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151. The effect of FOXA2 rs1209523 on glucose-related phenotypes and risk of type 2 diabetes in Danish individuals

Author

Banasik Karina, Hollensted Mette, Andersson Ehm, Sparsø Thomas, Sandbæk Annelli, Lauritzen Torsten, Jørgensen Torben, Witte Daniel R, Pedersen Oluf, and Hansen Torben

Subjects
Internal medicine, RC31-1245, Genetics, QH426-470
Abstract

Abstract Background Variations within the FOXA family have been studied for a putative contribution to the risk of type 2 diabetes (T2D), and recently the minor T-allele of FOXA2 rs1209523 was reported to associate with decreased fasting plasma glucose levels in a study using a weighted false discovery rate control procedure to enhance the statistical power of genome wide association studies in detecting associations between low-frequency variants and a given trait. Thus, the primary aim of this study was to investigate whether the minor T-allele of rs1205923 in FOXA2 associated with 1) decreased fasting plasma glucose and 2) a lower risk of developing T2D. Secondly, we investigated whether rs1205923 in FOXA2 associated with other glucose-related phenotypes. Methods The variant was genotyped in Danish individuals from four different study populations using KASPar® PCR SNP genotyping system. We examined for associations of the FOXA2 genotype with fasting plasma glucose and estimates of insulin release and insulin sensitivity following an oral glucose tolerance test in 6,162 Danish individuals from the population-based Inter99 study while association with T2D risk was assessed in 10,196 Danish individuals including four different study populations. Results The FOXA2 rs1209523 was not associated with fasting plasma glucose (effect size (β) = -0.03 mmol/l (95%CI: -0.07; 0.01), p = 0.2) in glucose-tolerant individuals from the general Danish population. Furthermore, when employing a case-control setting the variant showed no association with T2D (odds ratio (OR) = 0.82 (95%CI: 0.62-1.07), p = 0.1) among Danish individuals. However, when we performed the analysis in a subset of 6,022 non-obese individuals (BMI < 30 kg/m2) an association with T2D was observed (OR = 0.68 (95%CI: 0.49-0.94), p = 0.02). Also, several indices of insulin release and β-cell function were associated with the minor T-allele of FOXA2 rs1209523 in non-obese individuals. Conclusions We failed to replicate association of the minor T-allele of FOXA2 rs1209523 with fasting plasma glucose in a population based sample of glucose tolerant individuals. More extensive studies are needed in order to fully elucidate the potential role of FOXA2 in glucose homeostasis.

Published
2012
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152. Correction to:Soluble CD163, adiponectin, C-reactive protein and progression of dysglycaemia in individuals at high risk of type 2 diabetes mellitus: the ADDITION-PRO cohort (Diabetologia, 10.1007/s00125-016-4075-4)

Author

Deichgræber, Pia, Witte, Daniel R., Møller, Holger J., Skriver, Mette V., Richelsen, Bjørn, Jørgensen, Marit E., Johansen, Nanna B., and Sandbæk, Annelli

Abstract

The authors have discovered a coding error in the statistical analysis syntax file used for the mixed-effect model analyses in this paper. The error has led to differences (first decimal) in the estimates for the main results. Although the conclusions stand unaltered the actual change over time for many parameters is smaller than previously reported and the direction of change reversed for fasting insulin, HOMA-IR and HOMA-β.

Published
2018

154. Prospective Association Among Diabetes Diagnosis, HbA1c, Glycemia, and Frailty Trajectories in an Elderly Population

Author

Aguayo, Gloria A., primary, Hulman, Adam, additional, Vaillant, Michel T., additional, Donneau, Anne-Françoise, additional, Schritz, Anna, additional, Stranges, Saverio, additional, Malisoux, Laurent, additional, Huiart, Laetitia, additional, Guillaume, Michèle, additional, Sabia, Séverine, additional, and Witte, Daniel R., additional

Published
2019
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158. The minor C-allele of rs2014355 in ACADS is associated with reduced insulin release following an oral glucose load

Author

Pisinger Charlotta, Lauritzen Torsten, Sandbæk Annelli, Andersson Åsa, Sandholt Camilla H, Krarup Nikolaj T, Justesen Johanne M, Banasik Karina, Hornbak Malene, Witte Daniel R, Sørensen Thorkild IA, Pedersen Oluf, and Hansen Torben

Subjects
Internal medicine, RC31-1245, Genetics, QH426-470
Abstract

Abstract Background A genome-wide association study (GWAS) using metabolite concentrations as proxies for enzymatic activity, suggested that two variants: rs2014355 in the gene encoding short-chain acyl-coenzyme A dehydrogenase (ACADS) and rs11161510 in the gene encoding medium-chain acyl-coenzyme A dehydrogenase (ACADM) impair fatty acid β-oxidation. Chronic exposure to fatty acids due to an impaired β-oxidation may down-regulate the glucose-stimulated insulin release and result in an increased risk of type 2 diabetes (T2D). We aimed to investigate whether the two variants associate with altered insulin release following an oral glucose load or with T2D. Methods The variants were genotyped using KASPar® PCR SNP genotyping system and investigated for associations with estimates of insulin release and insulin sensitivity following an oral glucose tolerance test (OGTT) in a random sample of middle-aged Danish individuals (nACADS = 4,324; nACADM = 4,337). The T2D-case-control study involved a total of ~8,300 Danish individuals (nACADS = 8,313; nACADM = 8,344). Results In glucose-tolerant individuals the minor C-allele of rs2014355 of ACADS associated with reduced measures of serum insulin at 30 min following an oral glucose load (per allele effect (β) = -3.8% (-6.3%;-1.3%), P = 0.003), reduced incremental area under the insulin curve (β = -3.6% (-6.3%;-0.9%), P = 0.009), reduced acute insulin response (β = -2.2% (-4.2%;0.2%), P = 0.03), and with increased insulin sensitivity ISIMatsuda (β = 2.9% (0.5%;5.2%), P = 0.02). The C-allele did not associate with two other measures of insulin sensitivity or with a derived disposition index. The C-allele was not associated with T2D in the case-control analysis (OR 1.07, 95% CI 0.96-1.18, P = 0.21). rs11161510 of ACADM did not associate with any indices of glucose-stimulated insulin release or with T2D. Conclusions In glucose-tolerant individuals the minor C-allele of rs2014355 of ACADS was associated with reduced measures of glucose-stimulated insulin release during an OGTT, a finding which in part may be mediated through an impaired β-oxidation of fatty acids.

Published
2011
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159. Response to Comment on Andersen et al. Risk-Factor Trajectories Preceding Diabetic Polyneuropathy: ADDITION-Denmark. Diabetes Care 2018;41:1955–1962

Author

Andersen, Signe T., primary, Witte, Daniel R., additional, Andersen, Henning, additional, Bjerg, Lasse, additional, Bruun, Niels Henrik, additional, Jørgensen, Marit E., additional, Finnerup, Nanna B., additional, Lauritzen, Torsten, additional, Jensen, Troels S., additional, Tankisi, Hatice, additional, and Charles, Morten, additional

Published
2018
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161. Association of weight loss and weight loss maintenance following diabetes diagnosis by screening and incidence of cardiovascular disease and all‐cause mortality: An observational analysis of the ADDITION‐Europe trial.

Author

Strelitz, Jean, Sharp, Stephen J., Khunti, Kamlesh, Vos, Rimke C., Rutten, Guy E. H. M., Webb, David R., Witte, Daniel R., Sandbæk, Annelli, Wareham, Nicholas J., and Griffin, Simon J.

Subjects
WEIGHT loss, CARDIOVASCULAR disease related mortality, DIAGNOSIS of diabetes, WEIGHT gain, BODY mass index, DISEASE incidence, HEART disease related mortality
Abstract

Aims: Short‐term weight loss may lead to remission of type 2 diabetes but the effect of maintained weight loss on cardiovascular disease (CVD) is unknown. We quantified the associations between changes in weight 5 years following a diagnosis of diabetes, and incident CVD events and mortality up to 10 years after diagnosis. Materials and methods: Observational analysis of the ADDITION‐Europe trial of 2730 adults with screen‐detected type 2 diabetes from the UK, Denmark and the Netherlands. We defined weight change based on the maintenance at 5 years of weight loss achieved during the year after diabetes diagnosis, and as 5‐year overall change in weight. Incident CVD events (n = 229) and all‐cause mortality (n = 225) from 5 to 10 years follow‐up were ascertained from medical records. Results: Gaining >2% weight during the year after diabetes diagnosis was associated with higher hazard of all‐cause mortality versus maintaining weight [hazard ratio (95% confidence interval): 3.18 (1.30‐7.82)]. Losing ≥5% weight 1 year after diagnosis was also associated with mortality, whether or not weight loss was maintained at 5 years: 2.47 (0.99‐6.21) and 2.72 (1.17‐6.30), respectively. Losing ≥10% weight over 5 years was associated with mortality among those with body mass index <30 kg/m2 [4.62 (1.87‐11.42)]. Associations with CVD incidence were inconclusive. Conclusions: Both weight loss and weight gain after screen‐detected diabetes diagnosis were associated with higher mortality, but not CVD events, particularly among participants without obesity. The clinical implications of weight loss following a diagnosis of diabetes probably depend on its magnitude and timing, and may differ by body mass index status. Personalization of weight loss advice and support may be warranted. [ABSTRACT FROM AUTHOR]

Published
2021
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162. Patterns of obesity development before the diagnosis of type 2 diabetes: the whitehall ii cohort study

Author

Vistisen, Dorte, Witte, Daniel R., Tabak, Adam G., Herder, Christian, Brunner, Eric J., Kivimaki, Mika, and Faerch, Kristine

Subjects
Obesity -- Development and progression -- Research -- Diagnosis -- Analysis -- Complications and side effects -- Care and treatment, Type 2 diabetes -- Development and progression -- Research -- Diagnosis -- Analysis -- Causes of -- Complications and side effects -- Care and treatment, Biological sciences
Abstract

Background: Patients with type 2 diabetes vary greatly with respect to degree of obesity at time of diagnosis. To address the heterogeneity of type 2 diabetes, we characterised patterns of change in body mass index (BMI) and other cardiometabolic risk factors before type 2 diabetes diagnosis. Methods and Findings: We studied 6,705 participants from the Whitehall II study, an observational prospective cohort study of civil servants based in London. White men and women, initially free of diabetes, were followed with 5-yearly clinical examinations from 1991-2009 for a median of 14.1 years (interquartile range [IQR]: 8.7-16.2 years). Type 2 diabetes developed in 645 (1,209 person-examinations) and 6,060 remained free of diabetes during follow-up (14,060 person-examinations). Latent class trajectory analysis of incident diabetes cases was used to identify patterns of pre- disease BMI. Associated trajectories of cardiometabolic risk factors were studied using adjusted mixed-effects models. Three patterns of BMI changes were identified. Most participants belonged to the 'stable overweight' group (n = 604, 94%) with a relatively constant BMI level within the overweight category throughout follow-up. They experienced slightly worsening of beta cell function and insulin sensitivity from 5 years prior to diagnosis. A small group of 'progressive weight gainers' (n = 15) exhibited a pattern of consistent weight gain before diagnosis. Linear increases in blood pressure and an exponential increase in insulin resistance a few years before diagnosis accompanied the weight gain. The 'persistently obese' (n = 26) were severely obese throughout the whole 18 years before diabetes diagnosis. They experienced an initial beta cell compensation followed by loss of beta cell function, whereas insulin sensitivity was relatively stable. Since the generalizability of these findings is limited, the results need confirmation in other study populations. Conclusions: Three patterns of obesity changes prior to diabetes diagnosis were accompanied by distinct trajectories of insulin resistance and other cardiometabolic risk factors in a white, British population. While these results should be verified independently, the great majority of patients had modest weight gain prior to diagnosis. These results suggest that strategies focusing on small weight reductions for the entire population may be more beneficial than predominantly focusing on weight loss for high-risk individuals., Introduction Obesity is a well-established risk factor for type 2 diabetes; however, it is well-known that patients with type 2 diabetes vary greatly with respect to degree of adiposity at [...]

Published
2014
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163. Effect of secular trends on age-related trajectories of cardiovascular risk factors: the Whitehall II longitudinal study 1985–2009

Author

Hulmán, Adam, Tabák, Adam G, Nyári, Tibor A, Vistisen, Dorte, Kivimäki, Mika, Brunner, Eric J, and Witte, Daniel R

Subjects
Adult, Aged, 80 and over, Male, Aging, quantile regression, Smoking, blood pressure, cholesterol, Middle Aged, Lipids, Anthropometric Measures as Markers and Risk Factors, Body Mass Index, secular trend, Sex Factors, Socioeconomic Factors, ageing, Cardiovascular Diseases, Risk Factors, Body Composition, Humans, Female, Obesity, Longitudinal Studies, Aged
Abstract

Background: Secular trends in cardiovascular risk factors have been described, but few studies have examined simultaneously the effects of both ageing and secular trends within the same cohort. Methods: Development of cardiovascular risk factors over the past three decades was analysed using serial measurements from 10 308 participants aged from 35 to 80 years over 25 years of follow-up from five clinical examination phases of the Whitehall II study. Changes of body mass index, waist circumference, blood pressure and total and high-density lipoprotein cholesterol distribution characteristics were analysed with quantile regression models in the 57–61 age group. Age-related trajectories of risk factors were assessed by fitting mixed-effects models with adjustment for year of birth to reveal secular trends. Results: Average body mass index and waist circumference increased faster with age in women than in men, but the unfavourable secular trend was more marked in men. Distributions showed a fattening of the right tail in each consecutive phase, meaning a stronger increase in higher percentiles. Despite the higher obesity levels in younger birth cohorts, total cholesterol decreased markedly in the 57–61 age group along the entire distribution rather than in higher extremes only. Conclusion: The past three decades brought strong and heterogeneous changes in cardiovascular risk factor distributions. Secular trends appear to modify age-related trajectories of cardiovascular risk factors, which may be a source of bias in longitudinal analyses.

Published
2014

164. Prospective Association Among Diabetes Diagnosis, HbA1c, Glycemia, and Frailty Trajectories in an Elderly Population.

Author

Aguayo, Gloria A., Hulman, Adam, Vaillant, Michel T., Donneau, Anne-Françoise, Schritz, Anna, Stranges, Saverio, Malisoux, Laurent, Huiart, Laetitia, Guillaume, Michèle, Sabia, Séverine, and Witte, Daniel R.

Abstract

Objective: Frailty is a dynamic state of vulnerability in the elderly. We examined whether individuals with overt diabetes or higher levels of HbA1c or fasting plasma glucose (FG) experience different frailty trajectories with aging.Research Design and Methods: Diabetes, HbA1c, and FG were assessed at baseline, and frailty status was evaluated with a 36-item frailty index every 2 years during a 10-year follow-up among participants from the English Longitudinal Study of Ageing (ELSA). Mixed-effects models with age as time scale were used to assess whether age trajectories of frailty differed as a function of diabetes, HbA1c, and FG.Results: Among 5,377 participants (median age [interquartile range] 70 [65, 77] years, 45% men), 35% were frail at baseline. In a model adjusted for sex, participants with baseline diabetes had an increased frailty index over aging compared with those without diabetes. Similar findings were observed with higher levels of HbA1c, while FG was not associated with frailty. In a model additionally adjusted for income, social class, smoking, alcohol, and hemoglobin, only diabetes was associated with an increased frailty index. Among nonfrail participants at baseline, both diabetes and HbA1c level were associated with a higher increased frailty index over time.Conclusions: People with diabetes or higher HbA1c levels at baseline had a higher frailty level throughout later life. Nonfrail participants with diabetes or higher HbA1c also experienced more rapid deterioration of frailty level with aging. This observation could reflect a role of diabetes complications in frailty trajectories or earlier shared determinants that contribute to diabetes and frailty risk in later life. [ABSTRACT FROM AUTHOR]

Published
2019
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166. Human pancreatic islet 3D chromatin architecture provides insights into the genetics of type 2 diabetes

Author

Miguel-Escalada, Irene, primary, Bonàs-Guarch, Silvia, additional, Cebola, Inês, additional, Joan, Ponsa-Cobas, additional, Mendieta-Esteban, Julen, additional, Rolando, Delphine M.Y., additional, Javierre, Biola M., additional, Atla, Goutham, additional, Farabella, Irene, additional, Morgan, Claire C., additional, García-Hurtado, Javier, additional, Beucher, Anthony, additional, Morán, Ignasi, additional, Pasquali, Lorenzo, additional, Ramos, Mireia, additional, Appel, Emil V.R., additional, Linneberg, Allan, additional, Gjesing, Anette P., additional, Witte, Daniel R., additional, Pedersen, Oluf, additional, Grarup, Niels, additional, Ravassard, Philippe, additional, Torrents, David, additional, Mercader, Josep Maria, additional, Piemonti, Lorenzo, additional, Berney, Thierry, additional, Koning de, Eelco J.P., additional, Kerr-Conte, Julie, additional, Pattou, François, additional, Fedko, Iryna O., additional, Prokopenko, Inga, additional, Hansen, Torben, additional, Marti-Renom, Marc A., additional, Fraser, Peter, additional, and Ferrer, Jorge, additional

Published
2018
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168. Risk-Factor Trajectories Preceding Diabetic Polyneuropathy: ADDITION-Denmark

Author

Andersen, Signe T., primary, Witte, Daniel R., additional, Andersen, Henning, additional, Bjerg, Lasse, additional, Bruun, Niels Henrik, additional, Jørgensen, Marit E., additional, Finnerup, Nanna B., additional, Lauritzen, Torsten, additional, Jensen, Troels S., additional, Tankisi, Hatice, additional, and Charles, Morten, additional

Published
2018
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169. Pathophysiological Characteristics Underlying Different Glucose Response Curves: A Latent Class Trajectory Analysis From the Prospective EGIR-RISC Study

Author

Hulman, Adam, primary, Witte, Daniel R., additional, Vistisen, Dorte, additional, Balkau, Beverley, additional, Dekker, Jacqueline M., additional, Herder, Christian, additional, Hatunic, Mensud, additional, Konrad, Thomas, additional, Færch, Kristine, additional, and Manco, Melania, additional

Published
2018
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170. Publisher Correction: Re-analysis of public genetic data reveals a rare X-chromosomal variant associated with type 2 diabetes

Author

Bonàs-Guarch, Sílvia, primary, Guindo-Martínez, Marta, additional, Miguel-Escalada, Irene, additional, Grarup, Niels, additional, Sebastian, David, additional, Rodriguez-Fos, Elias, additional, Sánchez, Friman, additional, Planas-Fèlix, Mercè, additional, Cortes-Sánchez, Paula, additional, González, Santi, additional, Timshel, Pascal, additional, Pers, Tune H., additional, Morgan, Claire C., additional, Moran, Ignasi, additional, Atla, Goutham, additional, González, Juan R., additional, Puiggros, Montserrat, additional, Martí, Jonathan, additional, Andersson, Ehm A., additional, Díaz, Carlos, additional, Badia, Rosa M., additional, Udler, Miriam, additional, Leong, Aaron, additional, Kaur, Varindepal, additional, Flannick, Jason, additional, Jørgensen, Torben, additional, Linneberg, Allan, additional, Jørgensen, Marit E., additional, Witte, Daniel R., additional, Christensen, Cramer, additional, Brandslund, Ivan, additional, Appel, Emil V., additional, Scott, Robert A., additional, Luan, Jian’an, additional, Langenberg, Claudia, additional, Wareham, Nicholas J., additional, Pedersen, Oluf, additional, Zorzano, Antonio, additional, Florez, Jose C, additional, Hansen, Torben, additional, Ferrer, Jorge, additional, Mercader, Josep Maria, additional, and Torrents, David, additional

Published
2018
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171. Risk Factors for Incident Diabetic Polyneuropathy in a Cohort With Screen-Detected Type 2 Diabetes Followed for 13 Years: ADDITION-Denmark

Author

Andersen, Signe T., primary, Witte, Daniel R., additional, Dalsgaard, Else-Marie, additional, Andersen, Henning, additional, Nawroth, Peter, additional, Fleming, Thomas, additional, Jensen, Troels M., additional, Finnerup, Nanna B., additional, Jensen, Troels S., additional, Lauritzen, Torsten, additional, Feldman, Eva L., additional, Callaghan, Brian C., additional, and Charles, Morten, additional

Published
2018
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173. Re-analysis of public genetic data reveals a rare X-chromosomal variant associated with type 2 diabetes

Author

Bonàs-Guarch, Sílvia, primary, Guindo-Martínez, Marta, additional, Miguel-Escalada, Irene, additional, Grarup, Niels, additional, Sebastian, David, additional, Rodriguez-Fos, Elias, additional, Sánchez, Friman, additional, Planas-Fèlix, Mercè, additional, Cortes-Sánchez, Paula, additional, González, Santi, additional, Timshel, Pascal, additional, Pers, Tune H., additional, Morgan, Claire C., additional, Moran, Ignasi, additional, Atla, Goutham, additional, González, Juan R., additional, Puiggros, Montserrat, additional, Martí, Jonathan, additional, Andersson, Ehm A., additional, Díaz, Carlos, additional, Badia, Rosa M., additional, Udler, Miriam, additional, Leong, Aaron, additional, Kaur, Varindepal, additional, Flannick, Jason, additional, Jørgensen, Torben, additional, Linneberg, Allan, additional, Jørgensen, Marit E., additional, Witte, Daniel R., additional, Christensen, Cramer, additional, Brandslund, Ivan, additional, Appel, Emil V., additional, Scott, Robert A., additional, Luan, Jian’an, additional, Langenberg, Claudia, additional, Wareham, Nicholas J., additional, Pedersen, Oluf, additional, Zorzano, Antonio, additional, Florez, Jose C, additional, Hansen, Torben, additional, Ferrer, Jorge, additional, Mercader, Josep Maria, additional, and Torrents, David, additional

Published
2018
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174. Prevalence of micro- and macrovascular diabetes complications at time of type 2 diabetes diagnosis and associated clinical characteristics: A cross-sectional baseline study of 6958 patients in the Danish DD2 cohort

Author

Gedebjerg, Anne, primary, Almdal, Thomas Peter, additional, Berencsi, Klara, additional, Rungby, Jørgen, additional, Nielsen, Jens Steen, additional, Witte, Daniel R., additional, Friborg, Søren, additional, Brandslund, Ivan, additional, Vaag, Allan, additional, Beck-Nielsen, Henning, additional, Sørensen, Henrik Toft, additional, and Thomsen, Reimar Wernich, additional

Published
2018
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177. is involved in the development of nonalcoholic fatty liver disease

Author

Vazquez-Chantada, Mercedes, Gonzalez-Lahera, Aintzane, Martinez-Arranz, Ibon, Garcia-Monzon, Carmelo, Regueiro, Manuela M., Garcia-Rodriguez, Juan L., Schlangen, Karin A., Mendibil, Iñaki, Rodriguez-Ezpeleta, Naiara, Lozano, Juan J., Banasik, Karina, Justesen, Johanne M., Joergensen, Torben, Witte, Daniel R., Lauritzen, Torsten, Hansen, Torben, Pedersen, Oluf, Veyrie, Nicolas, Clement, Karine, Tordjman, Joan, Tran, Albert, Le Marchand-Brustel, Yannik, Buque, Xabier, Aspichueta, Patricia, Echevarria-Uraga, Jose J., Martin-Duce, Antonio, Caballeria, Joan, Gual, Philippe, Castro, Azucena, Mato, Jose M., Martinez-Chantar, Maria L., and Aransay, Ana M.

Published
2013
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178. Discovery of rare variants associated with blood pressure regulation through meta-analysis of 1.3 million individuals

Author

Surendran, Praveen, Feofanova, Elena V., Lahrouchi, Najim, Ntalla, Ioanna, Karthikeyan, Savita, Cook, James, Chen, Lingyan, Mifsud, Borbala, Yao, Chen, Kraja, Aldi T., Cartwright, James H., Hellwege, Jacklyn N., Giri, Ayush, Tragante, Vinicius, Thorleifsson, Gudmar, Liu, Dajiang J., Prins, Bram P., Stewart, Isobel D., Cabrera, Claudia P., Eales, James M., Akbarov, Artur, Auer, Paul L., Bielak, Lawrence F., Bis, Joshua C., Braithwaite, Vickie S., Brody, Jennifer A., Daw, E. Warwick, Warren, Helen R., Drenos, Fotios, Nielsen, Sune Fallgaard, Faul, Jessica D., Fauman, Eric B., Fava, Cristiano, Ferreira, Teresa, Foley, Christopher N., Franceschini, Nora, Gao, He, Giannakopoulou, Olga, Giulianini, Franco, Gudbjartsson, Daniel F., Guo, Xiuqing, Harris, Sarah E., Havulinna, Aki S., Helgadottir, Anna, Huffman, Jennifer E., Hwang, Shih-Jen, Kanoni, Stavroula, Kontto, Jukka, Larson, Martin G., Li-Gao, Ruifang, Lindström, Jaana, Lotta, Luca A., Lu, Yingchang, Luan, Jian’an, Mahajan, Anubha, Malerba, Giovanni, Masca, Nicholas G. D., Mei, Hao, Menni, Cristina, Mook-Kanamori, Dennis O., Mosen-Ansorena, David, Müller-Nurasyid, Martina, Paré, Guillaume, Paul, Dirk S., Perola, Markus, Poveda, Alaitz, Rauramaa, Rainer, Richard, Melissa, Richardson, Tom G., Sepúlveda, Nuno, Sim, Xueling, Smith, Albert V., Smith, Jennifer A., Staley, James R., Stanáková, Alena, Sulem, Patrick, Thériault, Sébastien, Thorsteinsdottir, Unnur, Trompet, Stella, Varga, Tibor V., Velez Edwards, Digna R., Veronesi, Giovanni, Weiss, Stefan, Willems, Sara M., Yao, Jie, Young, Robin, Yu, Bing, Zhang, Weihua, Zhao, Jing-Hua, Zhao, Wei, Zhao, Wei, Evangelou, Evangelos, Aeschbacher, Stefanie, Asllanaj, Eralda, Blankenberg, Stefan, Bonnycastle, Lori L., Bork-Jensen, Jette, Brandslund, Ivan, Braund, Peter S., Burgess, Stephen, Cho, Kelly, Christensen, Cramer, Connell, John, Mutsert, Renée de, Dominiczak, Anna F., Dörr, Marcus, Eiriksdottir, Gudny, Farmaki, Aliki-Eleni, Gaziano, J. Michael, Grarup, Niels, Grove, Megan L., Hallmans, Göran, Hansen, Torben, Have, Christian T., Heiss, Gerardo, Jørgensen, Marit E., Jousilahti, Pekka, Kajantie, Eero, Kamat, Mihir, Käräjämäki, AnneMari, Karpe, Fredrik, Koistinen, Heikki A., Kovesdy, Csaba P., Kuulasmaa, Kari, Laatikainen, Tiina, Lannfelt, Lars, Lee, I-Te, Lee, Wen-Jane, Linneberg, Allan, Martin, Lisa W., Moitry, Marie, Nadkarni, Girish, Neville, Matt J., Palmer, Colin N. A., Papanicolaou, George J., Pedersen, Oluf, Peters, James, Poulter, Neil, Rasheed, Asif, Rasmussen, Katrine L., Rayner, N. William, Mägi, Reedik, Renström, Frida, Rettig, Rainer, Rossouw, Jacques, Schreiner, Pamela J., Sever, Peter S., Sigurdsson, Emil L., Skaaby, Tea, Sun, Yan V., Sundstrom, Johan, Thorgeirsson, Gudmundur, Esko, Tõnu, Trabetti, Elisabetta, Tsao, Philip S., Tuomi, Tiinamaija, Turner, Stephen T., Tzoulaki, Ioanna, Vaartjes, Ilonca, Vergnaud, Anne-Claire, Willer, Cristen J., Wilson, Peter W. F., Witte, Daniel R., Yonova-Doing, Ekaterina, Zhang, He, Aliya, Naheed, Almgren, Peter, Amouyel, Philippe, Asselbergs, Folkert W., Barnes, Michael R., Blakemore, Alexandra I., Boehnke, Michael, Bots, Michiel L., Bottinger, Erwin P., Buring, Julie E., Chambers, John C., Chen, Yii-Der Ida, Chowdhury, Rajiv, Conen, David, Correa, Adolfo, Davey Smith, George, Boer, Rudolf A. de, Deary, Ian J., Dedoussis, George, Deloukas, Panos, Di Angelantonio, Emanuele, Elliott, Paul, Felix, Stephan B., Ferrières, Jean, Ford, Ian, Fornage, Myriam, Franks, Paul W., Franks, Stephen, Frossard, Philippe, Gambaro, Giovanni, Gaunt, Tom R., Groop, Leif, Gudnason, Vilmundur, Harris, Tamara B., Hayward, Caroline, Hennig, Branwen J., Herzig, Karl-Heinz, Ingelsson, Erik, Tuomilehto, Jaakko, Järvelin, Marjo-Riitta, Jukema, J. Wouter, Kardia, Sharon L. R., Kee, Frank, Kooner, Jaspal S., Kooperberg, Charles, Launer, Lenore J., Lind, Lars, Loos, Ruth J. F., Majumder, Abdulla al Shafi., Laakso, Markku, McCarthy, Mark I., Melander, Olle, Mohlke, Karen L., Murray, Alison D., Nordestgaard, Børge Grønne, Orho-Melander, Marju, Packard, Chris J., Padmanabhan, Sandosh, Palmas, Walter, Polasek, Ozren, Porteous, David J., Prentice, Andrew M., Province, Michael A., Relton, Caroline L., Rice, Kenneth, Ridker, Paul M., Rolandsson, Olov, Rosendaal, Frits R., Rotter, Jerome I., Rudan, Igor, Salomaa, Veikko, Samani, Nilesh J., Sattar, Naveed, Sheu, Wayne H.-H., Smith, Blair H., Soranzo, Nicole, Spector, Timothy D., Starr, John M., Sebert, Sylvain, Taylor, Kent D., Lakka, Timo A., Timpson, Nicholas J., Tobin, Martin D., van der Harst, Pim, van der Meer, Peter, Ramachandran, Vasan S., Verweij, Niek, Virtamo, Jarmo, Völker, Uwe, Weir, David R., Zeggini, Eleftheria, Charchar, Fadi J., Wareham, Nicholas J., Langenberg, Claudia, Tomaszewski, Maciej, Butterworth, Adam S., Caulfield, Mark J., Danesh, John, Edwards, Todd L., Holm, Hilma, Hung, Adriana M., Lindgren, Cecilia M., Liu, Chunyu, Manning, Alisa K., Morris, Andrew P., Morrison, Alanna C., O’Donnell, Christopher J., Psaty, Bruce M., Saleheen, Danish, Stefansson, Kari, Boerwinkle, Eric, Chasman, Daniel I., Levy, Daniel, Newton-Cheh, Christopher, Munroe, Patricia B., and Howson, Joanna M. M.

Abstract

Genetic studies of blood pressure (BP) to date have mainly analyzed common variants (minor allele frequency?>?0.05). In a meta-analysis of up to ~1.3 million participants, we discovered 106 new BP-associated genomic regions and 87 rare (minor allele frequency?=?0.01) variant BP associations (P?

Published
2020
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183. Effectiveness of Liraglutide and Lixisenatide in the Treatment of Type 2 Diabetes: Real-World Evidence from The Health Improvement Network (THIN) Database in the United Kingdom

Author

Feher, Michael, primary, Vega-Hernandez, Gabriela, additional, Mocevic, Emina, additional, Buysse, Brian, additional, Myland, Melissa, additional, Power, Geraldine S., additional, Nystrup Husemoen, Lise L., additional, Kim, Joseph, additional, and Witte, Daniel R., additional

Published
2017
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184. Does training of general practitioners for intensive treatment of people with screen-detected diabetes have a spillover effect on mortality and cardiovascular morbidity in ‘at risk’ individuals with normoglycaemia? Results from the ADDITION-Denmark cluster-randomised controlled trial

Author

Simmons, Rebecca K., primary, Bruun, Niels H., additional, Witte, Daniel R., additional, Borch-Johnsen, Knut, additional, Jørgensen, Marit E., additional, Sandbæk, Annelli, additional, and Lauritzen, Torsten, additional

Published
2017
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187. Does Training and Support of General Practitioners in Intensive Treatment of People with Screen-Detected Diabetes Improve Medication, Morbidity and Mortality in People with Clinically-Diagnosed Diabetes? Investigation of a Spill-Over Effect in a Cluster RCT

Author

Charles, Morten, primary, Skriver, Mette V., additional, Griffin, Simon J., additional, Simmons, Rebecca K., additional, Witte, Daniel R., additional, Dalsgaard, Else-Marie, additional, Lauritzen, Torsten, additional, and Sandbæk, Annelli, additional

Published
2017
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189. Genetic Correlation between Body Fat Percentage and Cardiorespiratory Fitness Suggests Common Genetic Etiology

Author

Schnurr, Theresia M., primary, Gjesing, Anette P., additional, Sandholt, Camilla H., additional, Jonsson, Anna, additional, Mahendran, Yuvaraj, additional, Have, Christian T., additional, Ekstrøm, Claus T., additional, Bjerregaard, Anne-Louise, additional, Brage, Soren, additional, Witte, Daniel R., additional, Jørgensen, Marit E., additional, Aadahl, Mette, additional, Thuesen, Betina H., additional, Linneberg, Allan, additional, Eiberg, Hans, additional, Pedersen, Oluf, additional, Grarup, Niels, additional, Kilpeläinen, Tuomas O., additional, and Hansen, Torben, additional

Published
2016
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190. Biomarkers of subclinical inflammation and increases in glycaemia, insulin resistance and beta-cell function in non-diabetic individuals: the Whitehall II study

Author

Herder, Christian, primary, Færch, Kristine, additional, Carstensen-Kirberg, Maren, additional, Lowe, Gordon D, additional, Haapakoski, Rita, additional, Witte, Daniel R, additional, Brunner, Eric J, additional, Roden, Michael, additional, Tabák, Adam G, additional, Kivimäki, Mika, additional, and Vistisen, Dorte, additional

Published
2016
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191. Heterogeneity in glucose response curves during an oral glucose tolerance test and associated cardiometabolic risk

Author

Hulman, Adam, primary, Simmons, Rebecca K., additional, Vistisen, Dorte, additional, Tabák, Adam G., additional, Dekker, Jacqueline M., additional, Alssema, Marjan, additional, Rutters, Femke, additional, Koopman, Anitra D. M., additional, Solomon, Thomas P. J., additional, Kirwan, John P., additional, Hansen, Torben, additional, Jonsson, Anna, additional, Gjesing, Anette Prior, additional, Eiberg, Hans, additional, Astrup, Arne, additional, Pedersen, Oluf, additional, Sørensen, Thorkild I. A., additional, Witte, Daniel R., additional, and Færch, Kristine, additional

Published
2016
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192. Reversion from prediabetes to normoglycaemia and risk of cardiovascular disease and mortality: the Whitehall II cohort study.

Author

Vistisen, Dorte, Kivimäki, Mika, Perreault, Leigh, Hulman, Adam, Witte, Daniel R., Brunner, Eric J., Tabák, Adam, Jørgensen, Marit E., and Færch, Kristine

Abstract

Aims/hypothesis: Reversion from prediabetes to normoglycaemia is accompanied by an improvement in cardiovascular risk factors, but it is unclear whether this translates into a reduction in risk of cardiovascular disease (CVD) events or death. Hence, we studied the probability of reversion from prediabetes to normoglycaemia and the associated risk of future CVD and death using data from the Whitehall II observational cohort study. Methods: Three glycaemic criteria for prediabetes (fasting plasma glucose [FPG] 5.6–6.9 mmol/l, 2 h plasma glucose [2hPG] 7.8–11.0 mmol/l, and HbA1c 39–47 mmol/mol [5.7–6.4%]) were assessed in 2002–2004 and 2007–2009 for 5193 participants free of known diabetes at enrolment. Among participants with prediabetes in the first examination, we calculated the probability of reversion to normoglycaemia by re-examination according to each glycaemic criterion. Poisson regression analysis was used to estimate and compare incidence rates of a composite endpoint of a CVD event or death in participants with prediabetes who did vs did not revert to normoglycaemia. Analyses were adjusted for age, sex, ethnicity and previous CVD. Results: Based on the FPG criterion, 820 participants had prediabetes and 365 (45%) of them had reverted to normoglycaemia in 5 years. The corresponding numbers were 324 and 120 (37%) for the 2hPG criterion and 1709 and 297 (17%) for the HbA1c criterion. During a median follow-up of 6.7 (interquartile range 6.3–7.2) years, 668 events of non-fatal CVD or death occurred among the 5193 participants. Reverting from 2hPG-defined prediabetes to normoglycaemia vs remaining prediabetic or progressing to diabetes was associated with a halving in event rate (12.7 vs 29.1 per 1000 person-years, p = 0.020). No association with event rate was observed for reverting from FPG-defined (18.6 vs 18.2 per 1000 person-years, p = 0.910) or HbA1c-defined prediabetes to normoglycaemia (24.5 vs 22.9 per 1000 person-years, p = 0.962). Conclusions/interpretation: Most people with HbA1c-defined prediabetes remained prediabetic or progressed to diabetes during 5 years of follow-up. In contrast, reversion to normoglycaemia was frequent among people with FPG- or 2hPG-defined prediabetes. Only reversion from 2hPG-defined prediabetes to normoglycaemia was associated with a reduction in future risk of CVD and death. [ABSTRACT FROM AUTHOR]

Published
2019
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193. Effect of duration and burden of microvascular complications on mortality rate in type 1 diabetes: an observational clinical cohort study.

Author

Bjerg, Lasse, Hulman, Adam, Carstensen, Bendix, Charles, Morten, Witte, Daniel R., and Jørgensen, Marit E.

Abstract

Aims/hypothesis: The role of burden and duration of multiple microvascular complications on mortality rate has not been explored in detail in type 1 diabetes. Taking complication burden and time-updated duration into account we aimed to quantify mortality rate in individuals with and without microvascular complications.Methods: This observational clinical cohort included 3828 individuals with type 1 diabetes attending the Steno Diabetes Center Copenhagen in 2001-2013. We used information on mortality and detailed clinical measures of microvascular complications from electronic patient records. Poisson models were used to model mortality rates according to complication burden.Results: During 26,665 person-years of follow-up, 503 deaths occurred. Compared with individuals without microvascular complications, the mortality rate ratio was 2.20 (95% CI 1.79, 2.69) for individuals with diabetic kidney disease, 1.72 (95% CI 1.39, 2.12) for individuals with neuropathy and 1.02 (95% CI 0.77, 1.37) for individuals with retinopathy, all adjusted for calendar time (year/month/day), age, duration of diabetes, sex, HbA1c, LDL-cholesterol, BMI, smoking status, systolic blood pressure, use of antihypertensive and lipid-lowering medication, and cardiovascular disease status. In individuals with two complications or more, the risk of mortality did not exceed the combined risk from each individual complication. Mortality rate ratios increased immediately after diagnosis of neuropathy and diabetic kidney disease. Mortality rate ratios were independent of the duration of neuropathy and retinopathy, while the mortality rate associated with diabetic kidney disease reached a stable level after approximately 3 years.Conclusions/interpretation: Neuropathy and diabetic kidney disease are strong and independent risk markers of mortality in type 1 diabetes, whereas no evidence of higher mortality rate was found for retinopathy. We found no indication that the mortality risk with multiple complications exceeds the risk conferred by each complication separately. The duration spent with microvascular complications had only a marginal effect on mortality. [ABSTRACT FROM AUTHOR]

Published
2019
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194. Genetic determinants of blood pressure traits are associated with carotid arterial thickening and plaque formation in patients with type 2 diabetes.

Author

Engelbrechtsen, Line, Appel, Vincent E., Schnurr, Theresia M., Lundby-Christensen, Louise, Skaaby, Thea, Linneberg, Allan, Drivsholm, Thomas, Witte, Daniel R., Jorgensen, Marit E., Grarup, Niels, Pedersen, Oluf, Hansen, Torben, and Vestergaard, Henrik

Abstract

Objectives: The aim of this study is to explore the contribution of genetically driven cardiometabolic risk factors for development of carotid arterial thickening in patients with type 2 diabetes. Methods: In total, 12 genetic risk scores for blood pressure, blood lipids and glycaemic traits were constructed. The genetic risk scores were tested for association with carotid intima-media thickness and plaques in patients with type 2 diabetes (n = 401) and in non-diabetic individuals (n = 648) and for association with glucose levels in two population-based cohorts (n = 1328 and n = 6161). Results: In patients with type 2 diabetes, the genetic risk scores for pulse pressure were positively associated with plaque formation (β = 0.036 ± 0.01 standard deviation/allele, p = 0.003). The genetic risk score for diastolic blood pressure was negatively associated with carotid intima-media thickness (β = –0.037 ± 0.01 standard deviation/allele, p = 0.005), although not significant after correction for multiple testing (p < 0.0042). In a meta-analysis of individuals with and without type 2 diabetes, the high-density lipoprotein genetic risk scores showed a trend towards an inverse association with carotid intima-media thickness and plaques, while the low-density lipoprotein genetic risk scores showed a trend towards a positive association with plaque formation but did reach the statistical threshold. Conclusion: Genetic loci for pulse pressure are associated with plaque formation among patients with type 2 diabetes, suggesting an underlying genetic contribution to arterial stiffening and atherosclerosis. [ABSTRACT FROM AUTHOR]

Published
2019
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196. Motivational counseling to reduce sitting time: A community-based randomized controlled trial in adults

Author

Aadahl, Mette, Linneberg, Allan, Møller, Trine C., Rosenørn, Solveig, Dunstan, David W., Witte, Daniel R., and Jørgensen, Torben

Abstract

Background Sedentary behavior is regarded as a distinct risk factor for cardiometabolic morbidity and mortality, but knowledge of the efficacy of interventions targeting reductions in sedentary behavior is limited. Purpose To investigate the effect of an individualized face-to-face motivational counseling intervention aimed at reducing sitting time. Design A randomized, controlled, observer-blinded, community-based trial with two parallel groups using open-end randomization with 1:1 allocation. Setting/participants A total of 166 sedentary adults were consecutively recruited from the population-based Health2010 Study. Intervention Participants were randomized to a control (usual lifestyle) or intervention group with four individual theory-based counseling sessions. Main outcome measures Objectively measured overall sitting time (ActivPAL 3TM, 7 days); secondary measures were breaks in sitting time, anthropometricmeasures, and cardiometabolic biomarkers, assessed at baseline and after 6 months. Data were collected in 2010–2012 and analyzed in 2013–2014 using repeated measures multiple regression analyses. Results Ninety-three participants were randomized to the intervention group and 73 to the control group, and 149 completed the study. The intervention group had a mean sitting time decrease of –0.27 hours/day, corresponding to 2.9% of baseline sitting time (hours/day); the control group increased mean sitting time by 0.06 hours/day. The between-group difference in change, –0.32 hours/day (95% CI=–0.87, 0.24, p=0.26), was not statistically significant. Significant differences in change in fasting serum insulin of –5.9 pmol/L (95% CI=–11.4, –0.5, p=0.03); homeostasis model assessment–estimated insulin resistance of –0.28 (95% CI=–0.53, –0.03, p=0.03); and waist circumference of –1.42 cm (95% CI=–2.54, –0.29, p=0.01) were observed in favor of the intervention group. Conclusions Although the observed decrease in sitting time was not significant, a community-based, individually tailored, theory-based intervention program aimed at reducing sitting time may be effective for increasing standing and improving cardiometabolic health in sedentary adults. Trial registration This study is registered at Clinicaltrials.gov (NCT00289237).

Published
2014

198. Insulin Resistance Is Accompanied by Increased Fasting Glucagon and Delayed Glucagon Suppression in Individuals With Normal and Impaired Glucose Regulation

Author

Færch, Kristine, primary, Vistisen, Dorte, additional, Pacini, Giovanni, additional, Torekov, Signe S., additional, Johansen, Nanna B., additional, Witte, Daniel R., additional, Jonsson, Anna, additional, Pedersen, Oluf, additional, Hansen, Torben, additional, Lauritzen, Torsten, additional, Jørgensen, Marit E., additional, Ahrén, Bo, additional, and Holst, Jens Juul, additional

Published
2016
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199. Functional and genetic epidemiological characterisation of theFFAR4(GPR120) p.R270H variant in the Danish population

Author

Vestmar, Marie A, primary, Andersson, Ehm A, additional, Christensen, Charlotte R, additional, Hauge, Maria, additional, Glümer, Charlotte, additional, Linneberg, Allan, additional, Witte, Daniel R, additional, Jørgensen, Marit E, additional, Christensen, Cramer, additional, Brandslund, Ivan, additional, Lauritzen, Torsten, additional, Pedersen, Oluf, additional, Holst, Birgitte, additional, Grarup, Niels, additional, Schwartz, Thue W, additional, and Hansen, Torben, additional

Published
2016
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