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  • 1
    Electronic Resource
    Electronic Resource
    Pancreatic Reg/pancreatic stone protein (PSP) gene expression does not correlate with beta-cell growth and regeneration in rats (1994)
    Springer
    Diabetologia 37 (1994), S. 994-999 
    Details
    ISSN: 1432-0428
    Keywords: Pancreas ; growth factors ; gene expression ; beta cells
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The Reg/pancreatic stone protein (PSP) gene is postulated to be an important regulator of pancreatic beta-cell growth. To investigate this hypothesis, we analysed the expression of the Reg/PSP gene following a 90% pancreatectomy and after chronic glucose infusion, two well-defined models of pancreatic beta-cell growth. There was a rapid induction of the Reg/PSP gene in the remnant pancreas after a 90% pancreatectomy in rats during the period of marked growth of the exocrine and islet tissue. However, a similar rapid, but smaller, induction of the Reg/PSP gene was observed in sham-operated rats and in non-surgical control rats in which there was no enhanced pancreatic growth. Furthermore, there was no pancreatic Reg/PSP gene induction in a model of selective beta-cell growth, the chronic glucose-infused rat. Thus, it is unlikely that Reg/PSP is a beta-cell specific growth factor, even though the function of this important pancreatic gene is still unknown.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00400462
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Pancreatic Reg/pancreatic stone protein (PSP) gene expression does not correlate with beta-cell growth and regeneration in rats (1994)
    Springer
    Diabetologia 37 (1994), S. 994-999 
    Details
    ISSN: 1432-0428
    Keywords: Key words Pancreas ; growth factors ; gene expression ; beta cells.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The Reg/pancreatic stone protein (PSP) gene is postulated to be an important regulator of pancreatic beta-cell growth. To investigate this hypothesis, we analysed the expression of the Reg/PSP gene following a 90 % pancreatectomy and after chronic glucose infusion, two well-defined models of pancreatic beta-cell growth. There was a rapid induction of the Reg/PSP gene in the remnant pancreas after a 90 % pancreatectomy in rats during the period of marked growth of the exocrine and islet tissue. However, a similar rapid, but smaller, induction of the Reg/PSP gene was observed in sham-operated rats and in non-surgical control rats in which there was no enhanced pancreatic growth. Furthermore, there was no pancreatic Reg/PSP gene induction in a model of selective beta-cell growth, the chronic glucose-infused rat. Thus, it is unlikely that Reg/PSP is a beta-cell specific growth factor, even though the function of this important pancreatic gene is still unknown. [Diabetologia (1994) 37: 994–999]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00400462
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
  • 3
    Electronic Resource
    Electronic Resource
    Beta-cell dysfunction in hyperglycaemic rat models: recovery of glucose-induced insulin secretion with lowering of the ambient glucose level (1991)
    Springer
    Diabetologia 34 (1991), S. 640-647 
    Details
    ISSN: 1432-0428
    Keywords: Animal models ; Type 2 (non-insulin-dependent) diabetes mellitus ; insulin secretion ; insulin treatment ; hypoglycaemia ; islets of Langerhans
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Glucose-induced insulin secretion is lost in the face of chronic hyperglycaemia. The same defect is present when normal rats are made hyperglycaemic by 48-h glucose infusions. Insulin secretory responses were mapped out during the post-infusion period in order to determine how long it takes for normal Beta-cell function to recover, and to identify factors which influence the rate of recovery. Male Sprague Dawley rats weighing 200–250 g were infused with 50% glucose or 77 mmol/l NaCl for 48 h. The glucose-infused rats were mildly hypoglycaemic for 14 h after the infusion ceased. Glucose-induced insulin secretion, absent at the end of the glucose infusion, was normal 6 h post-infusion. Such rapid recovery was not because of the short duration of hyperglycaemia; mild hypoglycaemia from a 5-h insulin infusion in 90% pancreatectomized rats resulted in a four-fold rise in glucose-induced insulin secretion. Under in vitro conditions, extreme glucose deprivation caused by perfusing the pancreas of glucose-infused rats with buffer devoid of glucose restored glucose-induced insulin secretion in just 37 min. Therefore, the suppression of glucose-induced insulin release by chronic hyperglycaemia is a dynamic situation that requires ongoing hyperglycaemia to prevent the reappearance of glucose responsiveness. This study shows recovery of glucose-induced insulin secretion after just 6 h of mild hypoglycaemia in vivo and even faster recovery with more severe glucose deprivation in vitro. Our results suggest that there is an inverse relationship between the rate of return of Beta-cell glucose responsiveness and the ambient glucose concentration.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00400993
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    Paper (German National Licenses)
    Fulltext
  • 4
    Electronic Resource
    Electronic Resource
    Beta-cell hypersensitivity for glucose precedes loss of glucose-induced insulin secretion in 90% pancreatectomized rats (1993)
    Springer
    Diabetologia 36 (1993), S. 1238-1244 
    Details
    ISSN: 1432-0428
    Keywords: Islets of Langerhans ; insulin secretion ; perfused pancreas ; glucose ; arginine ; partial pancreatectomy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Glucose-induced insulin secretion is impaired in the presence of chronic hyperglycaemia. Insulin secretion was studied in a diabetic rat model prior to the beta cells becoming non-responsive to glucose in order to map out the sequence of changes that accompany chronic hyperglycaemia. In vitro pancreas perfusions were carried out 1 and 2 weeks after a 90% pancreatectomy; controls underwent a sham pancreatectomy. One week post 90% pancreatectomy: (i) non-fasting plasma glucose values were 2–3 mmol/l above normal, (ii) the in vitro insulin response to 16.7 mmol/l glucose was 20 ± 4% of shams, a response that was appropriate for the surgical reduction in beta-cell mass, (iii) the beta-cell sensitivity for glucose was increased as reflected by left-shifted dose-response curves for glucose-induced insulin secretion (half maximal insulin output 5.7 mmol/l glucose vs 16.5 mmol/l glucose in shams) and glucose potentiation of arginine-induced insulin secretion (half maximal insulin output 3.5 mmol/l glucose vs 14.8 mmol/l glucose in shams). This heightened beta-cell sensitivity for glucose was not a result of the hyperglycaemia, because similarly reduced half-maximal insulin responses were found after a 60% pancreatectomy, a surgical procedure in which plasma glucose values remained normal. In summary, a rise in beta-cell sensitivity for glucose precedes the loss of glucose-induced insulin secretion in diabetic rats.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00400800
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    Paper (German National Licenses)
    Fulltext
  • 5
    Electronic Resource
    Electronic Resource
    Beta-cell hypersensitivity to glucose following 24-h exposure of rat islets to fatty acids (1997)
    Springer
    Diabetologia 40 (1997), S. 392-397 
    Details
    ISSN: 1432-0428
    Keywords: Keywords Palmitate ; long chain acyl-CoA esters ; Triacsin C ; glucose phosphorylation ; glucose utilization ; islets of Langerhans ; glucokinase ; hexokinase.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Prolonged exposure of islets to fatty acids results in a lowered glucose set-point for insulin secretion. We examined the mechanism in islets cultured for 24 h with 0.25 mmol/l palmitate. As expected, insulin secretion at 2.8 and 8.3 mmol/l glucose was increased in the palmitate-treated islets as opposed to no change at 27.7 mmol/l glucose. Co-culturing with 0.05 μg/ml Triacsin C, an inhibitor of long chain acyl-CoA synthetase, blocked this effect. Glucose utilization and oxidation showed the same pattern as insulin secretion, with the step-up for both measurements being fully manifest at 2.8 mmol/l glucose. Glucokinase Km and Vmax measured in islet extracts were unaffected by the palmitate. In contrast, hexokinase Vmax was increased by 25–35 % in both the cytoplasmic and mitochondrial-bound pools. Our data suggest prolonged exposure to fatty acids increased beta-cell hexokinase activity, thereby modifying the kinetics of glucose entry into the metabolic pathway and glucose-induced insulin secretion. The cellular mediator is likely an increased level of long chain fatty acyl-CoA esters. [Diabetologia (1997) 40: 392–397]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250050692
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    Paper (German National Licenses)
    Fulltext
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