SwePub
Sök i SwePub databas

  Utökad sökning

Träfflista för sökning "WFRF:(Vaag Allan) "

Sökning: WFRF:(Vaag Allan)

  • Resultat 61-70 av 97
Sortera/gruppera träfflistan
   
NumreringReferensOmslagsbildHitta
61.
  • Lund, Soren S, et al. (författare)
  • Impact of metformin versus repaglinide on non-glycaemic cardiovascular risk markers related to inflammation and endothelial dysfunction in non-obese patients with type 2 diabetes
  • 2008
  • Ingår i: European Journal of Endocrinology. - 1479-683X. ; 158:5, s. 631-641
  • Tidskriftsartikel (refereegranskat)abstract
    • Objective: In patients with type 2 diabetes mellitus (T2DM), biomarkers reflecting inflammation and endothelial dysfunction have been linked to cardiovascular disease (CVD biomarkers) and metabolic regulation. In T2DM patients, metformin and insulin secretagogues have demonstrated equal anti-hyperglycaemic potency. Here, we report the effect of metformin versus an insulin secretagogue, repaglinide, on CVD biomarkers in non-obese T2DM patients. Design and methods: Single-centre, double-masked, double-dummy, crossover study during 2x4 months involving 96 non-obese (body mass index <= 27kg/m(2)) insulin-naive T2DM patients. At enrolment, previous oral hypoglycaemic agents were stopped and the patients entered a 1-month run- on diet-only treatment. Hereafter, patients were randomized to either 2 mg repaglinide thrice daily followed by 1 g metformin twice daily or vice versa each during 4 months with a 1-month washout between interventions. Results: Levels of tumour necrosis factor-alpha, plasminogen activator inhibitor-1 antigen, tissue-type plasminogen activator antigen, von Willebrand factor, soluble intercellular adhesion molecule-1 and soluble E-selectin were significantly lower during metformin versus repaglinide treatments. In contrast, Amadori albumin and heart rate were higher during metformin versus repaglinide. Levels of interleukin-6. fibrinogen, soluble vascular cell adhesion molecule-1, asymmetric dimethylarginine and advanced glycation end products as well as glycaemic levels (previously reported) and 24-h blood pressure were similar between treatments. Adjustment for known macrovascular disease did not affect the between-treatment: effects. Conclusions: In non-obese T2DM patients, metformin was more effective in reducing selected biomarkers reflecting inflammation and endothelial dysfunction compared with repaglinide despite similar glycaemic levels between treatments.
  •  
62.
  • Lund, Soren S, et al. (författare)
  • Impact of metformin versus the prandial insulin secretagogue, repaglinide, on fasting and postprandial glucose and lipid responses in non-obese patients with type 2 diabetes
  • 2008
  • Ingår i: European Journal of Endocrinology. - 1479-683X. ; 158:1, s. 35-46
  • Tidskriftsartikel (refereegranskat)abstract
    • Objective: Non-obese patients with type 2 diabetes (T2DM) are characterized by predominant defective insulin secretion. However, in non-obese T2DM patients, metformin, targeting insulin resistance. is non-inferior to the prandial insulin secretagogue, repaglinide, controlling overall glycaemia (HbA(1c)). Whether the same apply for postprandial glucose and lipid metabolism is unknown. Here. we compared the effect of metformin versus repaglinide on postprandial metabolism in non-obese T2DM patients. Design: Single-centre. double-masked, double-dummy. crossover study during 2 X 4 months involving 96 non-obese (body mass index:! 2 7 kg/m(2)) insulin-naive T2DM patients. At enrolment, patients stopped prior oral hypoglycaemic agents therapies and after a 1-month run-in period on diet-only treatment, patients were randomized to repaglinide (2 mg) thrice daily followed by metformin (1 g) twice daily or vice versa each during 4 months with 1-month washout between interventions. Methods: Postprandial metabolism was evaluated by a standard test meal (3 515 kJ: 54%, fat, 13% protein and 33%, carbohydrate) with blood sampling 0-6 h postprandially. Results: Fasting levels and total area under the curve (AUC) for plasma glucose, triglycerides and free fatty acids (FFA) changed equally between treatments. In contrast, fasting levels and AUC of total cholesterol. low-density lipoprotein (LDL) cholesterol, non-high-density lipoprotein (non-HDL) cholesterol and serum insulin were lower during metformin than repaglinide (mean (95% confidence intervals), LDL cholesterol difference metformin versus repaglinide: AUC: -0.17mmol/l (-0.26; -0.08)). AUC differences remained significant after adjusting for fasting levels. Conclusions: In non-obese T2DM patients, metformin reduced postprandial levels of glycaemia, triglycerides and FFA similarly compared to the prandial insulin secretagogue, repaglinide. Furthermore, metformin reduced fasting and postprandial chotesterolaemia and insulinaemia compared with repaglinide. These data support prescription of metformin as the preferred drug in non-obese patients with T2DM targeting fasting and postprandial glucose and lipid metabolism.
  •  
63.
  • Lund, Søren Søgaard, et al. (författare)
  • Insulin regimens in type 2 diabetes.
  • 2010
  • Ingår i: New England Journal of Medicine. - 0028-4793. ; 362:10, s. 959-960
  • Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)
  •  
64.
  • Lund, S. S., et al. (författare)
  • Sustained postprandial decrease in plasma levels of LDL cholesterol in patients with type-2 diabetes mellitus
  • 2008
  • Ingår i: Scandinavian Journal of Clinical & Laboratory Investigation. - : Informa UK Limited. - 1502-7686 .- 0036-5513. ; 68:7, s. 628-640
  • Tidskriftsartikel (refereegranskat)abstract
    • Objective . Low density lipoprotein cholesterol (LDL-C) is an independent and modifiable risk factor for development of cardiovascular disease (CVD). Postprandial lipid metabolism has been linked to CVD, but little is known about the postprandial LDL-C profile in patients with type-2 diabetes (T2DM). We aimed to study the postprandial levels of LDL-C in T2DM patients. Material and methods . After an overnight fast, 74 T2DM patients, mean age approximately 60 years, were served a standard fat-rich meal of 3,515 kJ containing 54 % fat, 13 % protein and 33 % carbohydrates. Only drinking water was allowed postprandially. Blood samples were drawn at times 0 (fasting), 1.5, 3.0, 4.5 and 6.0 h (postprandial). In all samples, LDL-C was measured with modified beta quantification (separation by ultracentrifugation followed by measurement of infranate high density lipoprotein cholesterol (HLD-C) using a homogeneous assay). Results . At all postprandial times, levels of LDL-C showed highly significant (p<0.005) decreases compared to time 0 (mean [95 % CI] maximum change in LDL-C levels at 3.0 h: -0.16 mmol/L [-0.12; -0.20]; p<0.001). Independently of fasting LDL-C levels and ongoing statin therapy, LDL-C decreased significantly more in female compared to male patients postprandially (mean [95 % CI] maximum unadjusted change versus time 0 in LDL-C for men [n=56] at 3.0 h: -0.14 mmol/L [-0.19; -0.10], p<0.001; for women [n=18] at 4.5 h: -0.26 mmol/L [-0.35; -0.18], p<0.001; -0.14 mmol/L [-0.24; -0.05], p=0.005 between genders for the mean [95 % CI] fasting adjusted difference at 4.5 h in the change versus time 0 in LDL-C; gender by time interaction: p=0.007 (repeated measures mixed model)). Conclusions . In T2DM patients served a fat-rich meal, levels of LDL-C decreased significantly more in women compared to men postprandially, irrespective of fasting levels or ongoing statin therapy. This might have implications in the atherosclerotic process and on any difference in the risk of CVD between genders.
  •  
65.
  • Lund, S. S., et al. (författare)
  • Targeting hyperglycaemia with either metformin or repaglinide in non-obese patients with type 2 diabetes: results from a randomized crossover trial
  • 2007
  • Ingår i: Diabetes, Obesity and Metabolism. - : Wiley. - 1462-8902 .- 1463-1326. ; 9:3, s. 394-407
  • Tidskriftsartikel (refereegranskat)abstract
    • Aim: Metformin is the 'drug-of-first-choice' in obese patients with type 2 diabetes mellitus (T2DM) due to its antihyperglycaemic and cardiovascular protective potentials. In non-obese patients with T2DM, insulin secretagogues are empirically used as first choice. In this investigator-initiated trial, we evaluated the effect of metformin vs. an insulin secretagogue, repaglinide on glycaemic regulation and markers of inflammation and insulin sensitivity in non-obese patients with T2DM. Methods: A single-centre, double-masked, double-dummy, crossover study during 2 x 4 months involved 96 non-obese (body mass index <= 27 kg/m(2)) insulin-naive patients with T2DM. At enrolment, previous oral hypoglycaemic agents (OHA) were stopped and patients entered a 1-month run-in on diet-only treatment. Hereafter, patients were randomized to either repaglinide 2 mg thrice daily followed by metformin 1 g twice daily or vice versa each during 4 months with 1-month washout between interventions. Results: End-of-treatment levels of haemoglobin A(1c) (HbA(1c)), fasting plasma glucose, mean of seven-point home-monitored plasma glucose and fasting levels of high-sensitivity C-reactive protein and adiponectin were not significantly different between treatments. However, body weight, waist circumference, fasting serum levels of insulin and C-peptide were lower and less number of patients experienced hypoglycaemia during treatment with metformin vs. repaglinide. Both drugs were well tolerated. Conclusions: In non-obese patients with T2DM, overall glycaemic regulation was equivalent with less hypoglycaemia during metformin vs. repaglinide treatment for 2 x 4 months. Metformin was more effective targeting non-glycaemic cardiovascular risk markers related to total and abdominal body fat stores as well as fasting insulinaemia. These findings may suggest the use of metformin as the preferred OHA also in non-obese patients with T2DM.
  •  
66.
  • Lyssenko, Valeriya, et al. (författare)
  • Genetics of diabetes-associated microvascular complications
  • 2023
  • Ingår i: Diabetologia. - 0012-186X. ; 66:9, s. 1601-1613
  • Forskningsöversikt (refereegranskat)abstract
    • Diabetes is associated with excess morbidity and mortality due to both micro- and macrovascular complications, as well as a range of non-classical comorbidities. Diabetes-associated microvascular complications are those considered most closely related to hyperglycaemia in a causal manner. However, some individuals with hyperglycaemia (even those with severe hyperglycaemia) do not develop microvascular diseases, which, together with evidence of co-occurrence of microvascular diseases in families, suggests a role for genetics. While genome-wide association studies (GWASs) produced firm evidence of multiple genetic variants underlying differential susceptibility to type 1 and type 2 diabetes, genetic determinants of microvascular complications are mostly suggestive. Identified susceptibility variants of diabetic kidney disease (DKD) in type 2 diabetes mirror variants underlying chronic kidney disease (CKD) in individuals without diabetes. As for retinopathy and neuropathy, reported risk variants currently lack large-scale replication. The reported associations between type 2 diabetes risk variants and microvascular complications may be explained by hyperglycaemia. More extensive phenotyping, along with adjustments for unmeasured confounding, including both early (fetal) and late-life (hyperglycaemia, hypertension, etc.) environmental factors, are urgently needed to understand the genetics of microvascular complications. Finally, genetic variants associated with reduced glycolysis, mitochondrial dysfunction and DNA damage and sustained cell regeneration may protect against microvascular complications, illustrating the utility of studies in individuals who have escaped these complications.
  •  
67.
  • Lyssenko, Valeriya, et al. (författare)
  • Pleiotropic Effects of GIP on Islet Function Involve Osteopontin
  • 2011
  • Ingår i: Diabetes. - : American Diabetes Association. - 1939-327X .- 0012-1797. ; 60:9, s. 2424-2433
  • Tidskriftsartikel (refereegranskat)abstract
    • OBJECTIVE-The incretin hormone GIP (glucose-dependent insulinotropic polypeptide) promotes pancreatic beta-cell function by potentiating insulin secretion and beta-cell proliferation. Recently, a combined analysis of several genome-wide association studies (Meta-analysis of Glucose and Insulin-Related Traits Consortium [MAGIC]) showed association to postprandial insulin at the GIP receptor (GIPR) locus. Here we explored mechanisms that could explain the protective effects of GIP on islet function. RESEARCH DESIGN AND METHODS-Associations of GIPR rs10423928 with metabolic and anthropometric phenotypes in both nondiabetic (N = 53,730) and type 2 diabetic individuals (N = 2,731) were explored by combining data from 11 studies.Insulin secretion was measured both in vivo in nondiabetic subjects and in vitro in islets from cadaver donors. Insulin secretion was also measured in response to exogenous GIP. The in vitro measurements included protein and gene expression as well as measurements of beta-cell viability and proliferation. RESULTS-The A allele of GIPR rs10423928 was associated with impaired glucose- and GIP-stimulated insulin secretion and a decrease in BMI, lean body mass, and waist circumference. The decrease in BMI almost completely neutralized the effect of impaired insulin secretion on risk of type 2 diabetes. Expression of GIPR mRNA was decreased in human islets from carriers of the A allele or patients with type 2 diabetes. GIP stimulated osteopontin (OPN) mRNA and protein expression. OPN expression was lower in carriers of the A allele. Both GIP and OPN prevented cytokine-induced reduction in cell viability (apoptosis). In addition, OPN stimulated cell proliferation in insulin-secreting cells. CONCLUSIONS-These findings support beta-cell proliferative and antiapoptotic roles for GIP in addition to its action as an incretin hormone. Identification of a link between GIP and OPN may shed new light on the role of GIP in preservation of functional beta-cell mass in humans. Diabetes 60:2424-2433, 2011
  •  
68.
  • Main, Ailsa Maria, et al. (författare)
  • DNA methylation and gene expression of HIF3A : cross-tissue validation and associations with BMI and insulin resistance
  • 2016
  • Ingår i: Clinical Epigenetics. - : Springer Science and Business Media LLC. - 1868-7075 .- 1868-7083. ; 8:1
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: Associations between BMI and DNA methylation of hypoxia-inducible factor 3-alpha (HIF3A) in both blood cells and subcutaneous adipose tissue (SAT) have been reported. In this study, we investigated associations between BMI and HIF3A DNA methylation in the blood and SAT from the same individuals, and whether HIF3A gene expression in SAT and skeletal muscle biopsies showed associations with BMI and insulin resistance. Furthermore, we aimed to investigate gender specificity and heritability of these traits. Methods: We studied 137 first-degree relatives of type 2 diabetes (T2D) patients from 48 families, from whom we had SAT and muscle biopsies. DNA methylation of four CpG sites in the HIF3A promoter was analyzed in the blood and SAT by pyrosequencing, and HIF3A gene expression was analyzed in SAT and muscle by qPCR. An index of whole-body insulin sensitivity was estimated from oral glucose tolerance tests. Results: BMI was associated with HIF3A methylation at one CpG site in the blood, and there was a positive association between the blood and SAT methylation levels at a different CpG site within the individuals. The SAT methylation level did not correlate with HIF3A gene expression. Interestingly, HIF3A expression in SAT, but not in muscle, associated negatively with BMI and whole-body insulin resistance. We found a significant effect of familiality on HIF3A methylation levels in the blood and HIF3A expression levels in skeletal muscle. Conclusions: Our findings are in line with the previously reported link between BMI and DNA methylation of HIF3A in the blood. The tissue-specific results of HIF3A gene expression indicate that SAT is the more functional tissue in which a low expression may adversely affect whole-body insulin sensitivity.
  •  
69.
  • Naukkarinen, Jussi, et al. (författare)
  • Functional Variant Disrupts Insulin Induction of USF1 Mechanism for USF1-Associated Dyslipidemias
  • 2009
  • Ingår i: Circulation: Cardiovascular Genetics. - 1942-325X. ; 2:5, s. 245-522
  • Tidskriftsartikel (refereegranskat)abstract
    • Background-The upstream transcription factor 1 (USF1) gene is associated with familial combined hyperlipidemia, the most common genetic dyslipidemia in humans, as well as with various dyslipidemic changes in numerous other studies. Typical of complex disease-associated genes, neither the explicit mutations have been described nor the functional consequences for risk allele carriers been reported at the cellular or tissue level. Methods and Results-In this study, we aimed at describing the molecular mechanism through which the strongest associating intronic single-nucleotide polymorphism variant in USF1 is involved in the development of dyslipidemia. The effects of the risk variant on gene expression were studied in 2 relevant human tissues, fat and muscle. Global transcript profiles of 47 fat biopsies ascertained for carriership of the risk allele were tested for differential expression of known USF1 target genes as well as for broader effects on the transcript profile. Allelic imbalance of USF1 in fat was assessed using a quantitative sequencing approach. The possible allele-specific effect of insulin on the expression of USF1 was studied in 118 muscle biopsies before and after a euglycemic hyperinsulinemic clamp. The risk allele of single-nucleotide polymorphism rs2073658 seems to eradicate the inductive effect of insulin on the expression of USF1 in muscle and fat. The expression of numerous target genes is in turn perturbed in adipose tissue. Conclusions-In risk allele carriers, a defective response of USF1 to insulin results in the suboptimal response of relevant target genes that contributes to the enhanced risk of developing dyslipidemia and coronary heart disease. (Circ Cardiovasc Genet. 2009;2:522-529.)
  •  
70.
  • Nilsson, Emma A, et al. (författare)
  • Altered DNA Methylation and Differential Expression of Genes Influencing Metabolism and Inflammation in Adipose Tissue From Subjects With Type 2 Diabetes
  • 2014
  • Ingår i: Diabetes. - : American Diabetes Association. - 0012-1797 .- 1939-327X. ; 63:9, s. 2962-2976
  • Tidskriftsartikel (refereegranskat)abstract
    • Genetics, epigenetics, and environment may together affect the susceptibility for type 2 diabetes (T2D). Our aim was to dissect molecular mechanisms underlying T2D using genome-wide expression and DNA methylation data in adipose tissue from monozygotic twin pairs discordant for T2D and independent case-control cohorts. In adipose tissue from diabetic twins, we found decreased expression of genes involved in oxidative phosphorylation; carbohydrate, amino acid, and lipid metabolism; and increased expression of genes involved in inflammation and glycan degradation. The most differentially expressed genes included ELOVL6, GYS2, FADS1, SPP1 (OPN), CCL18, and IL1RN. We replicated these results in adipose tissue from an independent case-control cohort. Several candidate genes for obesity and T2D (e.g., IRS1 and VEGFA) were differentially expressed in discordant twins. We found a heritable contribution to the genome-wide DNA methylation variability in twins. Differences in methylation between monozygotic twin pairs discordant for T2D were subsequently modest. However, 15,627 sites, representing 7,046 genes including PPARG, KCNQ1, TCF7L2, and IRS1, showed differential DNA methylation in adipose tissue from unrelated subjects with T2D compared with control subjects. A total of 1,410 of these sites also showed differential DNA methylation in the twins discordant for T2D. For the differentially methylated sites, the heritability estimate was 0.28. We also identified copy number variants (CNVs) in monozygotic twin pairs discordant for T2D. Taken together, subjects with T2D exhibit multiple transcriptional and epigenetic changes in adipose tissue relevant to the development of the disease.
  •  
Skapa referenser, mejla, bekava och länka
  • Resultat 61-70 av 97
Typ av publikation
tidskriftsartikel (94)
forskningsöversikt (2)
konferensbidrag (1)
Typ av innehåll
refereegranskat (95)
övrigt vetenskapligt/konstnärligt (2)
Författare/redaktör
Vaag, Allan (85)
Ling, Charlotte (38)
Groop, Leif (34)
Poulsen, Pernille (24)
Perfilyev, Alexander (19)
Brøns, Charlotte (19)
visa fler...
Hansen, Torben (17)
Pedersen, Oluf (14)
Gillberg, Linn (14)
Ribel-Madsen, Rasmus (14)
Nilsson, Emma (12)
Almgren, Peter (12)
Rönn, Tina (11)
Ahlqvist, Emma (10)
Volkov, Petr (10)
Vaag, Allan A (10)
Hjort, Line (10)
Lyssenko, Valeriya (9)
Hansson, Ola (8)
Garcia-Calzon, Sonia (7)
Eriksson, Karl-Fredr ... (6)
Broholm, Christa (6)
Jørgensen, Sine W. (6)
Storgaard, Heidi (6)
Tuomi, Tiinamaija (5)
Ridderstråle, Martin (5)
Franks, Paul W. (5)
Madsbad, Sten (5)
Laakso, Markku (5)
Grarup, Niels (5)
Olsson, Anders H (5)
Arora, Geeti (5)
Beck-Nielsen, Hennin ... (5)
Parving, Hans Henrik (5)
Nilsson, Peter (4)
Kotova, Olga (4)
Stancáková, Alena (4)
Kuusisto, Johanna (4)
Pihlajamäki, Jussi (4)
Prasad, Rashmi B. (4)
Orho-Melander, Marju (4)
Ribel-Madsen, R. (4)
Eliasson, Lena (4)
Gjesing, Anette Prio ... (4)
Tarnow, Lise (4)
Scheele, Camilla (4)
Mortensen, Brynjulf (4)
Hansen, Ninna Schiøl ... (4)
Nielsen, Jens Steen (4)
Grunnet, Louise G. (4)
visa färre...
Lärosäte
Lunds universitet (92)
Göteborgs universitet (5)
Uppsala universitet (5)
Karolinska Institutet (5)
Mittuniversitetet (2)
Umeå universitet (1)
visa fler...
Kungliga Tekniska Högskolan (1)
Luleå tekniska universitet (1)
visa färre...
Språk
Engelska (97)
Forskningsämne (UKÄ/SCB)
Medicin och hälsovetenskap (94)
Naturvetenskap (1)

År

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