SwePub
Tyck till om SwePub Sök här!
Sök i SwePub databas

  Utökad sökning

Träfflista för sökning "L773:0940 5429 OR L773:1432 5233 ;lar1:(umu)"

Sökning: L773:0940 5429 OR L773:1432 5233 > Umeå universitet

  • Resultat 1-8 av 8
Sortera/gruppera träfflistan
   
NumreringReferensOmslagsbildHitta
1.
  • Bennet, Louise, et al. (författare)
  • Family history of diabetes and its relationship with insulin secretion and insulin sensitivity in Iraqi immigrants and native Swedes : a population-based cohort study
  • 2018
  • Ingår i: Acta Diabetologica. - : Springer Milan. - 0940-5429 .- 1432-5233. ; 55:3, s. 233-242
  • Tidskriftsartikel (refereegranskat)abstract
    • Aims Middle Eastern immigrants to western countries are at high risk of developing type 2 diabetes. However, the heritability and impact of rst-degree family history (FH) of type 2 diabetes on insulin secretion and action have not been adequately described. Methods Citizens of Malmö, Sweden, aged 30–75 years born in Iraq or Sweden were invited to participate in this population- based study. Insulin secretion (corrected insulin response and oral disposition index) and action (insulin sensitivity index) were assessed by oral glucose tolerance tests.Results In total, 45.7% of Iraqis (616/1348) and 27.4% of native Swedes (201/733) had FH in parent(s), sibling(s) or single parent and sibling, i.e., FH+. Approximately 8% of Iraqis and 0.7% of Swedes had ≥ 3 sibling(s) and parent(s) with diabetes, i.e., FH++. Irrespective of family size, prediabetes and diabetes increased with family burden (FH− 29.4%; FH+ 38.8%; FH++ 61.7%) without signi cant di erences across ethnicities. With increasing level of family burden, insulin secretion rather than insulin action decreased. Individuals with a combination of ≥ 3 siblings and parents with diabetes presented with the lowest levels of insulin secretion.Conclusions The Iraqi immigrant population often present with a strong familial burden of type 2 diabetes with the worst glycemic control and highest diabetes risk in individuals with ≥ 3 siblings and parents with diabetes. Our data show that in a population still free from diabetes familial burden in uences insulin secretion to a higher degree than insulin action and may be a logical target for intervention. 
  •  
2.
  • Håglin, Lena, et al. (författare)
  • Prediction of all-cause mortality in a patient population with hypertension and type 2 DM by using traditional risk factors and serum-phosphate, -calcium and -magnesium.
  • 2007
  • Ingår i: Acta Biabetologica. - : Springer Science and Business Media LLC. - 0940-5429 .- 1432-5233. ; 44:3
  • Tidskriftsartikel (refereegranskat)abstract
    • The aim of this study is to investigate whether the prediction of all-cause mortality from traditional risk factors is improved by adding electrolytes (serum-phosphate (S-P), serum-calcium (S-Ca) and serum-magnesium (S-Mg)) in a Cox regression. The study uses an 18-year follow-up of patients (n=2504) referred by physicians in primary health care and hospitals to the Vindeln Patient Education (VPE) Center, mainly with a diagnosis of hypertension (HT), type 2 diabetes mellitus (DM) and/or obesity.Cox regression, with the latest registered value and baseline values for risk factors, was used to study all-cause mortality in men and women. 221 out of 1096 men and 157 out of 1408 women died during the 18-year follow-up (20% and 11% respectively). The Cox regression analysis reveals that high blood glucose (B-Glu) and low S-Mg were significantly associated with increased all-cause mortality in the whole patient population as well as in men and women separately. Among women, type 2 DM and systolic blood pressure (SBP) and among men, high S-Ca, S-P, S-urate and body mass index (BMI) were the main predictors of all-cause mortality. There is significantly improved prediction of all-cause mortality with electrolytes added to the traditional risk factors. High B-Glu and low S-Mg in both men and women, and high S-Ca and S-P in men, are significantly associated with all-cause mortality. The metabolic disturbance in this high-risk group of patients can be more fully understood if ionic imbalance is included in the prediction of mortatlity.
  •  
3.
  • Larsson-Nyrén, G, et al. (författare)
  • Anion-selective amplification of glucose-induced insulin secretion.
  • 2002
  • Ingår i: Acta Diabetologica. - 0940-5429 .- 1432-5233. ; 39:1, s. 41-7
  • Tidskriftsartikel (refereegranskat)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.
  •  
4.
  • Lindgren, Marie, et al. (författare)
  • Cumulative incidence of type 1 diabetes in two cohorts of children with different national gluten recommendations in infancy
  • 2023
  • Ingår i: Acta Diabetologica. - : Springer. - 0940-5429 .- 1432-5233.
  • Tidskriftsartikel (refereegranskat)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.
  •  
5.
  • Mancera-Romero, J., et al. (författare)
  • Fasting apolipoprotein B48 is a marker for peripheral arterial disease in type 2 diabetes
  • 2013
  • Ingår i: Acta Diabetologica. - : Springer Science and Business Media LLC. - 0940-5429 .- 1432-5233. ; 50:3, s. 383-389
  • Tidskriftsartikel (refereegranskat)abstract
    • An earlier study showed that fasting and postprandial concentrations of apolipoprotein B48 were raised in patients with type 2 diabetes (DM2) and peripheral arterial disease (PAD) as compared with persons without DM2 or persons with DM2 but not PAD. The aim of this study was to confirm the association of PAD and B48 in a larger group of patients with DM2 and the relation of B48 with the preheparin lipoprotein lipase (LPL) mass. We studied 456 patients with DM2. PAD was defined as an ankle-brachial index (ABI) < 0.9. Apolipoprotein B48 was quantified by ELISA. Apo B48 was significantly higher in the group with an ABI < 0.9 than the groups with ABI of 0.9-1.3 and > 1.3 (10.7 +/- A 6.28 vs. 9.24 +/- A 5.5 vs. 9.17 +/- A 8.8 mg/L, ANOVA test, p < 0.05). B48 was independently associated with an ABI < 0.9 (OR 1.053; 95 % CI, 1.013-1.094; p < 0.05), together with smoking and duration of diabetes. The preheparin LPL mass was similar in the patients with and without PAD. In conclusion, we confirmed that fasting B48 is an independent marker of PAD in patients with DM2, unrelated to the preheparin LPL mass, statin therapy or glucose lowering treatment.
  •  
6.
  • Persson-Sjögren, Solveig, et al. (författare)
  • Effects of leptin, acetylcholine and vasoactive intestinal polypeptide on insulin secretion in isolated ob/ob mouse pancreatic islets
  • 2004
  • Ingår i: Acta Diabetologica. - Berlin : Springer. - 0940-5429 .- 1432-5233. ; 41:3, s. 104-112
  • Tidskriftsartikel (refereegranskat)abstract
    • Obesity is often accompanied by hyperleptinemia, hyperinsulinemia, and an increased parasympathetic tone. Obese-hyperglycemic mice (Umeå ob/ob) have functional leptin receptors and a raised parasympathetic tone. We studied insulin release in islets isolated from 9-month-old severely obese ob/ob mice. Leptin (0.5-18 nM) did not affect insulin release together with 2.8-20 mM glucose. Leptin (18 microM) had no effect in the presence of low glucose (2.8-5.5 mM), but increased insulin secretion in islets challenged with 11.1 or 16.7 mM glucose. Leptin at 18 microM increased insulin secretion stimulated by the parasympathetic neurotransmitters acetylcholine (ACh; 10 microM) or vasoactive intestinal peptide (VIP; 10 nM), and by 5 mM theophylline or 2.5 microM forskolin. Overnight culture increased the effect of 18 microM leptin, but no effects were observed with 18 nM leptin. Pretreatment of islets with phorbol 12-myristate 13-acetate (PMA) did not suggest any involvement of protein kinase C. In summary, a high concentration of leptin stimulates insulin release in the presence of stimulatory concentrations of glucose alone and with parasympathetic neurotransmitters. Hyperleptinemia and increased parasympathetic stimulation may in part cause the hyperinsulinemia observed in obesity. This may aggravate insulin resistance and the abnormal metabolism in diabetes mellitus.
  •  
7.
  •  
8.
  • Tanamas, Stephanie K., et al. (författare)
  • The performance of diabetes risk prediction models in new populations : the role of ethnicity of the development cohort
  • 2015
  • Ingår i: Acta Diabetologica. - : Springer Science and Business Media LLC. - 0940-5429 .- 1432-5233. ; 52:1, s. 91-101
  • Tidskriftsartikel (refereegranskat)abstract
    • It is believed that diabetes risk scores need to be ethnic specific. However, this prerequisite has not been tested. We examined the performance of several risk models, developed in various populations, in a Europid and a South Asian population. The performance of 14 published risk prediction models were tested in two prospective studies: the Australian Diabetes, Obesity and Lifestyle (AusDiab) study and the Mauritius non-communicable diseases survey. Eight models were developed in Europid populations; the remainder in various non-Europid populations. Model performance was assessed using area under the receiver operating characteristic curves (discrimination), Hosmer-Lemeshow tests (goodness-of-fit) and Brier scores (accuracy). In both AusDiab and Mauritius, discrimination was highest for a model developed in a mixed population (non-Hispanic white and African American) and lowest for a model developed in a Europid population. Discrimination for all scores was higher in AusDiab than in Mauritius. For almost all models, goodness-of-fit was poor irrespective of the ethnicity of the development cohort, and accuracy was higher in AusDiab compared to Mauritius. Our results suggest that similarity of ethnicity or similarity of diabetes risk may not be the best way of identifying models that will perform well in another population. Differences in study methodology likely account for much of the difference in the performance. Thus, identifying models which use measurements that are clearly described and easily reproducible for both research and clinical settings may be more important.
  •  
Skapa referenser, mejla, bekava och länka
  • Resultat 1-8 av 8

Kungliga biblioteket hanterar dina personuppgifter i enlighet med EU:s dataskyddsförordning (2018), GDPR. Läs mer om hur det funkar här.
Så här hanterar KB dina uppgifter vid användning av denna tjänst.

 
pil uppåt Stäng

Kopiera och spara länken för att återkomma till aktuell vy