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Sökning: L773:1262 3636 OR L773:1878 1780

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1.
  • Nilsson, Peter, et al. (författare)
  • Smoking is associated with increased HbA1c values and microalbuminuria in patients with diabetes--data from the National Diabetes Register in Sweden
  • 2004
  • Ingår i: Diabetes Metab. - 1262-3636 .- 1878-1780. ; 30:3, s. 261-8
  • Tidskriftsartikel (refereegranskat)abstract
    • OBJECTIVES: The aim was to examine trends in the proportion of smoking in diabetes patients, and to study associations between smoking, glycaemic control, and microalbuminuria. METHODS: Smoking habits were reported to the Swedish National Diabetes Register (NDR), with data from hospitals and primary health care. Patient characteristics included were age, gender, type of treatment, diabetes duration, HbA1c, BMI, blood pressure, antihypertensive and lipid-lowering drugs, and microalbuminuria. RESULTS: The proportion of smokers in type 1 diabetes was 12-15% during 1996-2001, it was high in females<30 years (12-16%), and was higher in the age group 30-59 years (13-17%) than in older (6-9%) patients. The corresponding proportion of smoking in type 2 diabetes was 10-12%, higher in those less than 60 years of age (17-22%) than in older (7-9%) patients. Smoking type 1 and type 2 patients in 2001 had higher mean HbA1c but lower mean BMI values than non-smokers. Smokers also had higher frequencies of microalbuminuria, in both type 1 (18 vs 14%) and type 2 (20% vs 13%) diabetes. Multiple logistic regression analyses disclosed that smoking was independently associated with elevated HbA1c levels (p<0.001) and microalbuminuria (p<0.001), but negatively with BMI (p<0.001), in both type 1 and type 2 diabetes. CONCLUSIONS: Smoking in patients with diabetes was widespread, especially in young female type 1, and in middle-aged type 1 and type 2 diabetes patients, and should be the target for smoking cessation campaigns. Smoking was associated with both poor glycaemic control and microalbuminuria, independently of other study characteristics.
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2.
  • Ahrén, Bo (författare)
  • Incretin dysfunction in type 2 diabetes: Clinical impact and future perspectives.
  • 2013
  • Ingår i: Diabetes & Metabolism. - : Elsevier BV. - 1878-1780 .- 1262-3636. ; 39:3, s. 195-201
  • Forskningsöversikt (refereegranskat)abstract
    • The incretin effect refers to the augmentation of insulin secretion after oral administration of glucose compared with intravenous glucose administration at matched glucose levels. The incretin effect is largely due to the release and action on beta-cells of the gut hormones glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1). This system has in recent years had considerable interest due to the success of incretin therapy as a glucose-lowering strategy in type 2 diabetes. In non-diabetic subjects, the incretin effect is responsible for 50-70% of insulin release during oral glucose administration. In type 2 diabetes patients, the incretin effect is impaired and contributes to only 20-35% of the insulin response to oral glucose. The reason for the defective incretin effect in type 2 diabetes has been the subject of many studies. Although the reports in the literature are mixed, most studies of GIP and GLP-1 secretory responses to oral glucose or a mixed meal have shown fairly normal results in type 2 diabetes. In contrast, the insulinotropic effects of both GIP and GLP-1 are impaired in type 2 diabetes with greater suppression of insulin secretion augmentation with GIP than with GLP-1. The suggested causes of these defects are a defective beta-cell receptor expression or post-receptor defects secondary to the diabetes milieu, defective beta-cell function in general resulting in defective incretin effect and genetic factors initiating incretin hormone resistance. Identifying the mechanisms in greater detail would be important for understanding the strengths, weaknesses and efficacy of incretin therapy in individual patients to more specifically target this glucose-lowering therapy.
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3.
  • Avall, K, et al. (författare)
  • The yin and yang of apolipoprotein CIII
  • 2018
  • Ingår i: Diabetes & metabolism. - : Elsevier BV. - 1878-1780 .- 1262-3636. ; 44:3, s. 303-304
  • Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)
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4.
  • Bennet, Louise, et al. (författare)
  • A family history of diabetes determines poorer glycaemic control and younger age of diabetes onset in immigrants from the Middle East compared with native Swedes
  • 2015
  • Ingår i: Diabetes & Metabolism. - : Elsevier BV. - 1262-3636 .- 1878-1780. ; 41:1, s. 45-54
  • Tidskriftsartikel (refereegranskat)abstract
    • Aims. - Immigrant populations from the Middle East develop diabetes earlier than indigenous European populations; however, the underlying etiology is poorly understood. This study looked at the risk factors associated with early diabetes onset and, in non-diabetics, glycaemic control in immigrants from Iraq compared with native Swedes. Methods. - This cross-sectional population-based study comprised 1398 Iraqi immigrants and 757 Swedes (ages 30-75 years) residing in the same area of Malmo, Sweden. Outcomes were age at diabetes onset and glycaemic control (HbA(1c)) as assessed by Cox proportional hazards and linear regression, respectively. Results. - In Iraqis vs Swedes, clustering in the family history (in two or more relatives) was more prevalent (23.2% vs 3.6%, P<0.001) and diabetes onset occurred earlier (47.6 years vs 53.4 years, P=0.001). Having an Iraqi background independently raised the hazard ratio (HR) for diabetes onset. Diabetes risk due to family history was augmented by obesity, with the highest HRs observed in obese participants with clustering in the family history (HR: 5.1, 95% CI: 3.2-8.2) after adjusting for country of birth and gender. In participants without previously diagnosed diabetes (Iraqis: n=1270; Swedes: n=728), HbA(1c), levels were slightly higher in Iraqis than in Swedes (4.5% vs 4.4%, P=0.038). This difference was explained primarily by clustering in the family history rather than age, obesity, lifestyle or socioeconomic status. Conclusion. - The study shows that the greater predisposition to diabetes in Middle Eastern immigrants may be explained by a more extensive family history of the disorder; clinical interventions tailored to Middle Eastern immigrants with such a family history are thus warranted.
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5.
  • Bodegard, J, et al. (författare)
  • Changes in body mass index following newly diagnosed type 2 diabetes and risk of cardiovascular mortality: A cohort study of 8486 primary-care patients
  • 2013
  • Ingår i: Diabetes & Metabolism. - : MASSON EDITEUR, 21 STREET CAMILLE DESMOULINS, ISSY, 92789 MOULINEAUX CEDEX 9, FRANCE. - 1262-3636 .- 1878-1780. ; 39:4, s. 306-313
  • Tidskriftsartikel (refereegranskat)abstract
    • Aims. - Elevated body mass index (BMI) is associated with an increased risk of type 2 diabetes and cardiovascular disease (CVD). This study explored the association between BMI changes in the first 18 months of newly diagnosed type 2 diabetes and the risk of long-term CVD mortality. less thanbrgreater than less thanbrgreater thanMethods. - A total of 8486 patients with newly diagnosed type 2 diabetes and no previous history of CVD or cancer were identified from 84 primary-care centres in Sweden. During the first year after diagnosis, patients were grouped according to BMI change: Increase, or andgt;= +1 BMI unit; unchanged, or between +1 and-1 BMI unit; and decrease, or andlt;=-1 BMI unit. Associations between BMI change and CVD mortality, defined as death from stroke, myocardial infarction or sudden death, were estimated using adjusted Cox proportional hazards models (NCT 01121315). less thanbrgreater than less thanbrgreater thanResults. - Baseline mean age was 60.0 years and mean BMI was 30.2 kg/m(2). Patients were followed for up to 9 years (median: 4.6 years). During the first 18 months, 53.4% had no change in their BMI, while 32.2% decreased and 14.4% increased. Compared with patients with unchanged BMI, those with an increased BMI had higher risks of CVD mortality (hazard ratio: 1.63, 95% CI: 1.11-2.39) and all-cause mortality (1.33, 1.01-1.76). BMI decreases had no association with these risks compared with unchanged BMI: 1.06 (0.76-1.48) and 1.06 (0.85-1.33), respectively. less thanbrgreater than less thanbrgreater thanConclusion. - Increased BMI within the first 18 months of type 2 diabetes diagnosis was associated with an increased long-term risk of CVD mortality. However, BMI decrease did not lower the long-term risk of mortality.
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6.
  • Carlsson, A C, et al. (författare)
  • Poor self-rated health is not associated with a high total allostatic load in type 2 diabetic patients--but high blood pressure is
  • 2011
  • Ingår i: Diabetes & Metabolism. - : Elsevier BV. - 1262-3636 .- 1878-1780. ; 37:5, s. 446-51
  • Tidskriftsartikel (refereegranskat)abstract
    • OBJECTIVE: Allostatic load has been linked to self-rated health (SRH), cardiovascular disease and mortality in non-diabetic individuals. The aim of this study was to construct an allostatic load score and to find any correlations with SRH. METHODS: The subjects included in the study came from a randomized, controlled trial of type 2 diabetes. Blood samples were drawn, urine was collected for 24h, and questionnaires, including SRH, were filled out on three occasions: at baseline; after the 10-week intervention; and at a follow-up 3 months after the intervention. Allostatic load was estimated using a wide range of variables, including systolic and diastolic blood pressure, pulse pressure, cortisol, catecholamines, HbA(1c), insulin, plasma glucose and waist circumference. RESULTS: There was no association between SRH and allostatic load. However, three other components were significantly correlated with allostatic load at the baseline investigation and the two follow-up investigations - namely, systolic blood pressure, diastolic blood pressure and HbA(1c). CONCLUSION: The absence of an association between allostatic load and SRH in diabetic individuals contrasts with previous findings in non-diabetic women, and shows that it is hazardous to apply findings in one population to another, especially diabetic and non-diabetic populations.
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7.
  • Carlsson, Axel C., et al. (författare)
  • The association between endostatin and kidney disease and mortality in patients with type 2 diabetes
  • 2016
  • Ingår i: Diabetes & Metabolism. - : Elsevier BV. - 1262-3636 .- 1878-1780. ; 42:5, s. 351-357
  • Tidskriftsartikel (refereegranskat)abstract
    • Aim. - Circulating endostatin, a biologically active derivate of collagen XVIII, is considered to be a marker of kidney disease and a risk factor for its related mortality. However, less is known of the role of endostatin in diabetes and the development of diabetic nephropathy. For this reason, our study investigated the associations between circulating endostatin and the prevalence and progression of kidney disease, and its mortality risk in patients with type 2 diabetes (T2D). Methods. - This was a cohort study of 607 patients with T2D (mean age: 61 years, 44% women). Estimated glomerular filtration rate (eGFR), calculated using the Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) creatinine equation, was used to assess the patients' kidney function decline and mortality. Results. - Of the total study cohort, 20 patients declined by >= 20% in eGFR over 4 years, and 44 died during the follow-up (mean duration: 6.7 years). At baseline, participants with diabetic nephropathy (defined as eGFR < 60 mL/min/1.73 m(2)) and/or microalbuminuria [defined as a urinary albumin-to-creatinine ratio (ACR) > 3 g/mol] had higher median levels of endostatin than those without nephropathy (62.7 mu g/L vs 57.4 mu g/L, respectively; P = 0.031). In longitudinal analyses adjusted for age, gender, baseline eGFR and ACR, higher endostatin levels were associated with a higher risk of decline (>= 20% in eGFR, OR per 1 SD increase: 1.73, 95% CI: 1.13-2.65) and a higher risk of mortality (HR per 1 SD increase: 1.57, 95% CI: 1.19-2.07). Conclusion. - In patients with T2D, circulating endostatin levels can predict the progression of kidney disease and mortality independently of established kidney disease markers. The clinical usefulness of endostatin as a risk marker in such patients merits further studies.
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8.
  • Dahlén, Elsa M, et al. (författare)
  • Abdominal Obesity and low grade Systemic Inflammation as Markers for Subclinical Organ Damage in type 2 diabetes
  • 2014
  • Ingår i: Diabetes & Metabolism. - : Elsevier. - 1262-3636 .- 1878-1780. ; 40:1, s. 76-81
  • Tidskriftsartikel (refereegranskat)abstract
    • The aim of this study was to explore associations between abdominal obesity, inflammatory markers, and subclinical organ damage in 740 patients with type 2 diabetes. Waist circumference (WC) and sagittal abdominal diameter (SAD) was measured. Blood samples were analyzed for; C-reactive protein (CRP), interleukin (IL) -1β and IL-6. Carotid intimamedia thickness (IMT) was evaluated by ultrasonography. Aortic pulse wave velocity (PWV) was measured with applanation tonometry.Abdominal obesity were significantly correlated with; IL-6, CRP (both p= <0.001, WC and SAD, respectively), IMT (WC p=0.012, SAD p=0.003) and PWV (p<0.001, for WC and SAD, respectively). In multiple linear regressions with IMT as dependent variable and age, sex, statins, systolic blood pressure (SBP), Body Mass Index (BMI), CRP and HbA1c, as independent variables, SAD (p=0.047) but not WC, remained associated with IMT. In stepwise linear regression, entering both SAD and WC, the association between SAD and PWV was stronger than the association between WC and PWV.We conclude that SAD and WC are feasible measures of obesity that provides information on inflammation, atherosclerosis and arterial stiffness in type 2 diabetes. However, SAD was slightly more robustly associated to subclinical organ damage, compared with WC.
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9.
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10.
  • Eliasson, Björn, 1959, et al. (författare)
  • Antihyperglycaemic treatment of type 2 diabetes : results from a national diabetes register
  • 2007
  • Ingår i: Diabetes & Metabolism. - : Elsevier BV. - 1262-3636 .- 1878-1780. ; 33:4, s. 269-276
  • Tidskriftsartikel (refereegranskat)abstract
    • Aim To describe clinical characteristics and antihyperglycaemic treatment patterns in patients with varying duration of diabetes. Methods We performed a cross-sectional survey of 61 890 type 2 diabetic (DM2) patients from the Swedish National Diabetes Register (NDR) in 2004. We also analysed the effect of types of treatment and risk factors on glycaemic control in a longitudinal cohort study from 1996 to 2004. HbA1c, risk factors and treatments were determined locally in primary care as well as hospital outpatient clinics. Results Insulin was frequently used in DM2 patients with long duration of diabetes, although the mean HbA1c increased and only a few in this group reached HbA1c < 7.0%. Patients showing long-term improvement in HbA1c (> 1%) from 1996 to 2004 were more often treated with insulin than with oral hypoglycaemic agents (OHA). During this period, the HbA1c levels leading to additional treatment decreased. A low BMI, decreasing BMI and not smoking were predictors of good long-term metabolic control. Hypertension and hyperlipidaemia were frequent in both newly diagnosed DM2 patients and in patients with a long duration of diabetes. Conclusions Insulin treatment was frequently used, particularly in patients with a long duration of DM2. The glycaemic control, which usually deteriorates over time, did not reach the recommended goal, despite the fact that complementary treatment was added at lower HbA1c levels in 2003 than in 1996. High frequencies of hypertension, hyperlipidaemia and high 10-year risks of coronary heart disease necessitate intensified risk factor control in the future.
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