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Träfflista för sökning "AMNE:(MEDICAL AND HEALTH SCIENCES) ;pers:(Groop Leif)"

Sökning: AMNE:(MEDICAL AND HEALTH SCIENCES) > Groop Leif

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1.
  • Arvidsson, Daniel, et al. (författare)
  • Vigorous Physical Activity may be Important for the Insulin Sensitivity in Immigrants From the Middle East and Native Swedes
  • 2015
  • Ingår i: Journal of Physical Activity & Health. - : Human Kinetics. - 1543-3080 .- 1543-5474. ; 12:2, s. 273-281
  • Tidskriftsartikel (refereegranskat)abstract
    • Purpose: To compare physical activity measures and their associations with insulin sensitivity, beta-cell function and body mass index (BMI) between Iraqi immigrants and native Swedes. Methods: A cross-sectional study of 493 Iraqis (58% men) and 469 Swedes (54% men) aged 30 to 75 years living in the city of Malmo, Sweden. Accelerometry was used for physical activity measures (sedentary time, breaks in sedentary time, moderate and vigorous physical activity, total counts). Insulin sensitivity index and oral disposal index were determined from an oral glucose tolerance test and BMI by body weight and height. Results: Iraqi men were less physically active than Swedish men, while the physical activity was more similar in the women. BMI was a strong predictor of insulin sensitivity and beta-cell function and frequently associated with the physical activity measures. BMI modified the associations of insulin sensitivity and beta-cell function with the physical activity measures to such extent that only VPA and total counts show direct associations with insulin sensitivity in addition to the indirect associations via BMI. Iraqi women demonstrated weaker associations compared with Swedish women. Conclusions: Physical activity and performed at vigorous intensity may be important mainly for the insulin sensitivity in Iraqi immigrants and native Swedes.
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2.
  • Quell, Jan D., et al. (författare)
  • Automated pathway and reaction prediction facilitates in silico identification of unknown metabolites in human cohort studies
  • 2017
  • Ingår i: Journal of Chromatography B: Analytical Technologies in the Biomedical and Life Sciences. - : Elsevier BV. - 1570-0232 .- 1873-376X. ; 1071, s. 58-67
  • Tidskriftsartikel (refereegranskat)abstract
    • Identification of metabolites in non-targeted metabolomics continues to be a bottleneck in metabolomics studies in large human cohorts. Unidentified metabolites frequently emerge in the results of association studies linking metabolite levels to, for example, clinical phenotypes. For further analyses these unknown metabolites must be identified. Current approaches utilize chemical information, such as spectral details and fragmentation characteristics to determine components of unknown metabolites. Here, we propose a systems biology model exploiting the internal correlation structure of metabolite levels in combination with existing biochemical and genetic information to characterize properties of unknown molecules.Levels of 758 metabolites (439 known, 319 unknown) in human blood samples of 2279 subjects were measured using a non-targeted metabolomics platform (LC-MS and GC-MS). We reconstructed the structure of biochemical pathways that are imprinted in these metabolomics data by building an empirical network model based on 1040 significant partial correlations between metabolites. We further added associations of these metabolites to 134 genes from genome-wide association studies as well as reactions and functional relations to genes from the public database Recon 2 to the network model. From the local neighborhood in the network, we were able to predict the pathway annotation of 180 unknown metabolites. Furthermore, we classified 100 pairs of known and unknown and 45 pairs of unknown metabolites to 21 types of reactions based on their mass differences. As a proof of concept, we then looked further into the special case of predicted dehydrogenation reactions leading us to the selection of 39 candidate molecules for 5 unknown metabolites. Finally, we could verify 2 of those candidates by applying LC-MS analyses of commercially available candidate substances. The formerly unknown metabolites X-13891 and X-13069 were shown to be 2-dodecendioic acid and 9-tetradecenoic acid, respectively.Our data-driven approach based on measured metabolite levels and genetic associations as well as information from public resources can be used alone or together with methods utilizing spectral patterns as a complementary, automated and powerful method to characterize unknown metabolites.
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3.
  • Middeldorp, Christel M., et al. (författare)
  • The Early Growth Genetics (EGG) and EArly Genetics and Lifecourse Epidemiology (EAGLE) consortia : design, results and future prospects
  • 2019
  • Ingår i: European Journal of Epidemiology. - : Springer Science and Business Media LLC. - 0393-2990 .- 1573-7284. ; 34:3, s. 279-300
  • Tidskriftsartikel (refereegranskat)abstract
    • The impact of many unfavorable childhood traits or diseases, such as low birth weight and mental disorders, is not limited to childhood and adolescence, as they are also associated with poor outcomes in adulthood, such as cardiovascular disease. Insight into the genetic etiology of childhood and adolescent traits and disorders may therefore provide new perspectives, not only on how to improve wellbeing during childhood, but also how to prevent later adverse outcomes. To achieve the sample sizes required for genetic research, the Early Growth Genetics (EGG) and EArly Genetics and Lifecourse Epidemiology (EAGLE) consortia were established. The majority of the participating cohorts are longitudinal population-based samples, but other cohorts with data on early childhood phenotypes are also involved. Cohorts often have a broad focus and collect(ed) data on various somatic and psychiatric traits as well as environmental factors. Genetic variants have been successfully identified for multiple traits, for example, birth weight, atopic dermatitis, childhood BMI, allergic sensitization, and pubertal growth. Furthermore, the results have shown that genetic factors also partly underlie the association with adult traits. As sample sizes are still increasing, it is expected that future analyses will identify additional variants. This, in combination with the development of innovative statistical methods, will provide detailed insight on the mechanisms underlying the transition from childhood to adult disorders. Both consortia welcome new collaborations. Policies and contact details are available from the corresponding authors of this manuscript and/or the consortium websites.
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4.
  • Ekman, Carl, et al. (författare)
  • Less pronounced response to exercise in healthy relatives to type 2 diabetic subjects compared with controls
  • 2015
  • Ingår i: Journal of applied physiology. - : American Physiological Society. - 8750-7587 .- 1522-1601. ; 119:9, s. 953-960
  • Tidskriftsartikel (refereegranskat)abstract
    • Healthy first-degree relatives with heredity of type 2 diabetes (FH+) are known to have metabolic inflexibility compared with subjects without heredity for diabetes (FH-). In this study, we aimed to test the hypothesis that FH+ individuals have an impaired response to exercise compared with FH-. Sixteen FH+ and 19 FH- insulin-sensitive men similar in age, peak oxygen consumption ((V) over dot(O2 peak)), and body mass index completed an exercise intervention with heart rate monitored during exercise for 7 mo. Before and after the exercise intervention, the participants underwent a physical examination and tests for glucose tolerance and exercise capacity, and muscle biopsies were taken for expression analysis. The participants attended, on average, 39 training sessions during the intervention and spent 18.8 MJ on exercise. (V) over dot(O2 peak)/kg increased by 14%, and the participants lost 1.2 kg of weight and 3 cm waist circumference. Given that the FH- group expended 61% more energy during the intervention, we used regression analysis to analyze the response in the FH+ and FH- groups separately. Exercise volume had a significant effect on (V) over dot(O2 peak), weight, and waist circumference in the FH- group, but not in the FH+ group. After exercise, expression of genes involved in metabolism, oxidative phosphorylation, and cellular respiration increased more in the FH- compared with the FH+ group. This suggests that healthy, insulin-sensitive FH+ and FH- participants with similar age, (V) over dot(O2 peak), and body mass index may respond differently to an exercise intervention. The FH+ background might limit muscle adaptation to exercise, which may contribute to the increased susceptibility to type 2 diabetes in FH+ individuals.
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5.
  • Andersen, Caroline, et al. (författare)
  • Worse glycaemic control in LADA patients than in those with type 2 diabetes, despite a longer time on insulin therapy
  • 2013
  • Ingår i: Diabetologia. - : Springer Science and Business Media LLC. - 0012-186X .- 1432-0428. ; 56:2, s. 252-258
  • Tidskriftsartikel (refereegranskat)abstract
    • Our aim was to study whether glycaemic control differs between individuals with latent autoimmune diabetes in adults (LADA) and patients with type 2 diabetes, and whether it is influenced by time on insulin therapy. We performed a retrospective study of 372 patients with LADA (205 men and 167 women; median age 54 years, range 35-80 years) from Swedish cohorts from SkAyenne (n = 272) and Vasterbotten (n = 100). Age- and sex-matched patients with type 2 diabetes were included as controls. Data on the use of oral hypoglycaemic agents (OHAs), insulin and insulin-OHA combination therapy was retrieved from the medical records. Poor glycaemic control was defined as HbA(1c) a parts per thousand yen7.0% (a parts per thousand yen53 mmol/mol) at follow-up. The individuals with LADA and with type 2 diabetes were followed for an average of 107 months. LADA patients were leaner than type 2 diabetes patients at diagnosis (BMI 27.7 vs 31.0 kg/m(2); p < 0.001) and follow-up (BMI 27.9 vs 30.2 kg/m(2); p < 0.001). Patients with LADA had been treated with insulin for longer than those with type 2 diabetes (53.3 vs 28.8 months; p < 0.001). There was no significant difference between the patient groups with regard to poor glycaemic control at diagnosis, but more patients with LADA (67.8%) than type 2 diabetes patients (53.0%; p < 0.001) had poor glycaemic control at follow-up. Patients with LADA had worse glycaemic control at follow-up compared with participants with type 2 diabetes (OR = 1.8, 95% CI 1.2, 2.7), adjusted for age at diagnosis, HbA(1c), BMI at diagnosis, follow-up time and duration of insulin treatment. Individuals with LADA have worse glycaemic control than patients with type 2 diabetes despite a longer time on insulin therapy.
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6.
  • Scott, Robert A., et al. (författare)
  • An Expanded Genome-Wide Association Study of Type 2 Diabetes in Europeans
  • 2017
  • Ingår i: Diabetes. - : American Diabetes Association. - 0012-1797 .- 1939-327X. ; 66:11, s. 2888-2902
  • Tidskriftsartikel (refereegranskat)abstract
    • To characterize type 2 diabetes (T2D)-associated variation across the allele frequency spectrum, we conducted a meta-analysis of genome-wide association data from 26,676 T2D case and 132,532 control subjects of European ancestry after imputation using the 1000 Genomes multiethnic reference panel. Promising association signals were followed up in additional data sets (of 14,545 or 7,397 T2D case and 38,994 or 71,604 control subjects). We identified 13 novel T2D-associated loci (P < 5 x 10(-8)), including variants near the GLP2R, GIP, and HLA-DQA1 genes. Our analysis brought the total number of independent T2D associations to 128 distinct signals at 113 loci. Despite substantially increased sample size and more complete coverage of low-frequency variation, all novel associations were driven by common single nucleotide variants. Credible sets of potentially causal variants were generally larger than those based on imputation with earlier reference panels, consistent with resolution of causal signals to common risk haplotypes. Stratification of T2D-associated loci based on T2D-related quantitative trait associations revealed tissue-specific enrichment of regulatory annotations in pancreatic islet enhancers for loci influencing insulin secretion and in adipocytes, monocytes, and hepatocytes for insulin action-associated loci. These findings highlight the predominant role played by common variants of modest effect and the diversity of biological mechanisms influencing T2D pathophysiology.
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7.
  • Strausz, Satu, et al. (författare)
  • Genetic analysis of obstructive sleep apnoea discovers a strong association with cardiometabolic health
  • 2021
  • Ingår i: European Respiratory Journal. - : European Respiratory Society (ERS). - 0903-1936 .- 1399-3003. ; 57:5, s. 1-17
  • Tidskriftsartikel (refereegranskat)abstract
    • There is currently limited understanding of the genetic aetiology of obstructive sleep apnoea (OSA). We aimed to identify genetic loci associated with OSA risk, and to test if OSA and its comorbidities share a common genetic background. We conducted the first large-scale genome-wide association study of OSA using the FinnGen study (217 955 individuals) with 16 761 OSA patients identified using nationwide health registries. We estimated 0.08 (95% CI 0.06.0.11) heritability and identified five loci associated with OSA (p<5.0×10-8): rs4837016 near GAPVD1 (GTPase activating protein and VPS9 domains 1), rs10928560 near CXCR4 (C-X-C motif chemokine receptor type 4), rs185932673 near CAMK1D (calcium/calmodulindependent protein kinase ID) and rs9937053 near FTO (fat mass and obesity-associated protein; a variant previously associated with body mass index (BMI)). In a BMI-adjusted analysis, an association was observed for rs10507084 near RMST/NEDD1 (rhabdomyosarcoma 2 associated transcript/NEDD1 γ-tubulin ring complex targeting factor). We found high genetic correlations between OSA and BMI (rg=0.72 (95% CI 0.62-0.83)), and with comorbidities including hypertension, type 2 diabetes, coronary heart disease, stroke, depression, hypothyroidism, asthma and inflammatory rheumatic disease (rg>0.30). The polygenic risk score for BMI showed 1.98-fold increased OSA risk between the highest and the lowest quintile, and Mendelian randomisation supported a causal relationship between BMI and OSA. Our findings support the causal link between obesity and OSA, and the joint genetic basis between OSA and comorbidities.
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8.
  • Tornberg, Åsa, et al. (författare)
  • Relation between cycling exercise capacity, fiber-type composition, and lower extremity muscle strength and muscle endurance.
  • 2011
  • Ingår i: Journal of Strength and Conditioning Research. - 1533-4287. ; 25:1, s. 16-22
  • Tidskriftsartikel (refereegranskat)abstract
    • Segerström, ÅB, Holmbäck, AM, Hansson, O, Elgzyri, T, Eriksson, K-F, Ringsberg, K, Groop, L, Wollmer, P, and Thorsson, O. Relation between cycling exercise capacity, fiber-type composition, and lower extremity muscle strength and muscle endurance. J Strength Cond Res 25(1): 16-22, 2011-The aim of the study was to determine the relation between peak oxygen uptake (&OV0312;o2peak), peak work rate (WRpeak), fiber-type composition, and lower extremity strength and endurance during a maximal incremental cycle test. Thirty-nine healthy sedentary men, aged 30-46, participated in the study. Subjects performed a maximal incremental cycle test and isokinetic knee extension (KE) and flexion (KF) strength and endurance tests at velocities of 60 and 180°·s. Muscle biopsies were taken from m. vastus lateralis and analyzed for fiber-type composition. A significant correlation existed between KE strength and &OV0312;o2peak and WRpeak. Also, KF endurance correlated significantly to &OV0312;o2peak and WRpeak. The KE endurance correlated significantly to WRpeak (rp = 0.32, p < 0.05) and almost significantly to &OV0312;o2peak (rp = 0.28, p = 0.06). Stepwise multiple regression analyses showed that KE strength, KF endurance, and the percentage of type I fibers could explain up to 40% of the variation in &OV0312;o2peak and WRpeak. The performance of sedentary subjects in a maximal incremental cycle test is highly affected by knee muscle strength and endurance. Fiber-type composition also contributes but to a smaller extent.
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9.
  • Tornberg, Åsa, et al. (författare)
  • Upper Body Muscle Strength and Endurance in Relation to Peak Exercise Capacity During Cycling in Healthy Sedentary Male Subjects.
  • 2011
  • Ingår i: Journal of Strength and Conditioning Research. - 1533-4287. ; 25, s. 1413-1417
  • Tidskriftsartikel (refereegranskat)abstract
    • Segerström, AB, Holmbäck, AM, Elzyri, T, Eriksson, KF, Ringsberg, K, Groop, L, Thorsson, O, and Wollmer, P. Upper body muscle strength and endurance in relation to peak exercise capacity during cycling in healthy sedentary male subjects. J Strength Cond Res 24(x): 000-000, 2010-The aim of this study was to investigate the relation between upper body muscle strength and endurance, and exercise capacity during an incremental cycle exercise test in sedentary healthy male subjects before and after 6 months of combined supervised group training. Exercise capacity was measured as maximal oxygen consumption (&OV0312;O2peak) and maximum work rate (WRpeak). Muscle strength and endurance of the upper body were assessed by bench press and isometric measurement of trunk extensor and flexor maximum voluntary contraction (MVC) and trunk extensor and flexor endurance. Thirty-one subjects were studied before and after the training period. Bench press and trunk extensor MVC correlated to exercise capacity at baseline and after training. Training improved &OV0312;O2peak and WRpeak. The correlation between trunk extensor MVC and exercise capacity improved after training. Upper body strength may affect exercise capacity by increasing the rider's ability to generate force on the handlebar that can be transmitted to the pedals. Resistance training of the arms, chest, and trunk may help improve cycling performance.
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10.
  • Ahlqvist, Emma, et al. (författare)
  • Genetics of type 2 diabetes
  • 2011
  • Ingår i: Clinical Chemistry. - : Oxford University Press (OUP). - 0009-9147 .- 1530-8561. ; 57:2, s. 241-254
  • Forskningsöversikt (refereegranskat)abstract
    • Background: Type 2 diabetes (T2D) is a complex disorder that is affected by multiple genetic and environmental factors. Extensive efforts have been made to identify the disease-affecting genes to better understand the disease pathogenesis, find new targets for clinical therapy, and allow prediction of disease.Content: Our knowledge about the genes involved in disease pathogenesis has increased substantially in recent years, thanks to genomewide association studies and international collaborations joining efforts to collect the huge numbers of individuals needed to study complex diseases on a population level. We have summarized what we have learned so far about the genes that affect T2D risk and their functions. Although more than 40 loci associated with T2D or glycemic traits have been reported and reproduced, only a minor part of the genetic component of the disease has been explained, and the causative variants and affected genes are unknown for many of the loci.Summary: Great advances have recently occurred in our understanding of the genetics of T2D, but much remains to be learned about the disease etiology. The genetics of T2D has so far been driven by technology, and we now hope that next-generation sequencing will provide important information on rare variants with stronger effects. Even when variants are known, however, great effort will be required to discover how they affect disease risk.
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