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Articles by T. Jorgensen
Total Records ( 5 ) for T. Jorgensen
  T. W. Boesgaard , S. I. Castella , G. Andersen , A. Albrechtsen , T. Sparso , K. Borch-Johnsen , T. Jorgensen , T. Hansen and O. Pedersen

Aims The glutamate decarboxylase gene (GAD2) encodes GAD65, an enzyme catalysing the production of the γ-aminobutyric acid (GABA) which interacts with neuropeptide Y to stimulate food intake. It has been suggested that in pancreatic islets, GABA serves as a functional regulator of pancreatic hormone release. Conflicting results have been reported concerning the potential impact of GAD2 variation on estimates of energy metabolism. The aim of this study was to elucidate potential associations between the GAD2−243A→G polymorphism and levels of body mass index (BMI) and estimates of glycaemia.

Methods Using high-throughput chip-based matrix-assisted laser desorption/ionization time-of-flight mass spectrometry, the GAD2−243A→G (rs2236418) polymorphism was genotyped in a population-based sample (Inter99) of 5857 middle-aged, unrelated Danish White subjects.

Results The G-allele was associated with modestly lower BMI (P = 0.01). In a case–control study of obesity, the G-allele frequency in 2582 participants with BMI < 25 kg/m2 was 19.5% (18.4–20.6) compared with 17.1% (15.5–18.8) in 968 participants having BMI ≥ 30 kg/m2 (P = 0.03), odds ratio 0.9 (0.7–1.0). Of the 5857 subjects, GG carriers had lower fasting plasma glucose levels (mmol/l) [AA (n = 3859) 5.6 ± 0.8; AG (n = 1792) 5.5 ± 0.8; GG (n = 206) 5.5 ± 0.8, P = 0.008] and lower 30-min oral glucose tolerance test (OGTT)-related plasma glucose levels (AA 8.7 ± 1.9; AG 8.6 ± 1.9; GG 8.6 ± 2.0, P = 0.04), adjusted for sex, age and BMI. Analysing subjects who were both normoglycaemic and glucose tolerant (n = 4431) GG carriers still had lower fasting plasma glucose concentrations: AA (n = 2895) 5.3 ± 0.4; AG (n = 1383) 5.3 ± 0.4; GG (n = 153) 5.2 ± 0.4 (P = 9.10−5).

Conclusion The present study suggests that the GAD2−243A→G polymorphism in a population of middle-aged White people associates with a modest reduction in BMI and fasting and OGTT-related plasma glucose levels.

  K. Faerch , A. Vaag , D. R. Witte , T. Jorgensen , O. Pedersen and K. Borch-Johnsen
  Aims  Screening and prevention strategies for Type 2 diabetes require insight into the aetiological and potentially different risk factors leading to early impairments of fasting plasma glucose (FPG) and 2-h post-load plasma glucose (2hPG) levels. We studied whether risk factors predicting subtle elevations of FPG levels were different from those predicting elevations of 2hPG levels in men and women.

Methods  We used baseline and 5-year follow-up data from middle-aged men and women with normal glucose tolerance (NGT) at baseline in the Danish population-based Inter99 study (n = 3164). Anthropometric and non-anthropometric baseline predictors of the 5-year FPG and 2hPG levels were estimated in linear regression models stratified by gender.

Results  In men, but not in women, smoking and family history of diabetes predicted increased FPG levels, whereas high physical activity predicted a decline in 2hPG levels. Among the anthropometric variables, large waist circumference was the strongest predictor of increased FPG levels in men, whereas high body mass index (BMI) was the strongest predictor of increased FPG levels in women. In both men and women, BMI and waist circumference were equally strong in predicting 2hPG levels. Furthermore, short height predicted increased 2hPG levels in men, and short height and low hip circumference predicted increased 2hPG levels in women.

Conclusions  Risk factors that predict future FPG levels are different from those predicting future 2hPG levels. Furthermore, different risk factors predict glycaemic levels in men compared with women. These findings indicate that different aetiological pathways may lead to Type 2 diabetes in men and women.

  S. B. Haugaard , O. Andersen , T. W. Hansen , J. Eugen-Olsen , A. Linneberg , S. Madsbad , M. H. Olsen , T. Jorgensen , K. Borch-Johnsen and J. Jeppesen
  Aim  To explore the putative association of new-onset diabetes and the soluble urokinase plasminogen activator receptor (suPAR), which is a new and stable plasma marker of immune function and low-grade inflammation. This association has been previously suggested by using the less sensitive International Classification of Disease system to detect incident diabetes in the Danish MONICA 10 cohort.

Methods  The Danish National Diabetes Register enabled more accurate identification of incident diabetes during a median follow-up of 13.8 years in the Danish MONICA 10 cohort (n = 2353 generally healthy individuals). The soluble urokinase plasminogen activator receptor was measured by the ELISA method. To fulfil model assumptions, outcome analyses were stratified by age, and further by smoking, owing to the interaction between the soluble urokinase plasminogen activator receptor and smoking on new-onset diabetes (P < 0.0001).

Results  New-onset diabetes (n = 182) was associated with increased soluble urokinase plasminogen activator receptor levels (P = 0.013). Among 699 middle-aged (41 and 51 years) and 564 older (61 and 71 years) non-smokers, participants in the upper soluble urokinase plasminogen activator receptor quartile had a sex- and age-adjusted relative risk of 6.01 (95% CI 2.17-16.6, P < 0.0006) and relative risk of 3.25 (95% CI 1.51-6.98, P = 0.0025), respectively, for new-onset diabetes compared with participants in the lowest quartile. This relationship remained significant after additional adjustments for C-reactive protein and leukocytes or fasting glucose and insulin or BMI (P < 0.05). The soluble urokinase plasminogen activator receptor was not related to incident diabetes among smokers (P ≥ 0.85).

Conclusions  In these explorative analyses, the soluble urokinase plasminogen activator receptor associated independently with incident diabetes in non-smokers, supporting an immune origin of Type 2 diabetes. Competing disease risk may explain lack of association among smokers.

  B. Guigas , J. E. de Leeuw van Weenen , N. van Leeuwen , A. M. Simonis-Bik , T. W. van Haeften , G. Nijpels , J. J. Houwing-Duistermaat , M. Beekman , J. Deelen , L. M. Havekes , B. W. J. H. Penninx , N. Vogelzangs , E. van t Riet , A. Dehghan , A. Hofman , J. C. Witteman , A. G. Uitterlinden , N. Grarup , T. Jorgensen , D. R. Witte , T. Lauritzen , T. Hansen , O. Pedersen , J. Hottenga , J. A. Romijn , M. Diamant , M. H. H. Kramer , R. J. Heine , G. Willemsen , J. M. Dekker , E. M. Eekhoff , H. Pijl , E. J. de Geus , P. E. Slagboom and L. M. t Hart


Modulation of dopamine receptor D2 (DRD2) activity affects insulin secretion in both rodents and isolated pancreatic β-cells. We hypothesized that single nucleotide polymorphisms in the DRD2/ANKK1 locus may affect susceptibility to Type 2 diabetes in humans.


Four potentially functional variants in the coding region of the DRD2/ANKK1 locus (rs1079597, rs6275, rs6277, rs1800497) were genotyped and analysed for Type 2 diabetes susceptibility in up to 25 000 people (8148 with Type 2 diabetes and 17687 control subjects) from two large independent Dutch cohorts and one Danish cohort. In addition, 340 Dutch subjects underwent a 2-h hyperglycaemic clamp to investigate insulin secretion. Since sexual dimorphic associations related to DRD2 polymorphisms have been previously reported, we also performed a gender-stratified analysis.


rs1800497 at the DRD2/ANKK1 locus was associated with a significantly increased risk for Type 2 diabetes in women (odds ratio 1.14 (1.06-1.23); = 4.1*10−4) but not in men (odds ratio 1.00 (95% CI 0.93-1.07); = 0.92) or the combined group. Although rs1800497 was not associated with insulin secretion, we did find another single nucleotide polymorphism in this locus, rs6275, to be associated with increased first-phase glucose-stimulated insulin secretion in women (= 5.5*10−4) but again not in men (= 0.34).


The present data identify DRD2/ANKK1 as a potential sex-specific Type 2 diabetes susceptibility gene.

  C Pisinger , M. M Jorgensen , N. E Moller , M Dossing and T. Jorgensen

Reviews state that there is a room for improvements of smoking cessation (SC) intervention in general practice.


In 2005, all 61 general practitioners (GPs) in four municipalities in Copenhagen, Denmark, were invited to participate. Twenty-four GPs accepted and were cluster randomized to one of three groups: Group A, referral to group-based SC counselling (national model), n = 10; Group B, referral to internet-based SC programme (newly developed), n = 8; or Group C, no referral (‘do as usual’), n = 6. A total of 1518/1914 smokers were included, and 760 returned a questionnaire at 1-year follow-up.


The participating GPs reported significantly more SC counselling than GPs who refused participation (P = 0.04). Self-reported point abstinence was 6.7% (40/600), 5.9% (28/476) and 5.7% (25/442) in Groups A, B and C, respectively. Only 40 smokers attended group-based SC counselling, and 75 logged in at the internet-based SC programme. In cluster analyses, we found no significant additional effect of referral to group-based (OR: 1.05; 95% CI: 0.6–1.8) or internet-based SC programmes (OR: 0.91; 95% CI: 0.6–1.4).


We found no additional effect on cessation rates of GPs' referring to group-based SC counselling or internet-based SC programme. This finding might, to some degree, be explained by the short time used by the GPs on SC counselling and the selection of the participating doctors.

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