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1. Whole-Exome Sequencing of 2,000 Danish Individuals and the Role of Rare Coding Variants in Type 2 Diabetes

Author

Lohmueller, Kirk E, Sparsø, Thomas, Li, Qibin, Andersson, Ehm, Korneliussen, Thorfinn, Albrechtsen, Anders, Banasik, Karina, Grarup, Niels, Hallgrimsdottir, Ingileif, Kiil, Kristoffer, Kilpeläinen, Tuomas O, Krarup, Nikolaj T, Pers, Tune H, Sanchez, Gaston, Hu, Youna, DeGiorgio, Michael, Jørgensen, Torben, Sandbæk, Annelli, Lauritzen, Torsten, Brunak, Søren, Kristiansen, Karsten, Li, Yingrui, Hansen, Torben, Wang, Jun, Nielsen, Rasmus, and Pedersen, Oluf

Subjects
Biological Sciences, Genetics, Medical and Health Sciences, Genetics & Heredity, Biological sciences, Biomedical and clinical sciences, Health sciences
Published
2014

2. Whole-exome sequencing of 2,000 Danish individuals and the role of rare coding variants in type 2 diabetes.

Author

Lohmueller, Kirk, Sparsø, Thomas, Li, Qibin, Andersson, Ehm, Korneliussen, Thorfinn, Albrechtsen, Anders, Banasik, Karina, Grarup, Niels, Hallgrimsdottir, Ingileif, Kiil, Kristoffer, Kilpeläinen, Tuomas, Krarup, Nikolaj, Pers, Tune, Sanchez, Gaston, Hu, Youna, Degiorgio, Michael, Jørgensen, Torben, Sandbæk, Annelli, Lauritzen, Torsten, Brunak, Søren, Kristiansen, Karsten, Li, Yingrui, Hansen, Torben, Wang, Jun, Pedersen, Oluf, and Nielsen, Rasmus

Subjects
Computational Biology, Denmark, Diabetes Mellitus, Type 2, Exome, Genetic Association Studies, Genetic Variation, Genotype, High-Throughput Nucleotide Sequencing, Humans, Models, Statistical, Open Reading Frames, Polymorphism, Single Nucleotide, White People
Abstract

It has been hypothesized that, in aggregate, rare variants in coding regions of genes explain a substantial fraction of the heritability of common diseases. We sequenced the exomes of 1,000 Danish cases with common forms of type 2 diabetes (including body mass index > 27.5 kg/m(2) and hypertension) and 1,000 healthy controls to an average depth of 56×. Our simulations suggest that our study had the statistical power to detect at least one causal gene (a gene containing causal mutations) if the heritability of these common diseases was explained by rare variants in the coding regions of a limited number of genes. We applied a series of gene-based tests to detect such susceptibility genes. However, no gene showed a significant association with disease risk after we corrected for the number of genes analyzed. Thus, we could reject a model for the genetic architecture of type 2 diabetes where rare nonsynonymous variants clustered in a modest number of genes (fewer than 20) are responsible for the majority of disease risk.

Published
2013

3. A genome-wide association search for type 2 diabetes genes in African Americans.

Author

Palmer, Nicholette D, McDonough, Caitrin W, Hicks, Pamela J, Roh, Bong H, Wing, Maria R, An, S Sandy, Hester, Jessica M, Cooke, Jessica N, Bostrom, Meredith A, Rudock, Megan E, Talbert, Matthew E, Lewis, Joshua P, DIAGRAM Consortium, MAGIC Investigators, Ferrara, Assiamira, Lu, Lingyi, Ziegler, Julie T, Sale, Michele M, Divers, Jasmin, Shriner, Daniel, Adeyemo, Adebowale, Rotimi, Charles N, Ng, Maggie CY, Langefeld, Carl D, Freedman, Barry I, Bowden, Donald W, Voight, Benjamin F, Scott, Laura J, Steinthorsdottir, Valgerdur, Morris, Andrew P, Dina, Christian, Welch, Ryan P, Zeggini, Eleftheria, Huth, Cornelia, Aulchenko, Yurii S, Thorleifsson, Gudmar, McCulloch, Laura J, Ferreira, Teresa, Grallert, Harald, Amin, Najaf, Wu, Guanming, Willer, Cristen J, Raychaudhuri, Soumya, McCarroll, Steve A, Langenberg, Claudia, Hofmann, Oliver M, Dupuis, Josée, Qi, Lu, Segrè, Ayellet V, van Hoek, Mandy, Navarro, Pau, Ardlie, Kristin, Balkau, Beverley, Benediktsson, Rafn, Bennett, Amanda J, Blagieva, Roza, Boerwinkle, Eric, Bonnycastle, Lori L, Boström, Kristina Bengtsson, Bravenboer, Bert, Bumpstead, Suzannah, Burtt, Noël P, Charpentier, Guillaume, Chines, Peter S, Cornelis, Marilyn, Couper, David J, Crawford, Gabe, Doney, Alex SF, Elliott, Katherine S, Elliott, Amanda L, Erdos, Michael R, Fox, Caroline S, Franklin, Christopher S, Ganser, Martha, Gieger, Christian, Grarup, Niels, Green, Todd, Griffin, Simon, Groves, Christopher J, Guiducci, Candace, Hadjadj, Samy, Hassanali, Neelam, Herder, Christian, Isomaa, Bo, Jackson, Anne U, Johnson, Paul RV, Jørgensen, Torben, Kao, Wen HL, Klopp, Norman, Kong, Augustine, Kraft, Peter, Kuusisto, Johanna, Lauritzen, Torsten, Li, Man, Lieverse, Aloysius, Lindgren, Cecilia M, Lyssenko, Valeriya, Marre, Michel, Meitinger, Thomas, and Midthjell, Kristian

Subjects
DIAGRAM Consortium, MAGIC Investigators, Humans, Diabetes Mellitus, Type 2, Genetic Predisposition to Disease, Case-Control Studies, Cohort Studies, Genotype, Polymorphism, Single Nucleotide, Adult, Aged, Middle Aged, African Americans, Female, Male, Meta-Analysis as Topic, Validation Studies as Topic, Genome-Wide Association Study, Diabetes Mellitus, Type 2, Polymorphism, Single Nucleotide, General Science & Technology
Abstract

African Americans are disproportionately affected by type 2 diabetes (T2DM) yet few studies have examined T2DM using genome-wide association approaches in this ethnicity. The aim of this study was to identify genes associated with T2DM in the African American population. We performed a Genome Wide Association Study (GWAS) using the Affymetrix 6.0 array in 965 African-American cases with T2DM and end-stage renal disease (T2DM-ESRD) and 1029 population-based controls. The most significant SNPs (n = 550 independent loci) were genotyped in a replication cohort and 122 SNPs (n = 98 independent loci) were further tested through genotyping three additional validation cohorts followed by meta-analysis in all five cohorts totaling 3,132 cases and 3,317 controls. Twelve SNPs had evidence of association in the GWAS (P

Published
2012

5. Natural selection affects multiple aspects of genetic variation at putatively neutral sites across the human genome.

Author

Lohmueller, Kirk E, Albrechtsen, Anders, Li, Yingrui, Kim, Su Yeon, Korneliussen, Thorfinn, Vinckenbosch, Nicolas, Tian, Geng, Huerta-Sanchez, Emilia, Feder, Alison F, Grarup, Niels, Jørgensen, Torben, Jiang, Tao, Witte, Daniel R, Sandbæk, Annelli, Hellmann, Ines, Lauritzen, Torsten, Hansen, Torben, Pedersen, Oluf, Wang, Jun, and Nielsen, Rasmus

Subjects
Animals, Humans, Pan troglodytes, Evolution, Molecular, Recombination, Genetic, Gene Frequency, Genetic Drift, Mutation, Genome, Human, Models, Genetic, Population, Genetic Variation, Selection, Genetic, Human Genome, Biotechnology, Genetics, Generic health relevance, Developmental Biology
Abstract

A major question in evolutionary biology is how natural selection has shaped patterns of genetic variation across the human genome. Previous work has documented a reduction in genetic diversity in regions of the genome with low recombination rates. However, it is unclear whether other summaries of genetic variation, like allele frequencies, are also correlated with recombination rate and whether these correlations can be explained solely by negative selection against deleterious mutations or whether positive selection acting on favorable alleles is also required. Here we attempt to address these questions by analyzing three different genome-wide resequencing datasets from European individuals. We document several significant correlations between different genomic features. In particular, we find that average minor allele frequency and diversity are reduced in regions of low recombination and that human diversity, human-chimp divergence, and average minor allele frequency are reduced near genes. Population genetic simulations show that either positive natural selection acting on favorable mutations or negative natural selection acting against deleterious mutations can explain these correlations. However, models with strong positive selection on nonsynonymous mutations and little negative selection predict a stronger negative correlation between neutral diversity and nonsynonymous divergence than observed in the actual data, supporting the importance of negative, rather than positive, selection throughout the genome. Further, we show that the widespread presence of weakly deleterious alleles, rather than a small number of strongly positively selected mutations, is responsible for the correlation between neutral genetic diversity and recombination rate. This work suggests that natural selection has affected multiple aspects of linked neutral variation throughout the human genome and that positive selection is not required to explain these observations.

Published
2011

7. Evidence of a liver–alpha cell axis in humans: hepatic insulin resistance attenuates relationship between fasting plasma glucagon and glucagonotropic amino acids

Author

Wewer Albrechtsen, Nicolai J., Færch, Kristine, Jensen, Troels M., Witte, Daniel R., Pedersen, Jens, Mahendran, Yuvaraj, Jonsson, Anna E., Galsgaard, Katrine D., Winther-Sørensen, Marie, Torekov, Signe S., Lauritzen, Torsten, Pedersen, Oluf, Knop, Filip K., Hansen, Torben, Jørgensen, Marit E., Vistisen, Dorte, and Holst, Jens J.

Published
2018
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15. The genetic architecture of type 2 diabetes

Author

Fuchsberger, Christian, Flannick, Jason, Teslovich, Tanya M., Mahajan, Anubha, Agarwala, Vineeta, Gaulton, Kyle J., Ma, Clement, Fontanillas, Pierre, Moutsianas, Loukas, McCarthy, Davis J., Rivas, Manuel A., Perry, John R. B., Sim, Xueling, Blackwell, Thomas W., Robertson, Neil R., Rayner, N. William, Cingolani, Pablo, Locke, Adam E., Tajes, Juan Fernandez, Highland, Heather M., Dupuis, Josee, Chines, Peter S., Lindgren, Cecilia M., Hartl, Christopher, Jackson, Anne U., Chen, Han, Huyghe, Jeroen R., van de Bunt, Martijn, Pearson, Richard D., Kumar, Ashish, Müller-Nurasyid, Martina, Grarup, Niels, Stringham, Heather M., Gamazon, Eric R., Lee, Jaehoon, Chen, Yuhui, Scott, Robert A., Below, Jennifer E., Chen, Peng, Huang, Jinyan, Go, Min Jin, Stitzel, Michael L., Pasko, Dorota, Parker, Stephen C. J., Varga, Tibor V., Green, Todd, Beer, Nicola L., Day-Williams, Aaron G., Ferreira, Teresa, Fingerlin, Tasha, Horikoshi, Momoko, Hu, Cheng, Huh, Iksoo, Ikram, Mohammad Kamran, Kim, Bong-Jo, Kim, Yongkang, Kim, Young Jin, Kwon, Min-Seok, Lee, Juyoung, Lee, Selyeong, Lin, Keng-Han, Maxwell, Taylor J., Nagai, Yoshihiko, Wang, Xu, Welch, Ryan P., Yoon, Joon, Zhang, Weihua, Barzilai, Nir, Voight, Benjamin F., Han, Bok-Ghee, Jenkinson, Christopher P., Kuulasmaa, Teemu, Kuusisto, Johanna, Manning, Alisa, Ng, Maggie C. Y., Palmer, Nicholette D., Balkau, Beverley, Stančáková, Alena, Abboud, Hanna E., Boeing, Heiner, Giedraitis, Vilmantas, Prabhakaran, Dorairaj, Gottesman, Omri, Scott, James, Carey, Jason, Kwan, Phoenix, Grant, George, Smith, Joshua D., Neale, Benjamin M., Purcell, Shaun, Butterworth, Adam S., Howson, Joanna M. M., Lee, Heung Man, Lu, Yingchang, Kwak, Soo-Heon, Zhao, Wei, Danesh, John, Lam, Vincent K. L., Park, Kyong Soo, Saleheen, Danish, So, Wing Yee, Tam, Claudia H. T., Afzal, Uzma, Aguilar, David, Arya, Rector, Aung, Tin, Chan, Edmund, Navarro, Carmen, Cheng, Ching-Yu, Palli, Domenico, Correa, Adolfo, Curran, Joanne E., Rybin, Denis, Farook, Vidya S., Fowler, Sharon P., Freedman, Barry I., Griswold, Michael, Hale, Daniel Esten, Hicks, Pamela J., Khor, Chiea-Chuen, Kumar, Satish, Lehne, Benjamin, Thuillier, Dorothée, Lim, Wei Yen, Liu, Jianjun, van der Schouw, Yvonne T., Loh, Marie, Musani, Solomon K., Puppala, Sobha, Scott, William R., Yengo, Loïc, Tan, Sian-Tsung, Taylor Jr., Herman A., Thameem, Farook, Wilson, Gregory, Wong, Tien Yin, Njølstad, Pål Rasmus, Levy, Jonathan C., Mangino, Massimo, Bonnycastle, Lori L., Schwarzmayr, Thomas, Fadista, João, Surdulescu, Gabriela L., Herder, Christian, Groves, Christopher J., Wieland, Thomas, Bork-Jensen, Jette, Brandslund, Ivan, Christensen, Cramer, Koistinen, Heikki A., Doney, Alex S. F., Kinnunen, Leena, Esko, Tõnu, Farmer, Andrew J., Hakaste, Liisa, Hodgkiss, Dylan, Kravic, Jasmina, Lyssenko, Valeriya, Hollensted, Mette, Jørgensen, Marit E., Jørgensen, Torben, Ladenvall, Claes, Justesen, Johanne Marie, Käräjämäki, Annemari, Kriebel, Jennifer, Rathmann, Wolfgang, Lannfelt, Lars, Lauritzen, Torsten, Narisu, Narisu, Linneberg, Allan, Melander, Olle, Milani, Lili, Neville, Matt, Orho-Melander, Marju, Qi, Lu, Qi, Qibin, Roden, Michael, Rolandsson, Olov, Swift, Amy, Rosengren, Anders H., Stirrups, Kathleen, Wood, Andrew R., Mihailov, Evelin, Blancher, Christine, Carneiro, Mauricio O., Maguire, Jared, Poplin, Ryan, Shakir, Khalid, Fennell, Timothy, DePristo, Mark, Hrabé de Angelis, Martin, Deloukas, Panos, Gjesing, Anette P., Jun, Goo, Nilsson, Peter, Murphy, Jacquelyn, Onofrio, Robert, Thorand, Barbara, Hansen, Torben, Meisinger, Christa, Hu, Frank B., Isomaa, Bo, Karpe, Fredrik, Liang, Liming, Peters, Annette, Huth, Cornelia, O’Rahilly, Stephen P., Palmer, Colin N. A., Pedersen, Oluf, Rauramaa, Rainer, Tuomilehto, Jaakko, Salomaa, Veikko, Watanabe, Richard M., Syvänen, Ann-Christine, Bergman, Richard N., Bharadwaj, Dwaipayan, Bottinger, Erwin P., Cho, Yoon Shin, Chandak, Giriraj R., Chan, Juliana C. N., Chia, Kee Seng, Daly, Mark J., Ebrahim, Shah B., Langenberg, Claudia, Elliott, Paul, Jablonski, Kathleen A., Lehman, Donna M., Jia, Weiping, Ma, Ronald C. W., Pollin, Toni I., Sandhu, Manjinder, Tandon, Nikhil, Froguel, Philippe, Barroso, Inês, Teo, Yik Ying, Zeggini, Eleftheria, Loos, Ruth J. F., Small, Kerrin S., Ried, Janina S., DeFronzo, Ralph A., Grallert, Harald, Glaser, Benjamin, Metspalu, Andres, Wareham, Nicholas J., Walker, Mark, Banks, Eric, Gieger, Christian, Ingelsson, Erik, Im, Hae Kyung, Illig, Thomas, Franks, Paul W., Buck, Gemma, Trakalo, Joseph, Buck, David, Prokopenko, Inga, Mägi, Reedik, Lind, Lars, Farjoun, Yossi, Owen, Katharine R., Gloyn, Anna L., Strauch, Konstantin, Tuomi, Tiinamaija, Kooner, Jaspal Singh, Lee, Jong-Young, Park, Taesung, Donnelly, Peter, Morris, Andrew D., Hattersley, Andrew T., Bowden, Donald W., Collins, Francis S., Atzmon, Gil, Chambers, John C., Spector, Timothy D., Laakso, Markku, Strom, Tim M., Bell, Graeme I., Blangero, John, Duggirala, Ravindranath, Tai, E. Shyong, McVean, Gilean, Hanis, Craig L., Wilson, James G., Seielstad, Mark, Frayling, Timothy M., Meigs, James B., Cox, Nancy J., Sladek, Rob, Lander, Eric S., Gabriel, Stacey, Burtt, Noël P., Mohlke, Karen L., Meitinger, Thomas, Groop, Leif, Abecasis, Goncalo, Florez, Jose C., Scott, Laura J., Morris, Andrew P., Kang, Hyun Min, Boehnke, Michael, Altshuler, David, and McCarthy, Mark I.

Published
2016
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20. Erratum:Role of fasting duration and weekday in incretin and glucose regulation

Author

Clemmensen, Kim K.B., Quist, Jonas S., Vistisen, Dorte, Witte, Daniel R., Jonsson, Anna, Pedersen, Oluf, Hansen, Torben, Holst, Jens J., Lauritzen, Torsten, Jørgensen, Marit E., Torekov, Signe, and Færch, Kristine

Abstract

The authors and journal apologise for errors in the above paper, which appeared in volume 9 part 4, pages 279-288. The errors relate to three values given in Table 2 on page 283. The value for Unadjusted upper 95% CI of 120 min plasma glucose should be 3.0, not 3.9, the value for Adjusted Estimate of Fasting plasma glucagon should be 0.0 not 0.3, and the value for Unadjusted Estimate of 30 min plasma GLP-1 should be -0.5 not -1.5. These errors do not affect the results or conclusions. The correct Table 2 is given in full below

Published
2021

23. Role of fasting duration and weekday in incretin and glucose regulation

Author

Clemmensen, Kim K B, primary, Quist, Jonas S, additional, Vistisen, Dorte, additional, Witte, Daniel R, additional, Jonsson, Anna, additional, Pedersen, Oluf, additional, Hansen, Torben, additional, Holst, Jens J, additional, Lauritzen, Torsten, additional, Jørgensen, Marit E, additional, Torekov, Signe, additional, and Færch, Kristine, additional

Published
2021
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26. Early Detection and Treatment of Type 2 Diabetes Reduce Cardiovascular Morbidity and Mortality: A Simulation of the Results of the Anglo-Danish-Dutch Study of Intensive Treatment in People With Screen-Detected Diabetes in Primary Care (ADDITION-Europe)

Author

Herman, William H., Ye, Wen, Griffin, Simon J., Simmons, Rebecca K., Davies, Melanie J., Khunti, Kamlesh, Rutten, Guy E.H.M., Sandbaek, Annelli, Lauritzen, Torsten, Borch-Johnsen, Knut, Brown, Morton B., and Wareham, Nicholas J.

Published
2015
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32. Effect of early intensive multifactorial therapy compared with routine care on self-reported health status, general well-being, diabetes-specific quality of life and treatment satisfaction in screen-detected type 2 diabetes mellitus patients (ADDITION-Europe): a cluster-randomised trial

Author

Van den Donk, Maureen, Griffin, Simon J., Stellato, Rebecca K., Simmons, Rebecca K., Sandbæk, Annelli, Lauritzen, Torsten, Khunti, Kamlesh, Davies, Melanie J., Borch-Johnsen, Knut, Wareham, Nicholas J., and Rutten, Guy E. H. M.

Published
2013
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33. Identification of KCNJ15 as a susceptibility gene in Asian patients with type 2 diabetes mellitus

Author

Okamoto, Koji, Iwasaki, Naoko, Nishimura, Chisa, Doi, Kent, Noiri, Eisei, Nakamura, Shinko, Takizawa, Miho, Ogata, Makiko, Fujimaki, Risa, Grarup, Niels, Pisinger, Charlotta, Borch-Johnsen, Knut, Lauritzen, Torsten, Sandbaek, Annelli, Hansen, Torben, Yasuda, Kazuki, Osawa, Haruhiko, Nanjo, Kishio, Kadowaki, Takashi, Kasuga, Masato, Pedersen, Oluf, Fujita, Toshiro, Kamatani, Naoyuki, Iwamoto, Yasuhiko, and Tokunaga, Katsushi

Subjects
Asians -- Genetic aspects, Chromosome mapping -- Usage, Gene expression -- Analysis, Type 2 diabetes -- Genetic aspects, Type 2 diabetes -- Care and treatment, Type 2 diabetes -- Risk factors, Biological sciences
Abstract

A study uses fine-mapping techniques of SNPs in a region of chromosome 21q and identifies potassium inwardly-rectifying channel, subfamily J, member 15 (KCNJ15) as a previously unreported susceptibility gene in Asian patients with type 2 diabetes mellitus (T2DM). It also shows that the KCNJ15 gene is expressed in human pancreatic beta cells, and demonstrates that a synonymous variant in KCNJ15 is significantly associated in T2DM among Asians.

Published
2010

35. Alanine aminotransferase and 20-year risk of major chronic diseases and death in a healthy cohort aged 30 to 49 years

Author

Jensen, Morten Daniel, Lauritzen, Torsten, Vilstrup, Hendrik, and Jepsen, Peter

Subjects
ALT, Short Report, cohort study, morbidity, Clinical Epidemiology, Morbidity, Mortality, Cohort study, mortality
Abstract

Morten Daniel Jensen,1 Torsten Lauritzen,2 Hendrik Vilstrup,1 Peter Jepsen1,3 1Department of Hepatology and Gastroenterology, Aarhus University Hospital, Aarhus, Denmark; 2Department of Public Health, Research Group for General Practice, University of Aarhus, Aarhus, Denmark; 3Department of Clinical Epidemiology, Aarhus University Hospital, Aarhus, DenmarkCorrespondence: Morten Daniel JensenDepartment of Hepatology and Gastroenterology, Aarhus University Hospital, Entrance C, Plan 1, Intersection C116, Palle Juul-Jensens Boulevard 99, Aarhus N 8200, DenmarkTel +45 27 59 75 49Email moje@clin.au.dkPurpose: Alanine aminotransferase is the most frequently used marker of liver cell injury. We examined the association between alanine aminotransferase levels and long-term absolute risks of morbidity and mortality in healthy Danish people aged 30– 49 years.Patients and Methods: We divided 671 healthy participants from the Ebeltoft Health Promotion Project into four categories based on their baseline alanine aminotransferase values: low (≤ 10U/l), medium-low (men: 11– 34U/l, women: 11– 22U/l), medium-high (men: 35– 69U/l, women: 23– 44U/l) and high (men: ≥ 70U/l, women: ≥ 45U/l), and followed them through Danish healthcare registries for up to 20 years. We examined mortality and absolute risks of liver disease, overall cancer, ischemic heart disease, and diabetes.Results: The risk of any cancer was highest for participants with “low alanine aminotransferase” or “high alanine aminotransferase” (20-year risk: 17.2% [95% confidence interval (CI): 6.3– 32.7%] and 18.2% [95% CI: 5.7– 36.3%], respectively). The risk of diabetes was highest for participants with “medium-high alanine aminotransferase” or “high alanine aminotransferase” (20-year risk: 12.1% [95% CI: 7.3– 18.3%] and 9.1% [95% CI: 1.6– 25.1%], respectively). Participants with “high alanine aminotransferase” had the highest 20-year risk of liver disease (20-year risk: 13.6% [95% CI: 3.4– 30.9%], while it was 1.0% or less in the other groups). The chance of being alive after 20 years without having been diagnosed with liver disease, cancer, ischemic heart disease, or diabetes was lowest in the “high alanine aminotransferase” group (50% [95% CI: 28– 68%]) and 72– 79% in the other groups.Conclusion: Our findings suggest that persons with high or abnormally low alanine aminotransferase measurements are at increased long-term risk of several chronic diseases.Keywords: ALT, mortality, morbidity, cohort study

Published
2020

36. Alanine Aminotransferase and 20-Year Risk of Major Chronic Diseases and Death in a Healthy Cohort Aged 30 to 49 Years

Author

Jensen,Morten Daniel, Lauritzen,Torsten, Vilstrup,Hendrik, Jepsen,Peter, Jensen,Morten Daniel, Lauritzen,Torsten, Vilstrup,Hendrik, and Jepsen,Peter

Abstract

Morten Daniel Jensen,1 Torsten Lauritzen,2 Hendrik Vilstrup,1 Peter Jepsen1,3 1Department of Hepatology and Gastroenterology, Aarhus University Hospital, Aarhus, Denmark; 2Department of Public Health, Research Group for General Practice, University of Aarhus, Aarhus, Denmark; 3Department of Clinical Epidemiology, Aarhus University Hospital, Aarhus, DenmarkCorrespondence: Morten Daniel JensenDepartment of Hepatology and Gastroenterology, Aarhus University Hospital, Entrance C, Plan 1, Intersection C116, Palle Juul-Jensens Boulevard 99, Aarhus N 8200, DenmarkTel +45 27 59 75 49Email moje@clin.au.dkPurpose: Alanine aminotransferase is the most frequently used marker of liver cell injury. We examined the association between alanine aminotransferase levels and long-term absolute risks of morbidity and mortality in healthy Danish people aged 30– 49 years.Patients and Methods: We divided 671 healthy participants from the Ebeltoft Health Promotion Project into four categories based on their baseline alanine aminotransferase values: low (≤ 10U/l), medium-low (men: 11– 34U/l, women: 11– 22U/l), medium-high (men: 35– 69U/l, women: 23– 44U/l) and high (men: ≥ 70U/l, women: ≥ 45U/l), and followed them through Danish healthcare registries for up to 20 years. We examined mortality and absolute risks of liver disease, overall cancer, ischemic heart disease, and diabetes.Results: The risk of any cancer was highest for participants with “low alanine aminotransferase” or “high alanine aminotransferase” (20-year risk: 17.2% [95% confidence interval (CI): 6.3– 32.7%] and 18.2% [95% CI: 5.7– 36.3%], respectively). The risk of diabetes was highest for participants with “medium-high alanine aminotransferase” or “high alanine aminotransferase” (20-year risk: 12.1% [95% CI: 7.3– 18.3%] and 9.1% [95% CI: 1.6&nd

Published
2020

37. Abdominal visceral and subcutaneous adipose tissue and associations with cardiometabolic risk in Inuit, Africans and Europeans:a cross-sectional study

Author

Rønn, Pernille Falberg, Andersen, Gregers Stig, Lauritzen, Torsten, Christensen, Dirk Lund, Aadahl, Mette, Carstensen, Bendix, Grarup, Niels, Jørgensen, Marit Eika, Rønn, Pernille Falberg, Andersen, Gregers Stig, Lauritzen, Torsten, Christensen, Dirk Lund, Aadahl, Mette, Carstensen, Bendix, Grarup, Niels, and Jørgensen, Marit Eika

Abstract

OBJECTIVES: Abdominal fat has been identified as a risk marker of cardiometabolic disease independent of overall adiposity. However, it is not clear whether there are ethnic disparities in this risk. We investigated the associations of visceral adipose tissue (VAT) and abdominal subcutaneous adipose tissue (SAT) with cardiometabolic risk factors in three ethnic diverse populations of Inuit, Africans and Europeans.DESIGN: Cross-sectional pooled study.SETTING: Greenland, Kenya and Denmark.METHODS: A total of 5113 participants (2933 Inuit, 1397 Africans and 783 Europeans) from three studies in Greenland, Kenya and Denmark were included. Measurements included abdominal fat distribution assessed by ultrasound, oral glucose tolerance test, hepatic insulin resistance, blood pressure and lipids. The associations were analysed using multiple linear regressions.RESULTS: Across ethnic group and gender, an increase in VAT of 1 SD was associated with higher levels of hepatic insulin resistance (ranging from 14% to 28%), triglycerides (8% to 16%) and lower high-density lipoprotein cholesterol (HDL-C, -1.0 to -0.05 mmol/L) independent of body mass index. VAT showed positive associations with most of the other cardiometabolic risk factors in Inuit and Europeans, but not in Africans. In contrast, SAT was mainly associated with the outcomes in Inuit and Africans. Of notice was that higher SAT was associated with higher HDL-C in African men (0.11 mmol/L, 95% CI: 0.03 to 0.18) and with lower HDL-C in Inuit (-0.07 mmol/L, 95% CI: -0.12 to -0.02), but not in European men (-0.02 mmol/L, 95% CI: -0.09 to 0.05). Generally weaker associations were observed for women. Furthermore, the absolute levels of several of the cardiometabolic outcomes differed between the ethnic groups.CONCLUSIONS: VAT and SAT were associated with several of the cardiometabolic risk factors beyond overall adiposity. Some of these associations were specific to ethnicity, suggesting

Published
2020

38. Role of fasting duration and weekday in incretin and glucose regulation

Author

Clemmensen, Kim K.B., Quist, Jonas S., Vistisen, Dorte, Witte, Daniel R., Jonsson, Anna, Pedersen, Oluf, Hansen, Torben, Holst, Jens J., Lauritzen, Torsten, Jørgensen, Marit E., Torekov, Signe, Færch, Kristine, Clemmensen, Kim K.B., Quist, Jonas S., Vistisen, Dorte, Witte, Daniel R., Jonsson, Anna, Pedersen, Oluf, Hansen, Torben, Holst, Jens J., Lauritzen, Torsten, Jørgensen, Marit E., Torekov, Signe, and Færch, Kristine

Abstract

Fasting duration has been associated with lower fasting blood glucose levels, but higher 2-h post-load levels, and research has indicated an adverse effect of ‘weekend behavior’ on human metabolism. We investigated associations of fasting duration and weekday of examination with glucose, insulin, glucagon and incretin responses to an oral glucose tolerance test (OGTT). This cross-sectional study is based on data from the ADDITION-PRO study, where 2082 individuals attended a health examination including an OGTT. Linear regression analysis was applied to study the associations of overnight fasting duration and day of the week with glucose, insulin, glucagon, glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide 1 (GLP-1) responses to an OGTT. We found that a 1 h longer fasting duration was associated with 1.7% (95% CI: 0.8,2.5) higher 2-h glucose levels, as well as a 3.0% (95% CI: 1.3,4.7) higher GIP and 2.3% (95% CI: 0.3,4.4) higher GLP-1 response. Fasting insulin levels were 20.6% (95% CI: 11.2,30.7) higher on Mondays compared to the other weekdays, with similar fasting glucose levels (1.7%, 95% CI: 0.0,3.4). In this study, longer overnight fasting duration was associated with a worsening of glucose tolerance and increased incretin response to oral glucose. We found higher fasting insulin levels on Mondays compared to the other days of the week, potentially indicating a worsened glucose regulation after the weekend.

Published
2020

45. Role of fasting duration and weekday in incretin and glucose regulation

Author

Clemmensen, Kim K B, primary, Quist, Jonas S, additional, Vistisen, Dorte, additional, Witte, Daniel R, additional, Jonsson, Anna, additional, Pedersen, Oluf, additional, Hansen, Torben, additional, Holst, Jens J, additional, Lauritzen, Torsten, additional, Jørgensen, Marit E, additional, Torekov, Signe, additional, and Færch, Kristine, additional

Published
2020
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47. The effect of training GPs in motivational interviewing on incident cardiovascular disease and mortality in people with screen-detected diabetes. Results from the ADDITION-Denmark randomised trial

Author

Charles, Morten, primary, Bruun, Niels Henrik, additional, Simmons, Rebecca, additional, Dalsgaard, Else-Marie, additional, Witte, Daniel, additional, Jorgensen, Marit, additional, Christensen, Bo, additional, Maindal, Helle Terkildsen, additional, Rubak, Sune, additional, Sandbaek, Annelli, additional, and Lauritzen, Torsten, additional

Published
2020
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49. Habitual physical activity is associated with lower fasting and greater glucose-induced GLP-1 response in men

Author

Janus, Charlotte, primary, Vistisen, Dorte, additional, Amadid, Hanan, additional, Witte, Daniel R, additional, Lauritzen, Torsten, additional, Brage, Søren, additional, Bjerregaard, Anne-Louise, additional, Hansen, Torben, additional, Holst, Jens J, additional, Jørgensen, Marit E, additional, Pedersen, Oluf, additional, Færch, Kristine, additional, and Torekov, Signe S, additional

Published
2019
Full Text
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