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  • 1
    Electronic Resource
    Electronic Resource
    Reduced sensitivity of dihydroxyacetone on ATP-sensitive K+ channels of pancreatic beta cells in GK rats (1994)
    Springer
    Diabetologia 37 (1994), S. 1082-1087 
    Details
    ISSN: 1432-0428
    Keywords: Dihydroxyacetone ; ATP-sensitive K+ channels ; GK rat ; glycerol phosphate shuttle ; pancreatic beta cell
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In the GK (Goto-Kakizaki) rat, a genetic model of non-insulin-dependent diabetes mellitus, glucose-induced insulin secretion is selectively impaired. In addition, it has been suggested by previous studies that impaired glucose metabolism in beta cells of the GK rat results in insufficient closure of ATP-sensitive K+ channels (KATP channels) and a consequent decrease in depolarization, leading to a decreased insulin release. We have recently reported that the site of disturbed glucose metabolism is probably located in the early stages of glycolysis or in the glycerol phosphate shuttle. In the present study, in order to identify the impaired metabolic step in diabetic beta cells, we have investigated insulin secretory capacity by stimulation with dihydroxyacetone (DHA), which is known to be directly converted to DHA-phosphate and to preferentially enter the glycerol phosphate shuttle. In addition, using the patch-clamp technique, we also have studied the sensitivity of DHA on the KATP channels of beta cells in GK rats. The insulin secretion in response to 5 mmol/l DHA with 2.8 mmol/l glucose was impaired, and DHA sensitivity of the KATP channels was reduced in beta cells of GK rats. From these results, we suggest that the intracellular site responsible for impaired glucose metabolism in pancreatic beta cells of GK rats is located in the glycerol phosphate shuttle.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00418371
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  • 2
    Electronic Resource
    Electronic Resource
    Hyperresponse in calcium-induced insulin release from electrically permeabilized pancreatic islets of diabetic GK rats and its defective augmentation by glucose (1995)
    Springer
    Diabetologia 38 (1995), S. 772-778 
    Details
    ISSN: 1432-0428
    Keywords: Key words Insulin release ; intracellular calcium ; exocytosis ; GK rat ; permeabilized islets.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In spontaneously diabetic GK rats, insulin secretion from pancreatic beta cells in response to glucose is selectively impaired, probably due to deficient intracellular metabolism of glucose and impaired closure of KATP channels during glucose stimulation. By using electrically permeabilized islets of GK rats, we explored the functional modulations in exocytotic steps distal to the rise in [Ca2 + ]i in the diabetic condition. At 30 nmol/l Ca2 + (basal conditions) insulin release was similar between GK and non-diabetic control Wistar rats. In response to 3.0 μmol/l Ca2 + (maximum stimulatory conditions), insulin release was significantly augmented in permeabilized GK islets (p 〈 0.01). Raising glucose concentrations from 2.8 to 16.7 mmol/l further augmented insulin release induced by 3.0 μmol/l Ca2 + from permeabilized control islets(p 〈 0.001), but had no effect on that from permeabilized GK islets. The stimulatory effect of glucose on insulin release from permeabilized control islets was partly inhibited by 2,4-dinitrophenol, an inhibitor of mitochondrial oxidative phosphorylation (p 〈 0.01). The hyperresponse to Ca2 + in GK islets may play a physiologically compensatory role on the putative functional impairment both in [Ca2 + ]i rise and energy state in response to glucose in diabetic β cells, and may explain the relative preservation of insulin release induced by non-glucose depolarizing stimuli, such as arginine, from pancreatic islets in non-insulin-dependent diabetes mellitus. [Diabetologia (1995) 38: 772–778]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250050351
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  • 3
    Electronic Resource
    Electronic Resource
    Reduced sensitivity of dihydroxyacetone on ATP-sensitive K+ channels of pancreatic beta cells in GK rats (1994)
    Springer
    Diabetologia 37 (1994), S. 1082-1087 
    Details
    ISSN: 1432-0428
    Keywords: Key words Dihydroxyacetone ; ATP-sensitive K+ channels ; GK rat ; glycerol phosphate shuttle ; pancreatic beta cell.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In the GK (Goto-Kakizaki) rat, a genetic model of non-insulin-dependent diabetes mellitus, glucose-induced insulin secretion is selectively impaired. In addition, it has been suggested by previous studies that impaired glucose metabolism in beta cells of the GK rat results in insufficient closure of ATP-sensitive K+ channels (KATP channels) and a consequent decrease in depolarization, leading to a decreased insulin release. We have recently reported that the site of disturbed glucose metabolism is probably located in the early stages of glycolysis or in the glycerol phosphate shuttle. In the present study, in order to identify the impaired metabolic step in diabetic beta cells, we have investigated insulin secretory capacity by stimulation with dihydroxyacetone (DHA), which is known to be directly converted to DHA-phosphate and to preferentially enter the glycerol phosphate shuttle. In addition, using the patch-clamp technique, we also have studied the sensitivity of DHA on the KATP channels of beta cells in GK rats. The insulin secretion in response to 5 mmol/l DHA with 2.8 mmol/l glucose was impaired, and DHA sensitivity of the KATP channels was reduced in beta cells of GK rats. From these results, we suggest that the intracellular site responsible for impaired glucose metabolism in pancreatic beta cells of GK rats is located in the glycerol phosphate shuttle. [Diabetologia (1994) 37: 1082–1087]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00418371
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    Paper (German National Licenses)
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  • 4
    Electronic Resource
    Electronic Resource
    Effects of Troglitazone (CS-045) on insulin secretion in isolated rat pancreatic islets and HIT cells: an insulinotropic mechanism distinct from glibenclamide (1995)
    Springer
    Diabetologia 38 (1995), S. 24-30 
    Details
    ISSN: 1432-0428
    Keywords: Key words Troglitazone (CS-045) ; insulin secretion ; pancreatic islets ; HIT-T15 cells ; glucose transport ; sulphonylurea receptor ; ATP-sensitive K++ channel.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In order to elucidate the direct effects of (±)-5-[4-(6-hydroxy-2, 5, 7, 8-tetramethylchroman-2-yl-methoxy) benzyl]-2,4-thiazolidinedione (Troglitazone), a newly-developed oral hypoglycaemic agent, on pancreatic beta-cell function, in vitro investigation of isolated rat pancreatic islets and a hamster beta-cell line (HIT cell) were performed. Troglitazone stimulates both glucose, and glibenclamide-induced insulin release at a concentration of 10−6 mol/l in these cells but, conversely, inhibits insulin secretion at 10−4 mol/l. Glucose uptake in HIT cells is similarly enhanced by 10−6 mol/l Troglitazone, but is reduced in the presence of 10−4 mol/l Troglitazone. However, a quantitative immunoblot analysis with a specific antibody for GLUT 2 glucose transporter revealed no significant change in GLUT 2 protein in HIT cells with 10−6 mol/l Troglitazone. Specific binding of [3H]-glibenclamide to beta-cell membranes is replaced by Troglitazone in a non-competitive manner, but 10−6 mol/l Troglitazone failed to eliminate ATP-sensitive K++ channel activity. These results suggest that Troglitazone has a putative non-competitive binding site at, or in the vicinity of, the sulphonylurea receptor in rat pancreatic islets and HIT cells and that the dual effect of Troglitazone on insulin secretory capacity is mediated through the modulation of glucose transport activity, possibly due to the modification of intrinsic activity in glucose transporter in pancreatic beta cells by this novel agent. [Diabetologia (1995) 38: 24–30]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250050249
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  • 5
    Electronic Resource
    Electronic Resource
    Effects of Troglitazone (CS-045) on insulin secretion in isolated rat pancreatic islets and HIT cells: an insulinotropic mechanism distinct from glibenclamide (1995)
    Springer
    Diabetologia 38 (1995), S. 24-30 
    Details
    ISSN: 1432-0428
    Keywords: Troglitazone (CS-045) ; insulin secretion ; pancreatic islets ; HIT-T15 cells ; glucose transport ; sulphonylurea receptor ; ATP-sensitive K++ channel
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In order to elucidate the direct effects of (±)-5-[4-(6-hydroxy-2, 5, 7, 8-tetramethylchroman-2-yl-methoxy) benzyl]-2,4-thiazolidinedione (Troglitazone), a newly-developed oral hypoglycaemic agent, on pancreatic beta-cell function, in vitro investigation of isolated rat pancreatic islets and a hamster beta-cell line (HIT cell) were performed. Troglitazone stimulates both glucose, and glibenclamide-induced insulin release at a concentration of 10−6 mol/l in these cells but, conversely, inhibits insulin secretion at 10−4 mol/l. Glucose uptake in HIT cells is similarly enhanced by 10−6 mol/l Troglitazone, but is reduced in the presence of 10−4 mol/l Troglitazone. However, a quantitative immunoblot analysis with a specific antibody for GLUT 2 glucose transporter revealed no significant change in GLUT 2 protein in HIT cells with 10−6 mol/l Troglitazone. Specific binding of [3H]-glibenclamide to beta-cell membranes is replaced by Troglitazone in a non-competitive manner, but 10−6 mol/l Troglitazone failed to eliminate ATP-sensitive K++ channel activity. These results suggest that Troglitazone has a putative non-competitive binding site at, or in the vicinity of, the sulphonylurea receptor in rat pancreatic islets and HIT cells and that the dual effect of Troglitazone on insulin secretory capacity is mediated through the modulation of glucose transport activity, possibly due to the modification of intrinsic activity in glucose transporter in pancreatic beta cells by this novel agent. [Diabetologia (1995) 38: 24–30]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02369349
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  • 6
    Electronic Resource
    Electronic Resource
    No evidence of linkage or diabetes-associated mutations in the transcription factors BETA2/NEUROD1 and PAX4 in Type II diabetes in France (1999)
    Springer
    Diabetologia 42 (1999), S. 480-484 
    Details
    ISSN: 1432-0428
    Keywords: Keywords MODY ; late-onset Type II diabetes ; transcription factors ; PAX4 ; BETA2/NEUROD1 ; SSCP.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Aims/hypothesis. The identification of mutations in hepatocyte nuclear factors-1α, –4α, –1β and insulin promoter factor-1 in maturity onset diabetes of the young (MODY) has highlighted the role that transcription factors may have in the development of diabetes. This result has focused molecular genetic studies of diabetes on other transcription factors expressed in the pancreatic beta cell. The basic helix-loop-helix transcription factor BETA2/NEUROD1 (gene symbol, NEUROD1) and the paired box homeodomain transcription factor PAX4 (PAX4) have an important role in islet and beta-cell development. We have examined the contribution of these transcription factors to the development of MODY and late-onset Type II (non-insulin-dependent) diabetes mellitus. Methods. Linkage studies have been done in MODY families reported to have no mutations in the five known MODY genes and in affected sibling pairs from families with late-onset Type II diabetes. Mutation screening of the coding regions of both genes was also realised by SSCP followed by sequencing in MODY patients and in probands with late-onset Type II diabetes. Results. There was no evidence of linkage with the markers for NEUROD1 and PAX4 either with MODY or late-onset Type II diabetes. Mutation screening showed single nucleotide polymorphisms, several of which resulted in amino acid substitutions : NEUROD1, Ala45Thr; PAX4, Pro321His and Pro334Ala. These amino acid sequence variants were not associated with Type II diabetes. Conclusion/interpretation. Our results indicate that NEUROD1 and PAX4 are not a common cause of either MODY or late-onset Type II diabetes in the French Caucasian population. [Diabetologia (1999) 42: 480–484]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250051182
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  • 7
    Electronic Resource
    Electronic Resource
    Glucagon, insulin and somatostatin secretion in response to sympathetic neural activation in streptozotocin-induced diabetic rats. A study with the isolated perfused rat pancreas in vitro (1992)
    Springer
    Diabetologia 35 (1992), S. 1035-1041 
    Details
    ISSN: 1432-0428
    Keywords: Glucagon ; insulin ; somatostatin ; streptozotocin ; sympathetic nerve ; diabetic rat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Changes in glucagon, insulin and somatostatin secretion induced by electrical splanchnic nerve stimulation were examined in rats treated with streptozotocin as neonates and as adults. In order to study the direct neural effects we used the isolated perfused rat pancreas with intact left splanchnic nerve in vitro. In normal rats splanchnic nerve stimulation causes significant decreases in insulin (30–40%) and somatostatin (30–50%) secretion at both 16.7 mmol/l and 1 mmol/l glucose concentrations. In the neonatal streptozotocin-diabetic rats splanchnic nerve stimulation at 16.7 mmol/l glucose decreased insulin secretion (14%) further than in the control rats (30%), however, somatostatin secretion did not decrease to the same extent. Similar results were also observed at the low (1 mmol/l) glucose concentration. On the other hand, percent decreases of insulin and somatostatin secretion induced by splanchnic nerve stimulation in the streptozotocin-diabetic rats were similar to the values observed in the normal control rats. The glucagon secretion in response to splanchnic nerve stimulation at 16.7 mmol/l glucose from pancreatic Alpha cells in both types of induced diabetes is exaggerated, and the degree of exaggeration seems to parallel the severity of the hyperglycaemia. However, the splanchnic nerve stimulation-induced glucagon secretion at 1 mmol/l glucose was impaired in the streptozotocin-diabetic rats, but not in the neonatal streptozotocin-diabetic rats. These data suggest that the sensitivity of diabetic Alpha and Delta cells to sympathetic neural activation are blunted, whereas the sensitivity of Beta cells is enhanced in the diabetic animal model.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02221678
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  • 8
    Electronic Resource
    Electronic Resource
    Biochemical characterization of 1,25(OH)2D3 receptors in chick embryonal duodenal cytosol (1982)
    Springer
    Calcified tissue international 34 (1982), S. 265-269 
    Details
    ISSN: 1432-0827
    Keywords: 1,25(OH)2D3 Receptor ; Chicken Duodenal Cytosol ; Chicken Embryo ; Affinity ; 1,25(OH)2D3 Concentration
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Notes: Summary This study presents measurements of serum vitamin D metabolites, calcium and phosphorus as well as measurements of the equilibrium dissociation constant for duodenal 1,25(OH)2D3 receptor in 15-, 18-, 19-, and 20-day chick embryos in comparison to that in 1- and 118-day-old chicks and to vitamin D-deficient chicks. The present results showed that: (a) serum 1,25(OH)2D and 24,25(OH)2D levels rise from 15 and 18 to days 19 and 20 of embryonic development while serum phosphate levels are stable; (b) serum calcium levels rise at hatching to adult levels; (c) the duodenal 1,25(OH)2D3 receptor is detectable in 15-day-old embryo and has a Kd similar to that of 118-day-old vitamin D-replete chicks; and (d) the activity of 1,25(OH)2D3 receptor in chick duodenal cytosol is maximal at hatching.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02411248
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  • 9
    Electronic Resource
    Electronic Resource
    Secondary hyperparathyroidism with 1,25-dihydroxyvitamin D deficiency and pseudohypoparathyroidism in childhood: Relationship between plasma 1,25-dihydroxyvitamin D and parathyroid hormone levels and urinary cyclic AMP response to exogenous PTH (1981)
    Springer
    European journal of pediatrics 135 (1981), S. 267-271 
    Details
    ISSN: 1432-1076
    Keywords: Pseudohypoparathyroidism ; Pseudopseudohypoparathyroidism ; 1,25-dihydroxyvitamin D
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract In order to clarify the complex interrelationship between serum calcium, 1,25-dihydroxyvitamin D (1,25(OH)2D), and parathyroid hormone (PTH), and the urinary excretion of cyclic AMP (cAMP) in response to exogenous PTH in pseudohypoparathyroidism (PHP) and related diseases, we investigated 3 patients with parathyroid disorders before and after treatment with 1α-hydroxyvitamin D3 (1α-OH-D3). Low plasma 1,25(OH)2D before treatment increased after giving 1α-OH-D3 (0.1 μg/kg/day), where-as high plasma PTH measured by the C-terminal assay (C-PTH) decreased in all 3. No response in urinary cAMP was found before or after treatment in 2 patients with PHP type I, despite the fall of plasma C-PTH. However, in one patient with extremely high plasma C-PTH but normal N-PTH (measured by a homologous radioimmunoassay using 1–34 human PTH), urinary cAMP response to exogenous PTH was increased after treatment with 1α-OH-D3. We suggest that he had pseudopseudohypoparathyroidism (PPHP) with Albright's hereditary osteodystrophy and a partial deficiency of renal 1α-hydroxylase. In this patient secondary hyperparathyroidism is thought to be due to 1,25(OH)2D deficiency, and the decreased responsiveness to exogenous PTH before treatment due to excess PTH occupying renal receptors.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00442101
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  • 10
    Electronic Resource
    Electronic Resource
    Activity of renal 25-hydroxyvitamin D3-1α-hydroxylase in a case of X-linked hypophosphataemic rickets (1984)
    Springer
    European journal of pediatrics 142 (1984), S. 219-222 
    Details
    ISSN: 1432-1076
    Keywords: Hypophosphataemic rickets ; 1,25(OH)2D ; 1α-hydroxylase
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract In 1974, a 2-year-old boy was diagnosed as having X-linked hypophosphataemic rickets (XLH) because of severe rickets and hypophosphataemia. The vitamin D metabolite concentrations, blood and urine chemistry and renal 25-hydroxyvitamin D3 (25 OHD3)-1α-hydroxlase were measured in 1982 (about 2 weeks after withdrawal of medication). 1α-hydroxylase was 392 pg/mg tissue/20 min in the patient, which was high compared with aged-matched controls (69.7±28.5 pg/mg tissue/20 min, mean ±SD, n=7). Our present studies showed that the 1α-hydroxylase activity in the patient with XLH was elevated. Therefore, the normal or low 1,25-dihydroxyvitamin D3 (1,25-(OH)2D3) concentrations in XLH patients could be due to accelerated catabolism of 1,25-(OH)2D3 or abnormally regulated 25OHD3-1α-hydroxylase in response to hypophosphataemia, although significantly elevated above that in normal controls.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00442454
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