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  • Type 2 (non-insulin-dependent) diabetes mellitus  (3)
  • Pancreas size  (2)
  • 1
    Electronic Resource
    Electronic Resource
    Pancreas size and insulin secretion: lack of association in non-diabetic subjects (1996)
    Springer
    Acta diabetologica 33 (1996), S. 274-276 
    Details
    ISSN: 1432-5233
    Keywords: Computer tomography ; Insulin secretion ; Pancreas size ; Diabetes mellitus
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Both type 1 and type 2 diabetes mellitus are associated with reduced pancreatic size. This could be caused by insulinopenia with loss of a trophic insulin effect and/or other factors associated with a diabetic state. To investigate the role of long-term moderate insulinemia per se, we compared the pancreatic size in healthy subjects with documented low (n=5) and high (n=5) insulin secretion. Insulin responses to a glucose clamp (11 mM) procedure were threefold higher in the high insulin responders (HIR) than low insulin responders (LIR). Age, body mass index (BMI), and blood glucose were similar between groups. Computed tomography showed no difference in total pancreatic size (total pancreas volume 84.8±29.4 ml in LIR, 79.8±8.4 ml in HIR; NS) nor in the size of various parts (caput, corpus, or cauda). We conclude that moderate hypoinsulinemia of long duration does not affect the pancreatic size.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00571563
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    Paper (German National Licenses)
    Fulltext
  • 2
    Electronic Resource
    Electronic Resource
    Pancreas size and insulin secretion: lack of association in non-diabetic subjects (1996)
    Springer
    Acta diabetologica 33 (1996), S. 274-276 
    Details
    ISSN: 1432-5233
    Keywords: Key words Computer tomography ; Insulin secretion ; Pancreas size ; Diabetes mellitus
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Both type 1 and type 2 diabetes mellitus are associated with reduced pancreatic size. This could be caused by insulinopenia with loss of a trophic insulin effect and/or other factors associated with a diabetic state. To investigate the role of long-term moderate insulinemia per se, we compared the pancreatic size in healthy subjects with documented low (n=5) and high (n=5) insulin secretion. Insulin responses to a glucose clamp (11 mM) procedure were threefold higher in the high insulin responders (HIR) than low insulin responders (LIR). Age, body mass index (BMI), and blood glucose were similar between groups. Computed tomography showed no difference in total pancreatic size (total pancreas volume 84.8±29.4 ml in LIR, 79.8±8.4 ml in HIR; NS) nor in the size of various parts (caput, corpus, or cauda). We conclude that moderate hypoinsulinemia of long duration does not affect the pancreatic size.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00571563
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
  • 3
    Electronic Resource
    Electronic Resource
    Abnormal insulin secretion and glucose metabolism in pancreatic islets from the spontaneously diabetic GK rat (1993)
    Springer
    Diabetologia 36 (1993), S. 3-8 
    Details
    ISSN: 1432-0428
    Keywords: Type 2 (non-insulin-dependent) diabetes mellitus ; pancreatic islets ; perfused pancreas ; glucose metabolism
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Insulin secretion and islet glucose metabolism were compared in pancreatic islets isolated from GK/Wistar (GK) rats with spontaneous Type 2 (non-insulin-dependent) diabetes mellitus and control Wistar rats. Islet insulin content was 24.5±3.1 μU/ng islet DNA in GK rats and 28.8±2.5 μU/ng islet DNA in control rats, with a mean (±SEM) islet DNA content of 17.3±1.7 and 26.5±3.4 ng (p 〈 0.05), respectively. Basal insulin secretion at 3.3 mmol/l glucose was 0.19±0.03 μ · ng islet DNA−1· h−1 in GK rat islets and 0.40±0.07 in control islets. Glucose (16.7 mmol/l) stimulated insulin release in GK rat islets only two-fold while in control islets five-fold. Glucose utilization at 16.7 mmol/l glucose, as measured by the formation of 3H2O from [5-3 H]glucose, was 2.4 times higher in GK rat islets (3.1±0.7 pmol · ng islet DNA−1 · h−1) than in control islets (1.3±0.1 pmol · ng islet DNA−1 · h−1; p〈0.05). In contrast, glucose oxidation, estimated as the production of 14CO2 from [U-14C]glucose, was similar in both types of islets and corresponded to 15±2 and 30±3 % (p〈0.001) of total glucose phosphorylated in GK and control islets, respectively. Glucose cycling, i. e. the rate of dephosphorylation of the total amount of glucose phosphorylated, (determined as production of labelled glucose from islets incubated with 3H2O) was 16.4±3.4% in GK rat and 6.4±1.0% in control islets, respectively (p〈0.01). We conclude that insulin secretion stimulated by glucose is markedly impaired in GK rat islets. Glucose metabolism is also altered in GK rat islets, with diminished ratio between oxidation and utilization of glucose, and increased glucose cycling, suggesting links between impaired glucose-induced insulin release and abnormal glucose metabolism.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00399086
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    Paper (German National Licenses)
    Fulltext
  • 4
    Electronic Resource
    Electronic Resource
    Screening for insulin receptor gene DNA polymorphisms associated with glucose intolerance in a Scandinavian population (1991)
    Springer
    Diabetologia 34 (1991), S. 265-270 
    Details
    ISSN: 1432-0428
    Keywords: Type 2 (non-insulin-dependent) diabetes mellitus ; insulin receptors ; restriction fragment length polymorphisms ; linkage disequilibrium ; blood glucose
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The significance of insulin receptor gene variants in the aetiology of Type 2 (non-insulin-dependent) diabetes mellitus has been investigated by analysis of restriction fragment length polymorphisms in a genetically homogeneous Swedish population. Seven polymorphisms were analysed, spanning functionally important regions of the insulin receptor locus. Four of these polymorphisms were mapped more accurately within the gene compared to previous studies. The genotype distribution was compared in 76 Type 2 diabetic patients and 84 healthy control subjects. No significant differences were found in the distribution of genotypes between diabetic and control subjects at the p〈 0.01 level. In order to study the possible association between quantitative measures of glucose metabolism and these DNA polymorphisms, the fasting glucose and insulin concentrations were compared in the different genotype groups of control subjects and mildly diabetic patients treated with diet. No differences in fasting glucose or insulin concentrations were found at the p〈 0.005 level of significance. In conclusion, no significant associations were found between insulin receptor gene DNA polymorphisms and glucose intolerance.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00405086
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    Paper (German National Licenses)
    Fulltext
  • 5
    Electronic Resource
    Electronic Resource
    Dexamethasone treatment fails to increase arginine-induced insulin release in healthy subjects with low insulin response (1992)
    Springer
    Diabetologia 35 (1992), S. 367-371 
    Details
    ISSN: 1432-0428
    Keywords: Insulin secretion ; Type 2 (non-insulin-dependent) diabetes mellitus ; glucagon secretion ; C-peptide ; arginine ; dexamethasone
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary We have compared insulin responses to L-arginine before and during dexamethasone treatment in healthy subjects, previously classified as subjects with either high or low insulin response according to a standardized glucose infusion test. Arginine stimulation was administered as a 150 mg/kg bolus followed by 10 mg·kg−1·min−1 to six subjects with high insulin response and to seven subjects with low insulin response. Before dexamethasone treatment the incremental insulin level during 0–10 min of arginine was higher in subjects with high (36.5±6.8 μU/ml) than in subjects with low response (14.5±2.3 μU/ml), p〈0.01 for difference. Dexamethasone treatment (6 mg/day for 60 h) markedly enhanced the insulin response to arginine in subjects with high response (+99% 0–30 min) but failed to affect the subjects with low response (+4% 0–30 min). The C-peptide response to arginine exhibited similar differences between groups. Decreased responsiveness to arginine in subjects with low insulin response, especially during dexamethasone treatment, suggests a Beta-cell capacity defect although a decreased potentiating-sensing effect of glucose cannot be completely ruled out.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00401204
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    Paper (German National Licenses)
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