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1.
  • Olsen, Henrik, et al. (författare)
  • Influence of glucose and insulin on transcapillary fluid absorption from the arm during lower body negative pressure in man
  • 2003
  • Ingår i: EUROPEAN JOURNAL OF APPLIED PHYSIOLOGY. - SPRINGER-VERLAG. - 1439-6319. ; 90:1-2, s. 138-143
  • Tidskriftsartikel (refereegranskat)abstract
    • This study examined the influence of insulin and glucose on the transcapillary fluid absorption during lower body negative pressure (LBNP) in humans. Ten healthy males 23 (1) years were exposed to LBNP of 45 cmH(2)O on two occasions: (1) before and during a hyperinsulinaemic clamp (HI) and (2) before and during a hyperglycaemic clamp (HG). Transcapillary fluid absorption and blood flow were recorded with volumetric technique. Forearm blood flow increased during HI from 2.3 (0.3) ml (100 ml)(-1) min(-1) to 3.3 (0.5) ml (100 ml)(-1) min(-1) (P<0.05). The haemodynamic response to LBNP was similar during HI and HG compared with control LBNP. Transcapillary fluid absorption during LBNP increased during HG from 0.044 (0.007) ml (100 ml)(-1) min(-1) to 0.059 (0.009) ml (100 ml)(-1) min(-1) (P<0.01), whereas it was unchanged during HI. In conclusion, hyperglycaemia augments transcapillary fluid absorption from skeletal muscle and skin during LBNP whereas hyperinsulinaemia has no such effect. This indicates that in human hyperglycaemia contributes to plasma volume restitution during hypovolaemic circulatory stress.
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2.
  • Weng, J., et al. (författare)
  • Functional consequences of mutations in the MODY4 gene (IPF1) and coexistence with MODY3 mutations
  • 2001
  • Ingår i: Diabetologia. - Springer-Verlag. - 0012-186x. ; 44:2, s. 249-258
  • Tidskriftsartikel (refereegranskat)abstract
    • Aims/hypothesis. The aim of this study was to examine the putative role of mutations in the insulin promoter 1 (IPF1) gene in early-onset diabetes. Methods. We carried out mutation screening of the IPF1 gene in 115 Scandinavian families with at least two members with onset of diabetes younger than 40 years. The allele frequencies were also tested in 183 unrelated patients with late-onset Type II (noninsulin-dependent) diabetes mellitus and in 92 nondiabetic control subjects. Results. Two novel IPF1 variants (G212R and P239Q) and one previously reported (D76N) IPF1 variant were identified in the 115 families (3.5%). The D76N variant was found in one MODY3 family (S315fsinsA of HNF1 alpha) and also in two families with late-onset Type II diabetes. The P239Q variant was identified in two families with early-onset diabetes including one with MODY3 (R272C of HNF1 alpha) and in three families with late-onset Type II diabetes. Despite the fact that the variants did not segregate completely with diabetes, the non-diabetic carriers of the IPF1 variants had increased blood glucose concentrations (p < 0.05) and reduced insulin:glucose ratios (p < 0.05) during an oral glucose tolerance test compared with non-diabetic family members without these variants. In addition, when the G212R and P239Q variants were expressed in cells without IPF1 i.e.. Nes2y cells, both variants showed about a 50% reduction in their ability to activate insulin gene transcription compared to wild-type IPF1, as measured by reporter gene assay. Conclusion/interpretation. Although mutations in the IPF-1 gene are rare in early- (3.5%) and late-onset (2.7%) Type II diabetes, they are functionally important and occur also in families with other MODY mutations.
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4.
  • Almqvist, E G, et al. (författare)
  • Hypothalamic-pituitary-adrenal response to different tests in type 1 diabetes mellitus
  • 2001
  • Ingår i: Scandinavian journal of clinical and laboratory investigation. - Scandinavian University Press. - 0036-5513. ; 61:7, s. 557-565
  • Tidskriftsartikel (refereegranskat)abstract
    • OBJECTIVE: To determine whether different tests of the adrenocorticotropic hormone (ACTH) reserve are influenced by diabetic state and metabolic control in newly diagnosed type 1 diabetic patients. DESIGN AND METHODS: We evaluated the ACTH reserve in 10 patients with uncomplicated type 1 diabetes during periods of poor and improved metabolic control and in 10 healthy subjects. The ACTH-cortisol secretion was assessed by a diurnal profile, an intravenous corticotropin-releasing hormone (CRH) test and an insulin tolerance test (ITT). RESULTS: The diurnal profiles were similar in all groups. CRH resulted in a diminished ACTH response during poor compared with improved metabolic control (mean+/-SD) (AUC 4950+/-4227 vs. 5847+/-3788 ng/L min, p<0.05). The response in the diabetic patients during improved metabolic control was of the same magnitude as in the control subjects (5934+/-1778 ng/L x min). ITT elicited a similar ACTH and cortisol response in the diabetic patients during poor and improved metabolic control as in the healthy control subjects. CONCLUSIONS: The ITT was uninfluenced by diabetic state and metabolic control and should therefore be considered the method of choice in evaluation of the ACTH reserve in patients with type 1 diabetes.
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5.
  • Antonelli, A, et al. (författare)
  • Autoimmunity to CD38 and GAD in Type I and Type II diabetes: CD38 and HLA genotypes and clinical phenotypes
  • 2002
  • Ingår i: Diabetologia. - Springer. - 0012-186X. ; 45:9, s. 1298-1306
  • Tidskriftsartikel (refereegranskat)abstract
    • Aims/hypothesis. Autoantibodies against CD38 have been found in some patients with Type II (non-insulin-dependent) diabetes mellitus and have been shown to stimulate insulin secretion by cultured human islets. We tested whether this new form of autoimmunity, (i) overlaps with anti-GAD autoimmunity, (ii) identifies an insulin-deficient phenotype, (iii) is under the influence of genetic factors. Methods. We screened 496 adults by immuno-blot analysis in the Botnia Study (298 with Type II and 98 with Type I (insulin-dependent) diabetes mellitus, 100 non-diabetic control subjects). Results. CD38-autoantibodies were found in 8.4% of Type II diabetic patients (p<0.003 vs 0% of control subjects), particularly in anti-GAD positive (14% vs 6% of anti-GAD negative, p=0.0004). CD38ab were also found in 4% of Type I diabetic patients; in the whole study group, 59% of anti-CD38 positive had DQB1 *02 compared with 38% of anti-CD38 negative (p=0.04). On the OGTT, beta-cell function (as the ratio of insulin-to-glucose areas) was impaired (p=0.02) only in association with anti-GAD positivity (3.2 +/- 3.1 U/mol, mean +/- SD) but not in anti-CD38 positive patients (5.6 +/- 2.9) as compared with patients free of autoimmunity (4.5 +/- 4.6, p=NS). In 44 Type II diabetic patients (22 negative and 22 positive for anti-CD38), no mutations were detected in any of the 8 exons, 5' end of intron 1 or the 5' and 3' untranslated regions of the CD38 gene. The previously described missense mutation (Arg140Trp) in exon 3 was not found in this cohort. There was no association between the PvUII polymorphism and clinical phenotype. Conclusion. Anti-CD38 autoimmunity identifies a clinical phenotype similar to non-autoimmune Type II diabetes, with relative preserved beta-cell function and weak genetic influence.
6.
  • Bengtsson, Kristina, et al. (författare)
  • Beta(2)-adrenergic receptor gene variation and hypertension in subjects with type 2 diabetes
  • 2001
  • Ingår i: Hypertension. - Lippincott Williams & Wilkins. - 1524-4563. ; 37:5, s. 1303-1308
  • Tidskriftsartikel (refereegranskat)abstract
    • The aim of this study was to investigate whether polymorphisms in the beta(2)-adrenergic receptor gene (5'LC-Arg19Cys, Arg16Gly, Gln27Glu) are associated with hypertension in patients with or without type 2 diabetes and with the blood pressure levels in normotensive sib pairs. The association study included 291 hypertensive patients without type 2 diabetes, 124 hypertensive patients with type 2 diabetes, and 265 healthy control subjects from SWEDEN: In addition, normotensive sib pairs that were discordant for the Arg16Gly (72 pairs) and Gln27Glu (40 pairs) polymorphisms were identified in type 2 diabetes families from FINLAND: Genotyping was performed using polymerase chain reaction-restriction fragment-length polymorphism analysis. Homozygous carriers of the Arg16 allele had a significantly increased odds ratio (OR) for hypertension in patients with type 2 diabetes (OR 2.14; 95% confidence interval CI, 1.05 to 4.33), particularly among lean (body mass index<27 kg/m(2)) patients (OR 3.47; 95% CI, 1.06 to 11.33). The Gln27 allele showed a weaker association to hypertension (OR 1.55; 95% CI, 1.00 to 2.41) and was found to be in linkage disequilibrium with the Cys19 allele of the 5'LC-Arg19Cys polymorphism. In the paired-sibling analysis, siblings with at least 1 copy of the Arg16 allele had higher systolic blood pressure (P=0.049), and nondiabetic siblings had a higher body mass index (P=0.026) than siblings homozygous for the Gly16 allele. These results indicate that the Arg16 allele of the beta(2)-adrenergic receptor gene confers an increased risk for hypertension in subjects with type 2 diabetes and is associated with higher blood pressure levels and higher body mass index in sib pairs who are discordant for the polymorphism.
7.
  • Bengtsson, Kristina, et al. (författare)
  • Polymorphism in the beta(1)-adrenergic receptor gene and hypertension
  • 2001
  • Ingår i: Circulation. - Lippincott Williams & Wilkins. - 1524-4539. ; 104:2, s. 187-190
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND: The Arg389 variant of the beta(1)-adrenergic receptor gene mediates a higher isoproterenol-stimulated adenylate cyclase activity than the Gly389 variant in vitro. We investigated whether the Arg389Gly or the Ser49Gly polymorphism is associated with hypertension in Scandinavians. Methods and Results-- A total of 292 unrelated, nondiabetic, hypertensive patients and 265 unrelated healthy control subjects were included in a case-control association study. From 118 families, 102 nondiabetic sibling pairs without antihypertensive medication who were discordant for the Arg389Gly polymorphism were selected for a sibling study. Allele and genotype frequencies of the Arg389Gly and Ser49Gly polymorphisms were compared between hypertensive patients and normotensive control subjects. Blood pressure and heart rate were compared between carriers of the different genotypes. In the case-control study, the age- and body mass index-adjusted odds ratio for hypertension in subjects homozygous for the Arg389 allele was 1.9 (95% confidence interval, 1.3 to 2.7; P=0.0005) when compared with carriers of 1 or 2 copies of the Gly389 allele. The genotype-discordant sibling pair analysis revealed that siblings homozygous for the Arg389 allele had significantly higher diastolic blood pressures (79.4+/-9.9 versus 76.0+/-10.1 mm Hg; P=0.003) and higher heart rates (68.3+/-11.0 versus 65.1+/-9.4 bpm; P=0.02) than siblings carrying 1 or 2 copies of the Gly389 allele. The Ser49Gly polymorphism was not associated with hypertension. CONCLUSION: Our data suggest that individuals homozygous for the Arg389 allele of the beta(1)-adrenergic receptor gene are at increased risk to develop hypertension.
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  • Resultat 1-10 av 88
  • [1]234567...9Nästa
 
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