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Articles by T. Hansen
Total Records ( 4 ) for T. Hansen
  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.

  T. D. Clausen , E. L. Mortensen , L. Schmidt , E. R. Mathiesen , T. Hansen , D. M. Jensen , S. Holm , L. Poulsen , M. From and P. Damm
  Aims  Maternal diabetes may affect offspring cognitive function. The objective of the study was to evaluate cognitive function and potential predictors hereof in adult offspring of women with Type 1 diabetes.

Methods  We conducted a follow-up study of adult offspring of women with Type 1 diabetes (n = 158) and a reference group from the background population (n = 118). The main outcome measure was offspring cognitive function measured by global cognitive score, derived from Raven's Progressive Matrices and three verbal subtests from the Weschler Adult Intelligence Scale.

Results  Offspring of women with Type 1 diabetes obtained lower global cognitive scores (94.8 vs. 100.0, P = 0.004) than offspring from the background population. When adjusted for confounders, the groups no longer differed significantly (difference 0.4, 95% CI -3.3 to 4.). Positive predictors of cognitive function in offspring of women with diabetes were family social class, parental educational level, maternal diabetes duration, male gender and offspring age, whereas parity ≥ 1 and gestational age < 34 weeks were negative predictors. We found no association with maternal glycaemia during pregnancy or with neonatal hypoglycaemia.

Conclusions  Impaired cognitive function in adult offspring of women with Type 1 diabetes compared with the background population apparently reflects differences with respect to well-known confounders. However, harmful effects of maternal hyperglycaemia may be mediated through delivery at < 34 weeks.

  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
 

Aims

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.

Methods

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.

Results

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).

Conclusion

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

  S. Djurovic , A.K. Kahler , B. Kulle , E.G. Jonsson , I. Agartz , S. Le Hellard , H. Hall , K.D. Jakobsen , T. Hansen , I. Melle , T. Werge , V.M. Steen and O.A. Andreassen
  There is considerable evidence of altered glutamatergic signalling in schizophrenia and a polymorphic variant of the GRIK3 glutamate receptor gene on 1p34-33 has previously been associated to this psychotic disorder. We therefore conducted a systematic association study with 30 HapMap-selected tagging SNPs across GRIK3 in three independent samples of Scandinavian origin from the Scandinavian Collaboration of Psychiatric Etiology (SCOPE), including a total of 839 cases with schizophrenia spectrum and 1473 healthy controls.

Four markers (rs6671364, rs17461259, rs472188, and rs535620) attained nominally significant P-values in both the genotypic (0.002, 0.02, 0.03, and 0.05, respectively) and allelic (0.001, 0.006, 0.03, and 0.02, respectively) association tests for the combined sample, and 2 additional markers (rs481047and rs1160751) displayed significance for the genotype (P-values: 0.03 and 0.04). Several haplotypes, that all included at least one of the four SNPs implicated by the single marker analysis, remained significant after adjustment for multiple testing using permutations with 10,000 shuffles. In addition we observed an association for two of the four significant GRIK3 markers (rs472188 and rs535620) to scores for negative symptoms on the PANSS scale.

The present results, although not robust, support the importance of more extensive investigations of GRIK3, given its potential role in mediating risk for schizophrenia.

 
 
 
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