| 41. |
- Isaksson, Mats, 1961, et al.
(author)
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Determination of potassium in the skeletal muscles by whole-body counting
- 2003
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In: Acta Diabetologica. - : Springer Science and Business Media LLC. - 0940-5429 .- 1432-5233. ; 40
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Journal article (peer-reviewed)abstract
- Changes in muscular function are related to nutritional status, disease and physical activity. To study these relationships, it is desirable to be able to determine the whole body potassium content, which is characteristic to the muscular tissue. This can be achieved by measurements in a whole-body counter, identifying contributions from the upper and lower parts of the body. In a whole-body counter with large plastic scintillators, a special measuring methodology is required. Such a method of measuring 40K in the leg muscles, extracting the part of the detector signal originating from the lower part of the body, has been developed and tested by independent phantom measurements. The results suggest that it is suited to perform regional measurements of body potassium but validation and implementation into clinical research are still necessary.
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| 42. |
- Karlsson, Maria G. E., et al.
(author)
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Peptide from glutamic acid decarboxylase similar to coxsackie B virus stimulates IFN- γ mRNA expression in Th1-like lymphocytes from children with recent-onset insulin-dependent diabetes mellitus
- 1998
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In: Acta Diabetologica. - : Springer Science and Business Media LLC. - 0940-5429 .- 1432-5233. ; 35:3, s. 137-144
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Journal article (peer-reviewed)abstract
- At the clinical onset of insulin-dependent diabetes mellitus (type 1 diabetes), inflammation within the pancreatic islets of Langerhans causes insulitis. CD4+ or Th-lymphocytes will be activated after stimulation resulting in interferon-gamma (IFN-γ) production by Th1-like lymphocytes and/or interleukin-4 (IL-4) secretion from Th2-like lymphocytes. The antigens responsible for this activation are unknown, but studies have suggested glutamic acid decarboxylase (GAD) to be a possible candidate. One peptide from this enzyme (amino acid 247–279) with a similar amino acid sequence to coxsackie B virus may cause lymphocyte proliferation in diabetic patients. In this study we have shown that this peptide activates Th1-like lymphocytes which produce increased amounts of IFN-γ mRNA, but seldom mRNA for IL-4. Lymphocytes from healthy HLA-matched controls (DR3/4) did not respond with an upregulated mRNA expression for these cytokines when stimulated by the GAD-peptide (P<0.05). A low or absent expression of IFN-γ mRNA was significantly correlated to a high fasting C-peptide at 3 months' duration (P<0.05). In conclusion, we suggest that GAD65 is involved in the development of type 1 diabetes and that the Th1-response may play a role in the destruction of β cells.
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| 43. |
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| 44. |
- Kurien, Matthew, et al.
(author)
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A nationwide population-based study on the risk of coma, ketoacidosis and hypoglycemia in patients with celiac disease and type 1 diabetes
- 2015
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In: Acta Diabetologica. - : Springer Milan. - 0940-5429 .- 1432-5233. ; 52:6, s. 1167-1174
-
Journal article (peer-reviewed)abstract
- Celiac disease (CD) may influence metabolic control in type 1 diabetes (T1D). This work examines whether CD in T1D influences hospital admissions due to coma, ketoacidosis and hypoglycemia.In population-based cohort study, individuals with CD were identified using biopsy data (1969-2008) from Sweden's 28 pathology departments. T1D was defined as a recorded diagnosis of T1D at age a parts per thousand currency sign30 years in the Swedish National Patient Register between 1964 and 2009. In total, 906 individuals had both T1D and CD and were matched for sex, age and calendar period with 4303 reference individuals. Through stratified Cox regression analysis, we modeled CD as a time-dependent covariate and estimated the risk of future coma, ketoacidosis and hypoglycemia, defined by relevant international classification of disease codes among T1D patients with and without CD.During follow-up, patients with both T1D and CD had 49 hospital admissions with diabetic coma, 91 episodes of ketoacidosis and 25 hypoglycemic events. Among patients with T1D, CD did not influence the risk of coma (adjusted HR 0.97; 95 % CI 0.72-1.32), ketoacidosis (adjusted HR 1.08; 95 % CI 0.86-1.34), or hypoglycemia (adjusted HR 1.34; 95 % CI 0.87-2.05). The absolute risk of coma was 621/100,000 person-years in T1D and CD (637 in controls). Corresponding figures for ketoacidosis were 1175/100,000 person-years in T1D and CD (1092 in controls) and for hypoglycemia 316/100,000 person-years (236 in controls). HRs for metabolic emergencies in T1D were similar in the first 5 years after T1D diagnosis as thereafter.Having a diagnosis of CD is unlikely to influence the risk of coma, ketoacidosis and hypoglycemia in T1D patients.
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| 45. |
- Köhler, Meike, et al.
(author)
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Joint modeling of longitudinal autoantibody patterns and progression to type 1 diabetes : results from the TEDDY study
- 2017
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In: Acta Diabetologica. - : Springer Science and Business Media LLC. - 1432-5233 .- 0940-5429. ; 54:11, s. 1009-1017
-
Journal article (peer-reviewed)abstract
- AIMS: The onset of clinical type 1 diabetes (T1D) is preceded by the occurrence of disease-specific autoantibodies. The level of autoantibody titers is known to be associated with progression time from the first emergence of autoantibodies to the onset of clinical symptoms, but detailed analyses of this complex relationship are lacking. We aimed to fill this gap by applying advanced statistical models.METHODS: We investigated data of 613 children from the prospective TEDDY study who were persistent positive for IAA, GADA and/or IA2A autoantibodies. We used a novel approach of Bayesian joint modeling of longitudinal and survival data to assess the potentially time- and covariate-dependent association between the longitudinal autoantibody titers and progression time to T1D.RESULTS: For all autoantibodies we observed a positive association between the titers and the T1D progression risk. This association was estimated as time-constant for IA2A, but decreased over time for IAA and GADA. For example the hazard ratio [95% credibility interval] for IAA (per transformed unit) was 3.38 [2.66, 4.38] at 6 months after seroconversion, and 2.02 [1.55, 2.68] at 36 months after seroconversion.CONCLUSIONS: These findings indicate that T1D progression risk stratification based on autoantibody titers should focus on time points early after seroconversion. Joint modeling techniques allow for new insights into these associations.
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| 46. |
- Larsson, Helena, et al.
(author)
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Baseline heterogeneity in glucose metabolism marks the risk for type 1 diabetes and complicates secondary prevention.
- 2015
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In: Acta Diabetologica. - : Springer Science and Business Media LLC. - 1432-5233 .- 0940-5429. ; 52:3, s. 473-481
-
Journal article (peer-reviewed)abstract
- Non-diabetic children with multiple islet autoantibodies were recruited to a secondary prevention trial. The objective was to determine the predictive value of baseline (1) HbA1c and metabolic variables derived from intravenous (IvGTT) and oral glucose tolerance tests (OGTT), (2) insulin resistance and (3) number, type and levels of islet autoantibodies, for progression to type 1 diabetes.
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| 47. |
- Larsson-Nyrén, G, et al.
(author)
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Anion-selective amplification of glucose-induced insulin secretion.
- 2002
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In: Acta Diabetologica. - 0940-5429 .- 1432-5233. ; 39:1, s. 41-7
-
Journal article (peer-reviewed)abstract
- The functional roles of anions on glucose-induced insulin secretion are poorly understood. We investigated the effects of the monovalent anions thiocyanate, iodide, bromide, nitrate and chloride on the dynamics of insulin secretion in isolated pancreatic islets from non-inbred Umeå ob/ob mice. All anion species (12 mM), except Cl-, significantly amplified glucose-induced (20 mM) first- and second-phase insulin secretion (selectivity sequence: SCN->NO3->I->Br->Cl-). Simultaneously, the anions reduced the lag-time prior to the initiation of the secretion (SCN-=I-=NO3->Br->Cl-). The results indicate that pancreatic beta-cell activation can be initiated and amplified by an anion-selective mechanism showing increasing degrees of activation in the order of the anion series of Hofmeister. On the basis of the strikingly similar anion selectivity of amplified secretion and shortened lag-phase, we suggest that both types of anion effects are caused by action at a single site on the beta-cell.
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| 48. |
- Lindehammer, Sabina, et al.
(author)
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Temporal trends of HLA genotype frequencies of type 1 diabetes patients in Sweden from 1986 to 2005 suggest altered risk
- 2008
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In: Acta Diabetologica. - : Springer Science and Business Media LLC. - 0940-5429 .- 1432-5233. ; 45:4, s. 231-5
-
Journal article (peer-reviewed)abstract
- The aim of this study was to compare the frequency of human leukocyte antigen (HLA) genotypes in 1-18-year-old patients with type 1 diabetes newly diagnosed in 1986-1987 (n = 430), 1996-2000 (n = 342) and in 2003-2005 (n = 171). We tested the hypothesis that the HLA DQ genotype distribution changes over time. Swedish type 1 diabetes patients and controls were typed for HLA using polymerase chain reaction amplification and allele specific probes for DQ A1* and B1* alleles. The most common type 1 diabetes HLA DQA1*-B1*genotype 0501-0201/0301-0302 was 36% (153/430) in 1986-1987 and 37% (127/342) in 1996-2000, but decreased to 19% (33/171) in 2003-2005 (P \ 0.0001). The 0501-0201/0501-0201 genotype increased from 1% in 1986-1987 to 7% in 1996-2000 (P = 0.0047) and to 5% in 2003-2005 (P > 0.05). This study in 1-18-year-old Swedish type 1 diabetes patients supports the notion that there is a temporal change in HLA risk.
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| 49. |
- Lindgren, Marie, et al.
(author)
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Cumulative incidence of type 1 diabetes in two cohorts of children with different national gluten recommendations in infancy
- 2024
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In: Acta Diabetologica. - : Springer. - 0940-5429 .- 1432-5233. ; 61:1, s. 35-41
-
Journal article (peer-reviewed)abstract
- Aims: Between 1985 and 1996, Sweden experienced an "epidemic" of celiac disease with a fourfold increase in incidence in young children. Timing and amount of gluten introduced during infancy have been thought to explain this "epidemic". We aimed to study whether the cumulative incidence of type 1 diabetes differs between children born during the "epidemic" compared to children born after.Methods: This is a national register study in Sweden comparing the cumulative incidence of type 1 diabetes in two birth cohorts of 240 844 children 0-17 years old born 1992-1993, during the "epidemic", and 179 530 children born 1997-1998, after the "epidemic". Children diagnosed with type 1 diabetes were identified using three national registers.Results: The cumulative incidence of type 1 diabetes by the age of 17 was statistically significantly higher in those born after the "epidemic" 0.77% than in those born during the "epidemic" 0.68% (p < 0.001).Conclusion: The incidence of type 1 diabetes is higher in those born after the epidemic compared to those born during the epidemic, which does not support the hypothesis that gluten introduction increases the incidence of T1D. Changes in gluten introduction did not halt the increased incidence of type 1 diabetes in Sweden.
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| 50. |
- Lundgren, Markus, et al.
(author)
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Influence of early-life parental severe life events on the risk of type 1 diabetes in children : the DiPiS study
- 2018
-
In: Acta Diabetologica. - : Springer Science and Business Media LLC. - 0940-5429 .- 1432-5233. ; 55:8, s. 797-804
-
Journal article (peer-reviewed)abstract
- Aims: Stress and severe life events (SLEs) modify autoimmune disease susceptibility. Here, we aimed to establish if SLEs reported by parents during the first 2 years of life influence the risk of developing type 1 diabetes (T1D) using data from the prospective Diabetes Prediction in Skåne (DiPiS) study. Methods: Prospective questionnaire data recorded at 2 months (n = 23,187) and 2 years of age (n = 3784) from the DiPiS cohort of children were included in the analysis. SLEs were analyzed both by groups and as a combined variable. A Cox proportional hazards model was used to calculate hazard ratios (HRs) for T1D diagnosis for the total cohort and for the HLA-DQ2/8 high-risk population. Affected first-degree relatives, HLA-DQ risk group, paternal education level, and parents’ country of birth were included as covariates. Results: There was a significantly increased risk of T1D in children with SLEs occurring during the child’s first 2 years of life for both the total cohort (HR 1.67; 95% CI 1.1, 2.7; p = 0.03) and the DQ2/8 cohort (HR 2.2; 95% CI 1.1, 4.2; p = 0.018). Subgroup analysis of events related to unemployment, divorce, or family conflict showed a significant hazard for these events occurring both during and after pregnancy in the DQ2/8 cohort (HR 2.17; 95% CI 1.1, 4.3; p = 0.03 and HR 4.98; 95% CI 2.3, 11; p < 0.001, respectively) and after pregnancy in the total cohort (multiple regression HR 2.07; 95% CI 1.01, 4.2; p = 0.047). Conclusions: Children of parents experiencing an SLE during the child’s first 2 years of life were at increased risk of T1D. Further studies including those measuring immune and stress-related biomarkers are necessary to validate the findings.
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