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Your search keyword '"Jørgensen, Torben"' showing total 12 results
Start Over Author "Jørgensen, Torben" Journal diabetes care
12 results on '"Jørgensen, Torben"'

10. Gene-Environment Interactions of Circadian-Related Genes for Cardiometabolic Traits

Author

Dashti, Hassan S., Follis, Jack L., Smith, Caren E., Tanaka, Toshiko, Garaulet, Marta, Gottlieb, Daniel J., Hruby, Adela, Jacques, Paul F., Kiefte-de Jong, Jessica C., Lamon-Fava, Stefania, Scheer, Frank A.J.L., Bartz, Traci M., Kovanen, Leena, Wojczynski, Mary K., Frazier-Wood, Alexis C., Ahluwalia, Tarunveer S., Perälä, Mia-Maria, Jonsson, Anna, Muka, Taulant, Kalafati, Ioanna P., Mikkilä, Vera, Ordovás, José M., Lemaitre, Rozenn N., Partonen, Timo, Ebeling, Tapani, Hopkins, Paul N., Paternoster, Lavinia, Lahti, Jari, Hernandez, Dena G., Toft, Ulla, Saxena, Richa, Vitezova, Anna, Kanoni, Stavroula, Raitakari, Olli T., Psaty, Bruce M., Perola, Markus, Männistö, Satu, Straka, Robert J., Hansen, Torben, Räikkönen, Katri, Ferrucci, Luigi, Grarup, Niels, Johnson, W. Craig, Rallidis, Loukianos, Kähönen, Mika, Siscovick, David S., Havulinna, Aki S., Astrup, Arne, Jørgensen, Torben, Chen, Tzu-An, Hofman, Albert, Deloukas, Panos, Viikari, Jorma S.A., Mozaffarian, Dariush, Pedersen, Oluf, Rotter, Jerome I., Uitterlinden, André G., Seppälä, Ilkka, Tiemeier, Henning, Salomaa, Veikko, Gharib, Sina A., Borecki, Ingrid B., Arnett, Donna K., Sørensen, Thorklid I.A., Eriksson, Johan G., Bandinelli, Stefania, Linneberg, Allan, Rich, Stephen S., Franco, Oscar H., Dedoussis, George, Lehtimäki, Terho, and Epidemiology

Subjects
medicine.medical_specialty, Endocrinology, Diabetes and Metabolism, Population, 030209 endocrinology & metabolism, Type 2 diabetes, 03 medical and health sciences, 0302 clinical medicine, Insulin resistance, SDG 3 - Good Health and Well-being, Internal medicine, Internal Medicine, medicine, Circadian rhythm, Allele, Epidemiology/Health Services Research, education, 030304 developmental biology, Glycemic, Advanced and Specialized Nursing, 0303 health sciences, education.field_of_study, business.industry, medicine.disease, Obesity, Endocrinology, Metabolic syndrome, business
Abstract

OBJECTIVE Common circadian-related gene variants associate with increased risk for metabolic alterations including type 2 diabetes. However, little is known about whether diet and sleep could modify associations between circadian-related variants (CLOCK-rs1801260, CRY2-rs11605924, MTNR1B-rs1387153, MTNR1B-rs10830963, NR1D1-rs2314339) and cardiometabolic traits (fasting glucose [FG], HOMA-insulin resistance, BMI, waist circumference, and HDL-cholesterol) to facilitate personalized recommendations. RESEARCH DESIGN AND METHODS We conducted inverse-variance weighted, fixed-effect meta-analyses of results of adjusted associations and interactions between dietary intake/sleep duration and selected variants on cardiometabolic traits from 15 cohort studies including up to 28,190 participants of European descent from the Cohorts for Heart and Aging Research in Genomic Epidemiology (CHARGE) Consortium. RESULTS We observed significant associations between relative macronutrient intakes and glycemic traits and short sleep duration ( CONCLUSIONS Our results suggest that lower carbohydrate intake and normal sleep duration may ameliorate cardiometabolic abnormalities conferred by common circadian-related genetic variants. Until further mechanistic examination of the nominally significant interactions is conducted, recommendations applicable to the general population regarding diet—specifically higher carbohydrate and lower fat composition—and normal sleep duration should continue to be emphasized among individuals with the investigated circadian-related gene variants.

Published
2015

12. Natural history of insulin sensitivity and insulin secretion in the progression from normal glucose tolerance to impaired fasting glycemia and impaired glucose tolerance: the Inter99 study.

Author

Faerch K, Vaag A, Holst JJ, Hansen T, Jørgensen T, and Borch-Johnsen K

Subjects
Blood Glucose analysis, Female, Follow-Up Studies, Glucose Intolerance blood, Humans, Insulin Secretion, Male, Middle Aged, Prediabetic State blood, Blood Glucose metabolism, Fasting blood, Glucose Intolerance physiopathology, Insulin metabolism, Prediabetic State physiopathology
Abstract

Objective: The aim of this study was to describe the natural history of insulin secretion and insulin sensitivity in the development of isolated impaired fasting glycemia (i-IFG), isolated impaired glucose tolerance (i-IGT), and combined IFG/IGT., Research Design and Methods: Baseline and 5-year follow-up data from the Inter99 study were used. Individuals with normal glucose tolerance (NGT) at baseline and i-IFG, i-IGT, combined IFG/IGT, or NGT at the 5-year follow-up were examined with an oral glucose tolerance test (n = 3,145). Insulin sensitivity index (ISI), homeostasis model assessment of insulin sensitivity (HOMA-IS), early-phase insulin release (EPIR), and insulin secretion relative to insulin action (disposition index) were estimated., Results: Five years before the pre-diabetes diagnoses (i-IFG, i-IGT, and IFG/IGT), ISI, HOMA-IS, EPIR, and disposition index were lower than in individuals who maintained NGT. During the 5-year follow-up, individuals developing i-IFG experienced a significant decline only in HOMA-IS, whereas individuals developing i-IGT experienced significant declines in ISI, EPIR, and disposition index. Individuals with IFG/IGT exhibited pronounced declines in ISI, HOMA-IS, EPIR, and disposition index during the 5-year follow-up., Conclusions: A stationary reduced insulin secretion followed by a decline in primarily hepatic insulin sensitivity characterizes the transition from NGT to i-IFG. In contrast, low whole-body insulin sensitivity with a secondary lack of beta-cell compensation is associated with the development of i-IGT. Thereby, i-IFG and i-IGT appear to result from different underlying mechanisms, which may have implications for the prevention and treatment of the diabetes that succeeds them.

Published
2009
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