of the radioactive uridine by the cells under hormonal influence, a mechanism by which insulin is observed to increase RNA synthesis in thymocytes in vitro. The action of growth hormone on thymocytes is specific, since thyroid-stimulating hormone (TSH), luteinizing hormone (LH), and heat-inactivated growth hormone are not effective. BGH has also a beneficial action on the regeneration of the thymus and spleen in starved rats.

THE EFFECT OF INSULIN ON THE UPTAKE OF MONOSACCHARIDES BY THE RAT LENS

1961 ◽  
Vol 22 (4) ◽  
pp. 361-369 ◽  
Author(s):  
RUTH LEVARI ◽  
W. KORNBLUETH ◽  
E. WERTHEIMER
Keyword(s):  
Lactic Acid ◽  
Glucose Uptake ◽  
Acid Production ◽  
Lactic Acid Production ◽  
Bicarbonate Buffer ◽  
Total Uptake ◽  
Order Of Magnitude ◽  
Normal Rat ◽  
Stimulation Of

SUMMARY 1. A direct stimulatory effect of insulin, in vitro, on the uptake of galactose, glucosamine and some pentoses by the intact lens, has been established. Stimulation of glucose uptake is perceptible only under certain conditions, and was more pronounced in a medium of bicarbonate buffer than in phosphate. 2. Insulin increased lactic acid production from glucose and from galactose. 3. Chronic diabetes decreased galactose uptake. Insulin, in vitro, restored the uptake to the level of that of normal rat lenses. 4. Phloridzin was found to cancel the effect of insulin. 5. The increase in uptake by insulin was of the same order of magnitude for glucose and galactose, irrespective of the total uptake. The decrease in uptake due to diabetes was quantitatively the same as the increase by insulin in normal rat lenses. The effect of insulin on lactic acid production was identical for both hexoses. 6. The possible existence of two pathways of glucose uptake in the rat lens is discussed.

Regulatory mechanism for the stimulatory action of genistein on glucose uptake in vitro and in vivo

2012 ◽  
Vol 23 (5) ◽  
pp. 501-509 ◽  
Author(s):  
Byung Geun Ha ◽  
Masato Nagaoka ◽  
Takayuki Yonezawa ◽  
Rima Tanabe ◽  
Je Tae Woo ◽  
...  
Keyword(s):  
Glucose Uptake ◽  
Regulatory Mechanism ◽  
Stimulatory Action

Role of NO generation in beta-adrenoceptor-mediated stimulation of rabbit airway ciliary motility

1995 ◽  
Vol 268 (6) ◽  
pp. C1342-C1347 ◽  
Author(s):  
J. Tamaoki ◽  
A. Chiyotani ◽  
M. Kondo ◽  
K. Konno
Keyword(s):  
Methyl Ester ◽  
Epithelial Cells ◽  
Beat Frequency ◽  
Ciliary Beat Frequency ◽  
Stimulatory Action ◽  
Maximal Increase ◽  
Ciliary Motility ◽  
Beta Adrenoceptor ◽  
Stimulation Of

To determine possible contribution of nitric oxide (NO) to the stimulatory action of beta-adrenoceptor agonist on ciliary motility, we measured ciliary beat frequency (CBF) of rabbit cultured tracheal epithelial cells by photoelectric method and NO release by specific amperometric sensors for this molecule in vitro. Salbutamol increased CBF, an effect that was potentiated by superoxide dismutase. Pretreatment of cells with NG-nitro-L-arginine methyl ester (L-NAME) attenuated the salbutamol-induced increase in CBF, causing a rightward displacement of the concentration-response curve by 2-2.5 log units, whereas NG-nitro-D-arginine methyl ester had no effect. The inhibitory effect of L-NAME was reversed by L-arginine but not by D-arginine. Immersion of the NO-selective electrode in the medium containing epithelial cells detected baseline current of 4.6-14.5 pA, which was abolished by L-NAME. Salbutamol dose-dependently increased the concentration of NO in the medium, the maximal increase being 56.2 +/- 5.3 nM (mean +/- SE; P < 0.001). These results suggest that NO is spontaneously released by airway epithelium and that the enhanced release of this molecule may play a role in the beta-adrenoceptor-mediated stimulation of ciliary motility

scholarly journals Nanoparticle Delivered Human Biliverdin Reductase-Based Peptide Increases Glucose Uptake by Activating IRK/Akt/GSK3 Axis: The Peptide Is Effective in the Cell and Wild-Type and Diabetic Ob/Ob Mice

2016 ◽  
Vol 2016 ◽  
pp. 1-15 ◽  
Author(s):  
Peter E. M. Gibbs ◽  
Tihomir Miralem ◽  
Nicole Lerner-Marmarosh ◽  
Mahin D. Maines
Keyword(s):  
Amino Acids ◽  
Cell Culture ◽  
Glucose Uptake ◽  
Animal Studies ◽  
Cultured Cells ◽  
Kinase Domain ◽  
Terminal Segment ◽  
Wild Type ◽  
Stimulation Of

Insulin’s stimulation of glucose uptake by binding to the IRK extracellular domain is compromised in diabetes. We have recently described an unprecedented approach to stimulating glucose uptake. KYCCSRK (P2) peptide, corresponding to the C-terminal segment of hBVR, was effective in binding to and inducing conformational change in the IRK intracellular kinase domain. Although myristoylated P2, made of L-amino acids, was effective in cell culture, its use for animal studies was unsuitable. We developed a peptidase-resistant formulation of the peptide that was efficient in both mice and cell culture systems. The peptide was constructed of D-amino acids, in reverse order, and blocked at both termini. Delivery of the encapsulated peptide to HepG2 and HSKM cells was confirmed by its prolonged effect on stimulation of glucose uptake (>6 h). The peptide improved glucose clearance in both wild-type and Ob/Ob mice; it lowered blood glucose levels and suppressed glucose-stimulated insulin secretion. IRK activity was stimulated in the liver of treated mice and in cultured cells. The peptide potentiated function of IRK’s downstream effector, Akt-GSK3-(α,β)axis. Thus, P2-based approach can be used for improving glucose uptake by cells. Also, it allows for screening peptidesin vitroand in animal models for treatment of diabetes.

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