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Biomedical subjects

H Greten

Publications and source records attributed to H Greten.

At least 127 records · Page 7Linked to original sources
PubMed1991

Association of Metformin's effect to increase insulin-stimulated glucose transport with potentiation of insulin-induced translocation of glucose transporters from intracellular pool to plasma membrane in rat adipocytes.

To examine the cellular mechanism of the antihyperglycemic action of metformin, we studied its effect on various functional and molecular parameters involved in the pathogenesis of insulin resistance. Isolated rat adipocytes were incubated with or without metformin (1-100 micrograms/ml) for 2 h at 37 degrees C followed by an incubation with or without insulin (1.72 nM). Metformin treatment had no significant effect on basal 3-O-methylglucose uptake. In contrast, metformin increased insulin-stimulated glucose transport in a dose-dependent manner up to 43 +/- 7%. This effect was neither associated with a significant effect of metformin on trace insulin binding (1.74 +/- 0.20% without metformin vs. 1.89 +/- 0.30% with metformin; P greater than 0.05) nor with an effect of metformin on insulin-receptor kinase activity as measured by 32P incorporation into the 95,000-Mr beta-subunit of the insulin receptor and an exogenous substrate, histone 2B.(ABSTRACT TRUNCATED AT 250 WORDS)

3-O-Methylglucose↗
PubMed1991

Evidence that metformin ameliorates cellular insulin-resistance by potentiating insulin-induced translocation of glucose transporters to the plasma membrane.

To examine the cellular mechanism of the antihyperglycemic action of metformin we studied the effect of metformin on various functional and molecular parameters involved in the pathogenesis of insulin resistance. Isolated rat adipocytes were incubated with or without metformin (1-100 micrograms/ml) for 2 hours at 37 degrees C followed by an incubation with or without insulin (10 ng/ml). Metformin treatment had no significant effect on basal 3-0 methylglucose uptake. In contrast, Metformin increased insulin-stimulated glucose transport in a dose dependent manner up to 43 +/- 7%. This effect was neither associated with a significant effect of Metformin on trace insulin binding, 1.74 +/- .2% (-M) vs. 1.89 +/- .3% (+M), P greater than 0.05, nor with an effect of metformin on in vivo activation of insulin receptor kinase activity as measured by 32P-incorporation into the 95 kDa beta-subunit of the insulin receptor and an exogenous substrate, histone 2B. Determination of glucose transporter numbers in subcellular membrane fractions, plasma membranes and low-density microsomes, using cytochalasin B binding and immunodetection revealed that metformin's effect to increase insulin-stimulated glucose transport is associated with a potentiation (38 +/- 5%) of insulin-induced translocation of glucose transporters from the intracellular pool to the plasma membrane, while the basal state was not significantly affected. Determination of specific glucose transporter mRNA-levels revealed that this metformin effect is not associated with an increase in glucose transporter gene expression.(ABSTRACT TRUNCATED AT 250 WORDS)

Adipose Tissue↗
PubMed1991

[Hyperlipidemias].

Explore the source record for details and available documents.

Combined Modality Therapy↗
PubMed1991

Modulation of platelet-derived growth factor A- and B-chain/c-sis mRNA by tumor necrosis factor and other agents in adenocarcinoma cells.

Human Platelet Derived Growth Factors (PDGF) are potent mitogens for mesenchymal cells and encoded by two related genes, the A- (or 1-) and B- (or 2-) chain. The latter is known as the human homolog (c-sis) of the v-sis oncogene. We investigated the expression and cytokine-mediated regulation of PDGF A- and B-chain mRNA in endoderm-derived cells, i.e. cultured human pancreatic adenocarcinoma cells. Northern blot analysis revealed that out of 14 cells lines 11 were positive for the A-chain and 10 for the B-chain. Tumor Necrosis Factor (TNF) -alpha and -beta, but not Interferon (IFN) -gamma, drastically upregulate the mRNA levels for PDGF B-chain and for the A-chain in a dose-dependent manner in nearly every pancreatic tumor cell line investigated (n = 6). With respect to the signal pathway stimulated by TNF, no evidence emerged for an activation of protein kinase A. The inhibition of protein kinase C by staurosporine (in the absence or presence of TNF) as well as its stimulation by PMA resulted in an increased mRNA level for the B-chain, indicating a functional role of PKC in this system. Furthermore, time course experiments and Cycloheximide treatment showed that the A- and B-chain mRNA are regulated by different mechanisms in transformed epithelial cells. Irrespective of these differences, the sum of their biological functions may contribute to the phenomenon of desmoplasia in pancreatic tumors by epithelial/mesenchymal interactions.

Adenocarcinoma↗
PubMed1990

[Color-coded Doppler sonography for phlebothrombosis].

Between November 1988 and February 1990, a total of 180 patients (76 men and 104 women; mean age 59 [17-79] years), suspected of having sustained a deep-vein or pelvic thrombosis were examined by colour Doppler ultrasound, the results being compared with those obtained by conventional phlebography. For 154 phlebographically confirmed acute venous thromboses (demonstrated by colour Doppler ultrasound in 153), four older thromboses (colour Doppler ultrasound: 7), and 22 without significant venous disease (colour Doppler ultrasound: 20), the specificity for colour Doppler ultrasound was 99%, its sensitivity 94%. In 49 patients with confirmed venous thrombosis thrombolytic treatment was started with 250,000 IU urokinase, followed by 62,500 IU hourly, the results being assessed by colour Doppler ultrasound and phlebography. This gave a specificity, compared with phlebography, of 99%, and a sensitivity of 97%. These data indicate that, in the diagnosis of venous thrombosis of the legs, colour Doppler ultrasound noninvasively provides information at least as reliable as phlebography. It may even be superior to phlebography in the demonstration of residual flow in partly thrombosed veins.

Adolescent↗
PubMed1990

[Modification of gas exchange and metabolism by various hemodialysis procedures].

We compared the effects of various dialysate composition on pulmonary and transdialyzer gas exchange in patients during hemodialysis. Under acetate hemodialysis there was a permanent loss of CO2 (45-68 ml/min) into the dialysate resulting in a significant decrease of arterial pO2, which can be explained by a reduced alveolar ventilation. The pulmonary oxygen uptake increased up to +20% during treatment, reflecting rising energy metabolism and possibly increased cardiopulmonary instability. Using different concentrates for bicarbonatehemodialysis we saw a moderate to clinical relevant uptake of CO2 (40-60 ml/min) from the dialysate into the blood of the patients, cause the pCO2 in the dialysate varied between 45 and 115 mmHg. Bicarbonate hemodialysis with high pCO2-levels in the dialysate led to hyperventilation and markedly increased oxygen consumption. In critically ill hemodialysis patients the pathophysiologic effects on pulmonary gas exchange of either acetatehemodialysis and bicarbonatehemodialysis with high pCO2 can explain the higher incidence of severe complications.

Acetates↗
PubMed1990

Biotinyl-high-density lipoproteins as a probe for the determination of high-density lipoprotein turnover in humans.

A simple and reliable method has been developed for the determination of high-density lipoprotein (HDL) turnover in humans. In this method, complex formation of [14C]methylavidin with biotinyl-HDL3 and subsequent precipitation of excess [14C]methylavidin with biotinyl-silica-gel is utilized for the detection of as little as 0.1 microgram of biotinyl-HDL3 (by protein)/ml of serum with high precision and reproducibility, at 7.9 +/- 0.9% (n = 7) of the peptidyl lysine modified. In serial dilutions and quadruplicate determinations the intra- and interassay variations were less than 4.7% and 5.2%, respectively (n = 5). Recovery of biotinyl-HDL3 averaged 92 +/- 5.7% throughout the working range of the assay (n = 4). Variations in the levels of HDL or very-low-density lipoprotein (VLDL) did not interfere with the measurement of biotinyl-HDL3 in serum. Also, results were not affected by storage of serum samples at -80 degrees C for up to 4 weeks. After reinjection of autologous biotinyl-HDL3 (0.12 mg protein/kg body wt.) into five normolipidemic male volunteers, typical decay curves were obtained. The mean half-life of biotinyl-HDL3 was 5.1 +/- 0.5 days, no different from that reported for radiolabeled HDL or radiolabeled HDL apolipoproteins. Routine immunobinding analysis did not reveal formation of antibodies with specificity towards HDL 4 weeks after the reinjection studies. From this it appears that biotinyl-HDL3 is a suitable probe and a safe and reliable alternative for the determination of HDL turnover in humans when application of radiolabeled HDL is not desirable.

Adult↗
PubMed1990

High-density lipoprotein particle uptake and selective uptake of high-density lipoprotein-associated cholesteryl esters by J774 macrophages.

High-density lipoprotein (HDL) cholesteryl esters are taken up by fibroblasts via HDL particle uptake and via selective uptake, i.e., cholesteryl ester uptake independent of HDL particle uptake. In the present study we investigated HDL selective uptake and HDL particle uptake by J774 macrophages. HDL3 (d = 1.125-1.21 g/ml) was labeled with intracellularly trapped tracers: 125I-labeled N-methyltyramine-cellobiose-apo A-I (125I-NMTC-apo A-I) to trace apolipoprotein A-I (apo A-I) and [3H]cholesteryl oleyl ether to trace cholesteryl esters. J774 macrophages, incubated at 37 degrees C in medium containing doubly labeled HDL3, took up 125I-NMTC-apo A-I, indicating HDL3 particle uptake (102.7 ng HDL3 protein/mg cell protein per 4 h at 20 micrograms/ml HDL3 protein). Apparent HDL3 uptake according to the uptake of [3H]cholesteryl oleyl ether (470.4 ng HDL3 protein/mg cell protein per 4 h at 20 micrograms/ml HDL3 protein) was in significant excess on 125I-NMTC-apo A-I uptake, i.e., J774 macrophages demonstrated selective uptake of HDL3 cholesteryl esters. To investigate regulation of HDL3 uptake, cell cholesterol was modified by preincubation with low-density lipoprotein (LDL) or acetylated LDL (acetyl-LDL). Afterwards, uptake of doubly labeled HDL3, LDL (apo B,E) receptor activity or cholesterol mass were determined. Preincubation with LDL or acetyl-LDL increased cell cholesterol up to approx. 3.5-fold over basal levels. Increased cell cholesterol had no effect on HDL3 particle uptake. In contrast, LDL- and acetyl-LDL-loading decreased selective uptake (apparent uptake 606 vs. 366 ng HDL3 protein/mg cell protein per 4 h in unloaded versus acetyl-LDL-loaded cells at 20 micrograms HDL3 protein/ml). In parallel with decreased selective uptake, specific 125I-LDL degradation was down-regulated. Using heparin as well as excess unlabeled LDL, it was shown that HDL3 uptake is independent of LDL (apo B,E) receptors. In summary, J774 macrophages take up HDL3 particles. In addition, J774 cells also selectively take up HDL3-associated cholesteryl esters. HDL3 selective uptake, but not HDL3 particle uptake, can be regulated.

Animals↗
PubMed1990

Mycobacterium kansasii infection limited to skin and lymph node in a patient with AIDS.

The case of a 36-year-old HIV-1-positive patient is presented. After an episode of Pneumocystis carinii pneumonia and cytomegalovirus retinitis a pruritic lesion developed on the thigh with subsequent intracutaneous abscess formation and regional lymph-node enlargement. Mycobacterium kansasii was demonstrated in lymph-node and abscess material. With a tuberculostatic triple-drug regimen the lesions resolved completely. Cutaneous involvement in the course of non-tuberculous mycobacteriosis in the acquired immunodeficiency syndrome is discussed.

Acquired Immunodeficiency Syndrome↗
PubMed1990

Lovastatin versus bezafibrate: efficacy, tolerability, and effect on urinary mevalonate.

Lovastatin and benzafibrate have proved effective in lowering low-density-lipoprotein (LDL) cholesterol and elevating high-density-lipoprotein (HDL) cholesterol. We compared their tolerability, safety, and effects on lipoproteins and urinary mevalonate excretion in a short-term study. Forty patients with primary hypercholesterolemia were enrolled in a single-blind randomized study with a diet/placebo period of 8 weeks and a treatment period of 12 weeks. Twenty patients received lovastatin (final average dose 70.5 mg/day), and 20 patients received bezafibrate 400 mg/day. LDL cholesterol was lowered by 35% (from 323 to 208 mg/dl) with lovastatin and by 8% (from 289 to 264 mg/dl) with benzafibrate. HDL cholesterol increased by 21 and 20% with lovastatin and benzafibrate, respectively. Twenty-four-hour urinary mevalonic acid output decreased by 37% during treatment with lovastatin and by 2% during treatment with bezafibrate. Thus, the lowering of cholesterol by lovastatin, but not by bezafibrate, can be attributed to inhibition of HMG CoA (3-hydroxy-3-methylglutaryl coenzyme A) reductase. Both lovastatin and bezafibrate are well tolerated.

Adult↗
PubMed1990

Potential mechanism of insulin resistance in ageing: impaired insulin-stimulated glucose transport due to a depletion of the intracellular pool of glucose transporters in Fischer rat adipocytes.

To examine the cellular mechanism responsible for impaired insulin action in ageing, we determined various in-vitro parameters involved in the pathogenesis of insulin resistance, i.e. basal and insulin-stimulated [14C]3-O-methylglucose transport (3OMG), 125I-labelled insulin binding, activation of insulin receptor kinase (IRKA) in intact cells, and number and subcellular distribution of glucose transporters in subcellular membrane fractions of adipocytes from 6- (FR-6) and 24- (FR-24) month-old Fischer rats. Ageing had no effect on basal 3OMG (12 +/- 4 vs 13 +/- 3 fmol/5 x 10(4) cells, means +/- S.E.M.); in contrast, in FR-24 rats insulin-stimulated 3OMG was markedly decreased by 43% when compared with that in FR-6 rats (158 +/- 14 vs 90 +/- 8 fmol/5 x 10(4) cells; P less than 0.01). Insulin binding to adipocytes from FR-6 rats was 2.40 +/- 0.38% compared with 2.28 +/- 0.47% in FR-24 (P not significant). Moreover, ageing had no significant effect on IRKA, as determined by insulin-stimulated (0, 1, 4 and 500 ng insulin/ml) 32P-incorporation into histone 2B. In subcellular membrane fractions, low density microsomes and plasma membranes, glucose transporter numbers were determined using [3H]cytochalasin B binding and immunodetection using an antiserum against the C-terminal peptide of the hepatoma-G2-glucose transporter. Cytochalasin B binding revealed that in the basal state the intracellular pool of glucose transporters was depleted in FR-24 by about 39% compared with low density microsomes from FR-6: (48.6 +/- 7.2 vs 29.8 +/- 5.5 pmol/mg membrane protein; P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

3-O-Methylglucose↗