Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
  • 1
    ISSN: 1433-2965
    Keywords: Bone density ; Calcitonin ; Females ; Nandrolone decanoate
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract This study used a randomized, 2 × 2 factorial design to evaluate over 2 years the effect of intranasal salmon calcitonin and intramuscular nandrolone decanoate on bone mass in elderly women with established osteoporosis. The study was double masked in relation to calcitonin and open in relation to nandrolone decanoate. One hundred and twenty-three women aged 60–88 years who had sustained a previous osteoporotic fracture, or had osteopenia, were recruited through an outpatient clinic. Women were assigned to one of four groups: (1) daily placebo nasal spray, (2) 400 IU intranasal calcitonin daily, (3) 20 intramuscular injections of 50 mg nandrolone decanoate (given as two courses of 10 injections) plus placebo nasal spray, or (4) 20 injections of 50 mg nandrolone decanoate plus 400 IU intranasal calcitonin daily. All subjects received 1000 mg calcium supplementation daily. Outcomes measured included changes in bone mineral density (BMD) at the lumbar spine, as measured by dual-energy quantitative computed tomography (DEQCT), in BMD of the proximal femur, and BMD and bone mineral content (BMC) of the lumbar spine and forearm, as measured by dual-energy X-ray absorptiometry (DXA). Significant positive changes from baseline in DXA BMC at the lumbar spine were observed over 2 years in the calcitonin group (5.0±1.9%, mean ± SE) and in the nandrolone deconate group (4.7±1.9%) but not in the placebo group (1.1±2.2%) or the combined therapy group (0.7±1.8%). Modelling based on the 2×2 factorial design revealed that nandrolone decanoate was associated with a 3.8±1.8% (p〈0.05) gain in DXA BMD at the proximal femur. Modelling also revealed that calcitonin treatment was associated with a loss of 11.5±4.7% in DEQCT BMD at the lumbar spine and a loss of 3.7±1.8% in DXA BMD at the proximal femur (p〈0.05). There was in vivo antagonism between the two medications of 7.9±3.9% for DXA BMC at the lumbar spine. Both agents caused positive changes from baseline in lumbar spine BMC. Nandrolone decanoate had beneficial effects on BMD at the proximal femur. This dose of intranasal calcitonin was associated with deleterious effects on trabecular BMD at the lumbar spine and total BMD at the proximal femur. There may be significant clinical antagonism between these two medications.
    Type of Medium: Electronic Resource
    Signatur Availability
    BibTip Others were also interested in ...
  • 2
    ISSN: 1432-0428
    Keywords: Key words: Hyaluronan ; prostaglandin ; sulphated proteoglycan ; glycosaminoglycan ; mesangial cell.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Exposure in vivo or in vitro to elevated glucose increases production of vasoactive prostaglandins by glomeruli and mesangial cells. This study aimed to determine whether this increased prostaglandin production could provide a link with later structural changes in diabetic nephropathy. Glomerular cores were prepared from control rats and streptozotocin-diabetic rats (3 weeks' duration). Over 24 h in culture hyaluronan production from diabetic glomerular cores was higher than production from control glomerular cores whether maintained in 5.6 mmol/l glucose (105.6 ± 15.5 vs 53.6 ± 8.5 ng hyaluronan per 250 glomerular cores, p 〈 0.001); in 25 mmol/l glucose (149.3 ± 34.8 vs 62.7 ± 7.8 ng hyaluronan per 250 glomerular cores, p 〈 0.01); or in 45 mmol/l glucose (176.8 ± 23.3 vs 102.0 ± 17.9 ng hyaluronan per 250 glomerular cores, p 〈 0.01). At 5.6 mmol/l glucose, exposure in vitro to prostaglandin E2 caused an increase in hyaluronan production [maximal at 10 − 9 mol/l prostaglandin E2, 237 ± 19 vs 42 ± 4, ng hyaluronan per 250 glomerular cores, p 〈 0.001 (control) and 195 ± 7 vs 103 ± 5, ng hyaluronan per 250 glomerular cores, p 〈 0.001 (diabetic) ]. In both control and diabetic glomerular cores hyaluronan production was reduced significantly by the cyclooxygenase inhibitor indomethacin (10−5 mol/l) [24.7 ± 3.33 vs 40.25 ± 4.11 ng hyaluronan per 250 glomerular cores, p 〈 0.05 (control) and 36.5 ± 6.25 vs 118.0 ± 22.6, p 〈 0.01 (diabetic) ]. A direct spectrophotometric microassay was used to determine the concentration of sulphated glycosaminoglycans derived from papain-digested glomerular core proteoglycans. Release of sulphated glycosaminoglycans from diabetic glomerular cores maintained at 5.6 mmol/l glucose was decreased [41.9 ± 1.1 vs 54.0 ± 1.0 μg of sulphated glycosaminoglycans (chondroitin sulphate) per 250 glomerular cores p 〈 0.01]. A decrease in sulphated glycosaminoglycans was also shown from control glomerular cores maintained at 25 mmol/l glucose. At this glucose concentration, addition of exogenous hyaluronan or prostaglandin E2 significantly reduced sulphated glycosaminoglycans from control and diabetic glomerular cores. It is concluded that increased prostaglandin production secondary to high glucose environment can lead to an increased glomerular hyaluronan synthesis. This can substantially affect the levels of sulphated glycosaminoglycans in the extracellular matrix. We propose that these effects provide a possible link between the initial biochemical consequences of hyperglycaemia and later structural changes seen in the glomerulus in diabetes. [Diabetologia (1995) 38: 298–305]
    Type of Medium: Electronic Resource
    Signatur Availability
    BibTip Others were also interested in ...
  • 3
    ISSN: 1432-0428
    Keywords: Caffeine ; neonatal rat ; sucrose supplementation ; pancreatic insulin ; insulin release ; proinsulin biosynthesis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Pancreatic function was investigated in neonatal suckling offspring of caffeine-ingesting dams, with or without maternal sucrose supplementation, throughout pregnancy and lactation. In offspring of rats ingesting caffeine without sucrose supplementation, there was initial hyperinsulinaemia, followed by a progressive fall of plasma insulin to subnormal levels. This fall in plasma insulin coincided with depletion of pancreatic insulin stores. Both the fall in plasma insulin and depletion of pancreatic insulin stores were prevented by sucrose supplementation of caffeine-ingesting dams. Offspring of dams fed sucrose alone and control offspring also maintained pancreatic insulin stores and circulating insulin levels over the first 14 days of postnatal life. Pancreases from offspring of caffeine-exposed animals tested in vitro showed enhanced sensitivity of the insulin release process to glucose. This was reflected in the glucose concentration required to elicit half-maximal insulin release (2.4 ± 0.2 mmol/l for caffeine offspring, 2.3 ± 0.2 mmol/l for caffeine with sucrose, 3.8 ± 0.3 mmol/l for sucrose and 4.1 ± 0.3 mmol/l for control offspring, mean ± SEM). In contrast, offspring of sucrose-supplemented (with or without caffeine) dams showed increased sensitivity of the proinsulin biosynthetic process to glucose, whereas offspring of dams ingesting caffeine alone showed no significant enhancement of the biosynthetic process compared with control offspring. Thus enhanced sensitivity of the insulin secretory process to glucose without a change in the sensitivity of the biosynthetic process in the offspring of the caffeine ingesting (nonsucrose supplemented) dams could explain the progressive depletion of pancreatic insulin stores and eventual hypoinsulinaemia seen in this group.
    Type of Medium: Electronic Resource
    Signatur Availability
    BibTip Others were also interested in ...
  • 4
    ISSN: 1432-0428
    Keywords: Diabetic nephropathy ; albuminuria ; aldose reductase inhibitors ; prostaglandins
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effect of two structurally unrelated aldose reductase inhibitors, sorbinil and ponalrestat, on glomerular prostaglandin production and urinary albumin excretion was investigated in rats with diabetes induced by streptozotocin. It was found that both aldose reductase inhibitors, when administered from the time of induction of the diabetes, significantly decreased the raised urinary albumin excretion in the diabetic rats, although it remained elevated compared with non-diabetic rats. Glomerular prostaglandin E and 6-ketoprostaglandin F1α production was significantly increased in glomeruli obtained from the diabetic rats. Inhibition of aldose reductase caused a reduction in the raised glomerular prostaglandin production, although this remained above that observed in the non-diabetic rats. Subsequent experiments were performed to determine whether the effects of the aldose reductase inhibitors could be explained by effects on glomerular filtration rate. It was found that ponalrestat, at a dose which markedly reduced urinary albumin excretion, did not significantly affect glomerular filtration rate in non-diabetic rats, rats with untreated streptozotocin-induced diabetes and rats with diabetes partially treated with low dose insulin. Glomerular sorbitol concentrations were significantly elevated in untreated diabetic rats as early as two weeks after the induction of diabetes. It is concluded that the administration of aldose reductase inhibitors from the time of induction of diabetes significantly reduces glomerular prostaglandin production and urinary albumin excretion. The latter effect is not due to an effect on glomerular filtration rate. Increased polyol pathway activity may account in part for the increased glomerular prostaglandin production and urinary albumin excretion in early experimental diabetes.
    Type of Medium: Electronic Resource
    Signatur Availability
    BibTip Others were also interested in ...
  • 5
    Electronic Resource
    Electronic Resource
    Springer
    Diabetologia 35 (1992), S. 499-504 
    ISSN: 1432-0428
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary A large number of experimental studies in animals and retrospective or non-randomised prospective studies in humans provide support for the concept that the microvascular complications of diabetes mellitus are dependent on hyperglycaemia. This review focuses on four potential bio-chemical pathways linking hyperglycaemia to changes within the kidney which can plausibly be linked to the functional and structural changes characterising diabetic nephropathy. These four pathways are the polyol pathway, non-enzymatic glycation, glucose autoxidation and de novo synthesis of diacylglycerol leading to protein kinase C and phospholipase A2 activation. Rather than being independent, there are several potential interactions between these four pathways which may explain confusing and overlapping effects observed in studies examining inhibitors of individual pathways. As many of the steps which follow on glucose metabolism are subject to modification by dietary and pharmacological means, the further delineation of the pathogenetic sequence leading to tissue damage in diabetes should allow a logical and effective approach to the prevention or treatment of the complications of diabetes.
    Type of Medium: Electronic Resource
    Signatur Availability
    BibTip Others were also interested in ...
  • 6
    ISSN: 1432-0428
    Keywords: Hyaluronan ; prostaglandin ; sulphated proteoglycan ; glycosaminoglycan ; mesangial cell
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Exposure in vivo or in vitro to elevated glucose increases production of vasoactive prostaglandins by glomeruli and mesangial cells. This study aimed to determine whether this increased prostaglandin production could provide a link with later structural changes in diabetic nephropathy. Glomerular cores were prepared from control rats and streptozotocin-diabetic rats (3 weeks' duration). Over 24 h in culture hyaluronan production from diabetic glomerular cores was higher than production from control glomerular cores whether maintained in 5.6 mmol/l glucose (105.6±15.5 vs 53.6±8.5 ng hyaluronan per 250 glomerular cores, p〈0.001); in 25 mmol/l glucose (149.3±34.8 vs 62.7±7.8 ng hyaluronan per 250 glomerular cores, p〈0.01); or in 45 mmol/l glucose (176.8±23.3 vs 102.0±17.9 ng hyaluronan per 250 glomerular cores, p〈0.01). At 5.6 mmol/l glucose, exposure in vitro to prostaglandin E2 caused an increase in hyaluronan production [maximal at 10−9 mol/l prostaglandin E2, 237±19 vs 42±4, ng hyaluronan per 250 glomerular cores, p〈0.001 (control) and 195±7 vs 103±5, ng hyaluronan per 250 glomerular cores, p〈0.001 (diabetic)]. In both control and diabetic glomerular cores hyaluronan production was reduced significantly by the cyclooxygenase inhibitor indomethacin (10−5 mol/l) [24.7±3.33 vs 40.25±4.11 ng hyaluronan per 250 glomerular cores, p〈0.05 (control) and 36.5±6.25 vs 118.0±22.6, p〈0.01 (diabetic)]. A direct spectrophotometric microassay was used to determine the concentration of sulphated glycosaminoglycans derived from papain-digested glomerular core proteoglycans. Release of sulphated glycosaminoglycans from diabetic glomerular cores maintained at 5.6 mmol/l glucose was decreased [41.9±1.1 vs 54.0±1.0 Μg of sulphated glycosaminoglycans (chondroitin sulphate) per 250 glomerular cores p〈0.01]. A decrease in sulphated glycosaminoglycans was also shown from control glomerular cores maintained at 25 mmol/l glucose. At this glucose concentration, addition of exogenous hyaluronan or prostaglandin E2 significantly reduced sulphated glycosaminoglycans from control and diabetic glomerular cores. It is concluded that increased prostaglandin production secondary to high glucose environment can lead to an increased glomerular hyaluronan synthesis. This can substantially affect the levels of sulphated glycosaminoglycans in the extracellular matrix. We propose that these effects provide a possible link between the initial biochemical consequences of hyperglycaemia and later structural changes seen in the glomerulus in diabetes.
    Type of Medium: Electronic Resource
    Signatur Availability
    BibTip Others were also interested in ...
  • 7
    Electronic Resource
    Electronic Resource
    Springer
    Diabetologia 7 (1971), S. 302-307 
    ISSN: 1432-0428
    Keywords: NZO mouse ; plasma growth hormone ; suppression after glucose
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Résumé L'hormone de croissance immunoréactive (IRGH) plasmatique a été mesurée par une méthode radio-immunologique dans des conditions de base et après l'administration de glucose chez la souris obèse de la Nouvelle-Zélande (NZO) et aussi chez une souche de souris témoins. On a constaté plus de variabilité de IRGH plasmatique chez la souris NZO que chez la souche de souris témoins dans les conditions de base, mais il n'y avait pas de différence notable entre la moyenne logarithmique de IRGH plasmatique dans les deux souches de souris. D'ailleurs dans toutes les deux races il y avait une suppression rapide de IRGH plasmatique après l'administration de glucose. Il paraît peu probable que l'hypersécrétion pituitaire de l'hormone de croissance explique les anomalies métaboliques observées chez la souris NZO.
    Abstract: Zusammenfassung Das Wachstumshormon im Plasma wurde unter Anwendung der Radioimmunomethode unter basalen Bedingungen und nach Zufuhr von Glucose bei der New Zealand obese mouse (NZO) und einer Kontrollzucht gemessen. Unter basalen Bedingungen bestand bei den NZO-Mäusen eine größere Variabilität des immunreaktiven Wachstumshormons im Plasma (IRGH) als bei der Kontrollzucht; es fand sich jedoch kein wesentlicher Unterschied des mittleren logarithmischen Plasma-IRGH bei den beiden Zuchten. Darüberhinaus erfolgte nach Zufuhr von Glucose bei beiden Zuchten eine schnelle Suppression des Plasma-IRGH. Es ist unwahrscheinlich, daß die pituitäre Hypersekretion des Wachstumshormons für die metabolischen Anomalien bei der NZO-Maus verantwortlich zu machen ist.
    Notes: Summary Plasma growth hormone was measured by radioimmunoassay under basal conditions and after glucose administration in the New Zealand Obese (NZO) mouse and in a control strain. There was greater variability of plasma IRGH in the NZO mice than in the control strain under basal conditions, but there was no significant difference between the mean log plasma IRGH in the two strains. Moreover, in both strains rapid suppression of plasma IRGH occurred following glucose administration. It appears unlikely that pituitary hypersecretion of growth hormone accounts for the metabolic abnormalities observed in the NZO mouse.
    Type of Medium: Electronic Resource
    Signatur Availability
    BibTip Others were also interested in ...
  • 8
    ISSN: 1432-0428
    Keywords: islet activating protein, NZO mice ; insulin secretion ; insulin responsiveness ; soleus muscle
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effect of islet activating protein on glucose tolerance, insulin secretion and insulin responsiveness was studied in the NZO mouse, a model of non-insulin dependent diabetes and obesity. A single IV injection of 5 ng/g body weight islet activating protein markedly lowered plasma glucose and the glucose response to IP glucose administration, measured 5 days later (mean±SEM, plasma glucose levels 0, 10, 30 and 60 min after glucose 6.0±0.9, 14.6±1.3, 14.1±1.3 and 13.2±1.7 mmol/l in islet activating protein-treated NZO mice versus 12.8±1.6, 27.8±3.4, 34.7±4.1, 39.1±3.8 mmol/l in carrier-treated NZO mice). There was no difference in fasting plasma insulin levels between islet activating protein and carrier-treated mice. No response of plasma insulin to glucose occurred in the carrier-treated mice, but a highly significant insulin response to glucose was seen in the islet activating protein-treated mice. The in vitro responsiveness of pancreatic islets of islet activating protein-treated NZO mice to glucose was improved, and the inhibitory effect of adrenaline on insulin secretion was reduced. The in vivo hypoglycaemic response to exogenous insulin was not improved by islet activating protein and a demonstrated defect in the insulin sensitivity and responsiveness of glucose utilization by isolated soleus muscle was not reversed by islet activating protein treatment. It is concluded that islet activating protein is highly effective in improving glucose tolerance and insulin secretion in NZO mice, and that the improvement in glucose tolerance occurs without demonstrable improvement in the responsiveness to exogenous insulin or sensitivity of soleus muscle to insulin.
    Type of Medium: Electronic Resource
    Signatur Availability
    BibTip Others were also interested in ...
  • 9
    ISSN: 1433-2965
    Keywords: Adolescence ; Bone density ; Calcium supplementation ; Twins
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The effect of calcium supplementation on bone mineral density (BMD) was evaluated in female twin pairs aged 10–17 years with a mean age of 14 years. Forty-two twin pairs (22 monozygotic, 20 dizygotic; (including one monozygotic pair from a set of triplets) completed at least 6 months of the intervention: 37 pairs to 12 months and 28 pairs to 18 months. BMD was measured by dual-energy X-ray absorptiometry (DXA). In a double-blind manner, one twin in each pair was randomly assigned to receive daily a 1000 mg effervescent calcium tablet (Sandocal 1000), and the other a placebo tablet similar in taste and appearance to the calcium supplement but containing no calcium. Compliance (at least 80% tablets consumed), as measured by tablet count, was 85% in the placebo group and 83% in the calcium group over the 18 months of the study, on average increasing dietary calcium to over 1600 mg/day. There was no within-pair difference in the change in height or weight. When the effect of calcium supplementation on BMD was compared with placebo at approximately 6, 12 and 18 months, it was found that there was a 0.015±0.007 g/ cm2 greater increase in BMD (1.62±0.84%) at the spine in those on calcium after 18 months. At the end of the first 6 months there was a significant within-pair difference of 1.53±0.56% at the spine and 1.27±0.50% at the hip. However, there were no significant differences in the changes in BMD after the initial effect over the first 6 months. Therefore, we found an increase in BMD at the spine with calcium supplementation in females with a mean age of 14 years. The greatest effect was seen in the first 6 months; thereafter the difference was maintained, but there was no accelerated increase in BMD associated with calcium supplementation. The continuance of the intervention until the attainment of peak bone mass and follow-up after cessation of calcium supplementation will be important in clarifying the optimal timing for increased dietary calcium and the sustained, long-term effects of this intervention.
    Type of Medium: Electronic Resource
    Signatur Availability
    BibTip Others were also interested in ...
  • 10
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] In a previous report10, we described inhibition of the conversion of 25-hydroxycholecalciferol (25 HCC) to 1,25 DHCC in vitro after incubation of isolated chick kidney tubules with 1,25 DHCC. We show here that this inhibition is not due to a direct competitive effect of 1,25 DHCC, but that it is ...
    Type of Medium: Electronic Resource
    Signatur Availability
    BibTip Others were also interested in ...
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...