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  • fluid secretion  (8)
  • genetics  (4)
  • insulin  (4)
  • 1
    Electronic Resource
    Electronic Resource
    Evidence for a Na+/K+/Cl− cotransport system in basolateral membrane vesicles from the rabbit parotid (1986)
    Springer
    The journal of membrane biology 94 (1986), S. 143-152 
    Details
    ISSN: 1432-1424
    Keywords: fluid secretion ; exocrine gland ; chloride transport
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology
    Notes: Summary Sodium (22Na) transport was studied in a basolateral membrane vesicle preparation from rabbit parotid. Sodium uptake was markedly dependent on the presence of both K+ and Cl− in the extravesicular medium, being reduced 5 times when K+ was replaced by a nonphysiologic cation and 10 times when Cl− was replaced by a nonphysiologic anion. Sodium uptake was stimulated by gradients of either K+ or Cl− (relative to nongradient conditions) and could be driven against a sodium concentration gradient by a KCl gradient. No effect of membrane potentials on KCl-dependent sodium flux could be detected, indicating that this is an electroneutral process. A KCl-dependent component of sodium flux could also be demonstrated under equuilibrium exchange conditions, indicating a direct effect of K+ and Cl− on the sodium transport pathway. KCl-dependent sodium uptake exhibited a hyperbolic dependence on sodium concentration consistent with the existence of a single-transport system withK m =3.2mm at 80mm KCl and 23°C. Furosemide inhibited this transporter withK 0.5=2×10−4 m (23°C). When sodium uptake was measured as a function of potassium and chloride concentrations a hyperbolic dependence on [K] (Hill coefficient =1.31±0.07) were observed, consistent with a Na/K/Cl stoichiometry of 1∶1∶2. Taken together these data provide strong evidence for the electroneutral coupling of sodium and KCl movements in this preparation and strongly support the hypothesis that a Na+/K+/Cl− cotransport system thought to be associated with transepithelial chloride and water movements in many exocrine glands is present in the parotid acinar basolateral membrane.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01871194
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  • 2
    Electronic Resource
    Electronic Resource
    Plasma proinsulin, C-peptide and insulin in diagnostic suppression tests for insulinomas (1977)
    Springer
    Diabetologia 13 (1977), S. 571-577 
    Details
    ISSN: 1432-0428
    Keywords: Insulinoma ; malignant insulinoma ; proinsulin ; C-peptide ; insulin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The value of plasma insulin, human C-peptide and proinsulin estimation in the diagnosis of 15 insulinomas has been investigated. Measurement of plasma proinsulin in an overnight fasting sample diagnosed all the insulinomas studied, irrespective of the plasma glucose. Patients with insulinomas had plasma proinsulin in the range 0.04–4.2 pmol/l and normal values were less than 0.01 pmol/ml. If hypoglycaemia was present, an inappropriately raised plasma immunoreactive insulin (including proinsulin) was diagnostic, but this assay was of little assistance if the plasma glucose was normal. Hypoglycaemia was induced with fish insulin in twelve patients with insulinomas and eight normal subjects. Using an antiserum which did not detect fish insulin, but cross-reacted with human proinsulin, the endogenous immunoreactive insulin was suppressed in the normal subjects, but all insulinoma patients had impaired suppression. Assay of plasma human C-peptide, or of the combined immunoreactive C-peptide and proinsulin, discriminated less well and did not clearly diagnose three insulinomas which secreted proinsulin rather than insulin and C-peptide. Plasma human proinsulin values during induced hypoglycaemia gave excellent discrimination and should detect insulinomas irrespective of their degree of histological differentiation. The assay of plasma human proinsulin allows a suppression test to be performed with hypoglycaemia induced by any type of insulin. A raised plasma proinsulin in proportion to C-peptide suggests an undifferentiated insulinoma, which may be more likely to be malignant.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01236309
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  • 3
    Electronic Resource
    Electronic Resource
    Twenty-four hour profiles of plasma C-peptide in Type 1 (insulin-dependent) diabetic children (1982)
    Springer
    Diabetologia 22 (1982), S. 245-249 
    Details
    ISSN: 1432-0428
    Keywords: Type 1 diabetes ; diabetic children ; blood glucose profiles ; insulin ; C-peptide ; B cell
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Twenty-four hour profiles of plasma C-peptide an index of endogenous insulin secretion, were performed in 15 Type 1 (insulin-dependent) diabetic children. Plasma C-peptide was detectable in six children, of whom four (‘C-peptide producers’) had peak values above normal fasting levels. In each of the six children with residual B cell function, there was a close correlation between plasma C-peptide and simultaneous blood glucose (r〉 0.50, p〈 0.05). Post-breakfast peak blood glucose was 10.2 ± 1.7 mmol/l (mean ±SEM) in the ‘C-peptide producers’ and 18.7 ± 1.7 mmol/l in the 11 children with low or no detectable C-peptide. Mean M-value, an index of deviation from an ideal blood glucose, was lower in the ‘C-peptide producers’ (p〈0.05). It is concluded that residual functioning B cells in diabetic children behave physiologically in that insulin secretion fluctuates in accordance with the prevailing blood glucose; and that the pattern of action of injected insulin is more critical in non-C-peptide producers who lack the post-prandial dampening effect provided by residual endogenous insulin secretion.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00281299
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  • 4
    Electronic Resource
    Electronic Resource
    Analysis of the HepG2/erythrocyte glucose transporter locus in a family with Type 2 (non-insulin-dependent) diabetes and obesity (1989)
    Springer
    Diabetologia 32 (1989), S. 266-269 
    Details
    ISSN: 1432-0428
    Keywords: Type 2 (non-insulin-dependent) diabetes ; genetics ; linkage ; glucose transporter
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary A recent report has shown an association between a specific Xba1 restriction fragment of the human HepG2-Erythrocyte glucose transporter gene and Type 2 (non-insulin dependent) diabetes. To further examine the significance of this finding we have studied Type 2 diabetic pedigrees for linkage between the Xba1 alleles of this glucose transporter gene and diabetes. One large pedigree, in which the diabetic phenotype was associated with obesity and insulin resistance, was informative. In this family the disease did not co-segregate with the glucose transporter locus. Formal linkage analysis was performed assuming autosomal dominant inheritance with age-dependent penetrance. At putative gene frequencies of 0.01 and 0.001 the logarithin of the odds for linkage versus non-linkage at a recombination fraction of 0.001 was −1.84 and −3.32 respectively (a value of 〈-2 indicates definite non-linkage). Genetic variations in the HepG2-Erythrocyte glucose transporter gene are unlikely to be responsible for the development of diabetes in this pedigree.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00285296
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  • 5
    Electronic Resource
    Electronic Resource
    UK Prospective Diabetes Study (UKPDS) 14: association of angiotensin-converting enzyme insertion/deletion polymorphism with myocardial infarction in NIDDM (1995)
    Springer
    Diabetologia 38 (1995), S. 948-952 
    Details
    ISSN: 1432-0428
    Keywords: Key words Non-insulin-dependent diabetes mellitus ; myocardial infarction ; angiotensin-converting enzyme ; genetics ; risk factors.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The deletion allele of the insertion/deletion polymorphism of the angiotensin-converting enzyme gene has been suggested to be an independent risk factor for myocardial infarction, particularly in subjects judged to be “low-risk” by the criteria of lipid status and body mass index. In a prospective, matched case-control study, we have investigated the role of this polymorphism as a risk factor for myocardial infarction in 173 newly-diagnosed British Caucasian non-insulin-dependent diabetic subjects taken from the United Kingdom Prospective Diabetes Study who subsequently developed myocardial infarction and 297 control subjects from the same study population matched for known cardiovascular risk factors including age at diagnosis of diabetes, gender, blood pressure, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, triglyceride and smoking habit. A trend towards increased risk conferred by homozygosity for the deletion allele was observed in cases (odds ratio 1.63, p = 0.09). When the population was stratified according to the matched risk factors, the deletion allele was associated with myocardial infarction in those with low plasma low-density lipoprotein cholesterol (odds ratio 3.67, p = 0.002), or low triglyceride (odds ratio 3.14, p = 0.005). The strongest association of the deletion allele with myocardial infarction was observed in subjects with both low low-density lipoprotein cholesterol and low triglyceride levels (odds ratio 9.0, p 〈 0.001). These results show that the deletion allele is a risk factor for myocardial infarction in non-insulin-dependent diabetic patients who have a favourable lipid profile. [Diabetologia (1995) 38: 948–952]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00400584
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  • 6
    Electronic Resource
    Electronic Resource
    Multiple restriction fragment length polymorphisms at the GLUT2 locus: GLUT2 haplotypes for genetic analysis of Type 2 (non-insulin-dependent) diabetes mellitus (1991)
    Springer
    Diabetologia 34 (1991), S. 817-821 
    Details
    ISSN: 1432-0428
    Keywords: Type 2 (non-insulin-dependent) diabetes mellitus ; genetics ; liver/islet glucose transporter gene ; restriction fragment length polymorphism ; population association study
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The liver/islet glucose transporter (GLUT2) is expressed in the liver and in the Beta cells of pancreatic islets and is a candidate gene for the inherited defect in Type 2 (non-insulin-dependent) diabetes mellitus. A series of restriction fragment length polymorphisms have been identified using a GLUT2 cDNA probe with five restriction enzymes in a British white Caucasian population. Five independent restriction fragment length polymorphisms detected by restriction enzymes EcoRI (two restriction fragment length polymorphisms termed EcoRI-1, EcoRI-2), TaqI (two restriction fragment length polymorphisms termed TaqI-1, TaqI-2), and BclI (BclI-2) were used to construct GLUT2 haplotypes. Significant linkage disequilibrium was observed between four polymorphic sites EcoRI-2, TaqI-1, TaqI-2 and BclI-2 but linkage disequilibrium was not observed with EcoRI-1 polymorphic site and the other four sites. The frequencies of GLUT2 restriction fragment length polymorphisms and haplotypes in 50 Type 2 diabetic subjects and 50 non-diabetic control subjects show no significant differences suggesting that it is unlikely that there is a single major defect of this gene contributing to the inherited susceptibility to Type 2 diabetes in a Caucasian population.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00408357
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  • 7
    Electronic Resource
    Electronic Resource
    UK Prospective Diabetes Study (UKPDS) 14: association of angiotensin-converting enzyme insertion/deletion polymorphism with myocardial infarction in NIDDM (1995)
    Springer
    Diabetologia 38 (1995), S. 948-952 
    Details
    ISSN: 1432-0428
    Keywords: Non-insulin-dependent diabetes mellitus ; myocardial infarction ; angiotensin-converting enzyme ; genetics ; risk factors
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The deletion allele of the insertion/deletion polymorphism of the angiotensin-converting enzyme gene has been suggested to be an independent risk factor for myocardial infarction, particularly in subjects judged to be “low-risk” by the criteria of lipid status and body mass index. In a prospective, matched case-control study, we have investigated the role of this polymorphism as a risk factor for myocardial infarction in 173 newly-diagnosed British Caucasian non-insulin-dependent diabetic subjects taken from the United Kingdom Prospective Diabetes Study who subsequently developed myocardial infarction and 297 control subjects from the same study population matched for known cardiovascular risk factors including age at diagnosis of diabetes, gender, blood pressure, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, triglyceride and smoking habit. A trend towards increased risk conferred by homozygosity for the deletion allele was observed in cases (odds ratio 1.63, p=0.09). When the population was stratified according to the matched risk factors, the deletion allele was associated with myocardial infarction in those with low plasma low-density lipoprotein cholesterol (odds ratio 3.67, p=0.002), or low triglyceride (odds ratio 3.14, p=0.005). The strongest association of the deletion allele with myocardial infarction was observed in subjects with both low low-density lipoprotein cholesterol and low triglyceride levels (odds ratio 9.0, p〈0.001). These results show that the deletion allele is a risk factor for myocardial infarction in non-insulin-dependent diabetic patients who have a favourable lipid profile.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00400584
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  • 8
    Electronic Resource
    Electronic Resource
    Sulphonylurea therapy doubles B-cell response to glucose in Type 2 diabetic patients (1985)
    Springer
    Diabetologia 28 (1985), S. 809-814 
    Details
    ISSN: 1432-0428
    Keywords: Sulphonylureas ; insulin ; C-peptide ; insulin resistance ; hyperglycaemic clamp
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effect of sulphonylurea therapy for 3 weeks on glucose-stimulated insulin secretion and insulin resistance was studied in Type 2 diabetic patients. The fasting plasma insulin and C-peptide concentrations on diet alone were compared with each subject's fasting concentrations on sulphonylurea treatment at a lower fasting plasma glucose and at the original diet-alone glycaemic level obtained by the hyperglycaemic clamp technique. At this isoglycaemic level (mean 11 mmol/l), plasma insulin levels increased from 6.9 mU/l on diet alone to 12.1 mU/l on sulphonylurea treatment (p〈0.01). The subjects were also studied by the hyperglycaemic clamp technique at mean glycaemic levels of 13 mmol/l before and after sulphonylurea treatment; the incremental insulin response was similarly enhanced from 7.6±3.5 to 13.7±6.9 mU/l (p〈0.02) respectively. Sulphonylureas appear to reduce glycaemia by enhancing B-cell function two-fold. In the patients studied this was from approximately 21% to 37% of a normal response. Insulin resistance assessed by the same hyperglycaemic clamps as endogenous plasma insulin concentrations divided by glucose infusion rates was unchanged by sulphonylurea therapy (mean 4.37 compared to 4.40 mU. 1−1·mg−1·kg·min on diet alone).
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00291069
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  • 9
    Electronic Resource
    Electronic Resource
    Homeostasis model assessment: insulin resistance and β-cell function from fasting plasma glucose and insulin concentrations in man (1985)
    Springer
    Diabetologia 28 (1985), S. 412-419 
    Details
    ISSN: 1432-0428
    Keywords: β-cell function ; insulin resistance ; mathematical model ; intravenous glucose tolerance test ; glucose clamp ; insulin receptors ; Type 2 diabetes ; insulin ; glucose
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The steady-state basal plasma glucose and insulin concentrations are determined by their interaction in a feedback loop. A computer-solved model has been used to predict the homeostatic concentrations which arise from varying degrees of β-cell deficiency and insulin resistance. Comparison of a patient's fasting values with the model's predictions allows a quantitative assessment of the contributions of insulin resistance and deficient β-cell function to the fasting hyperglycaemia (homeostasis model assessment, HOMA). The accuracy and precision of the estimate have been determined by comparison with independent measures of insulin resistance and β-cell function using hyperglycaemic and euglycaemic clamps and an intravenous glucose tolerance test. The estimate of insulin resistance obtained by homeostasis model assessment correlated with estimates obtained by use of the euglycaemic clamp (Rs = 0.88, p 〈 0.0001), the fasting insulin concentration (Rs = 0.81, p 〈 0.0001), and the hyperglycaemic clamp, (Rs = 0.69, p 〈 0.01). There was no correlation with any aspect of insulin-receptor binding. The estimate of deficient β-cell function obtained by homeostasis model assessment correlated with that derived using the hyperglycaemic clamp (Rs = 0.61, p 〈 0.01) and with the estimate from the intravenous glucose tolerance test (Rs = 0.64, p 〈 0.05). The low precision of the estimates from the model (coefficients of variation: 31% for insulin resistance and 32% for β-cell deficit) limits its use, but the correlation of the model's estimates with patient data accords with the hypothesis that basal glucose and insulin interactions are largely determined by a simple feed back loop.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00280883
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  • 10
    Electronic Resource
    Electronic Resource
    Evidence that up-regulation of the parotid Na+-K+-2Cl- cotransporter by hypertonic shrinkage is not duplicated by isotonic shrinkage (1997)
    Springer
    Molecular and cellular biochemistry 169 (1997), S. 21-25 
    Details
    ISSN: 1573-4919
    Keywords: salivary glands ; volume regulation ; fluid secretion ; osmoregulation ; stimulus-secretion coupling ; intracellular signalling
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract The application of Ca2+ mobilizing secretagogues to rat parotid acini results in a significant decrease in cell volume (15-30%) due to isotonic salt loss. It is often assumed that the effects of such an isotonic volume decrease can be mimicked by anisotonic cell shrinkage. We demonstrate that the Na+-K+-2Cl- cotransporter in these cells is up-regulated by Ca2+ mobilizing secretagogues as well as by cell shrinkage in hypertonic media. However, we find that although the protein kinase inhibitors staurosporine (0.3 μM) and K252a (0.6 μM) significantly blunt the latter up-regulation, they are without effect on the former. These observations suggest that hypertonic and isotonic shrinkage do not result in the activation of the same intracellular signalling pathways, and indicate that anisotonic volume perturbations may not provide good experimental models of physiologic isotonic volume changes.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1006878324913
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