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Sökning: swepub > (2000-2011) > Groop Leif > Ridderstråle Martin

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21.
  • Nilsson, Emma A, et al. (författare)
  • Genetic and Nongenetic Regulation of CAPN10 mRNA Expression in Skeletal Muscle.
  • 2005
  • Ingår i: Diabetes. - : American Diabetes Association. - 1939-327X .- 0012-1797. ; 54:10, s. 3015-3020
  • Tidskriftsartikel (refereegranskat)abstract
    • The gene encoding calpain-10 (CAPN10) has been identified as a candidate gene for type 2 diabetes. Our aim was to study the impact of genetic (heritability and polymorphisms) and nongenetic (insulin, free fatty acids, and age) factors on CAPN10 mRNA expression in skeletal muscle using two different study designs. Muscle biopsies were obtained before and after hyperinsulinemic-euglycemic clamps from 166 young and elderly monozygotic and dizygotic twins as well as from 15 subjects with normal (NGT) or impaired glucose tolerance (IGT) exposed to an Intralipid infusion. We found hereditary effects on both basal and insulin-exposed CAPN10 mRNA expression. Carriers of the type 2 diabetes–associated single nucleotide polymorphism (SNP)-43 G/G genotype had reduced CAPN10 mRNA levels compared with subjects carrying the SNP-43 A-allele. Age had no significant influence on CAPN10 mRNA levels. Insulin had no significant effect on CAPN10 mRNA levels, neither in the twins nor in the basal state of the Intralipid study. However, after a 24-h infusion of Intralipid, we noted a significant increase in CAPN10 mRNA in response to insulin in subjects with NGT but not in subjects with IGT. In conclusion, we provide evidence that mRNA expression of CAPN10 in skeletal muscle is under genetic control. Glucose-tolerant but not glucose-intolerant individuals upregulate their CAPN10 mRNA levels in response to prolonged exposure to fat.
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22.
  • Nilsson, Emma A, et al. (författare)
  • Role of the FOXC2 -512C>T polymorphism in type 2 diabetes: possible association with the dysmetabolic syndrome.
  • 2005
  • Ingår i: International Journal of Obesity. - : Springer Science and Business Media LLC. - 1476-5497 .- 0307-0565. ; 29:Dec 14, s. 268-274
  • Tidskriftsartikel (refereegranskat)abstract
    • OBJECTIVE: Overexpression of the human transcription factor FOXC2 gene ( FOXC2) protects against insulin resistance in mice and a common FOXC2 polymorphism (-512C > T) has been suggested to be associated with insulin resistance in humans. Here, we addressed the potential role for FOXC2 as a candidate gene for type 2 diabetes and associated phenotypes. MATERIALS AND METHODS: A case-control study was performed in 390 type 2 diabetic patients and 307 control subjects. The number of patients was increased to a total of 768 subjects for further study of phenotypic differences relating to the dysmetabolic syndrome relative to genetic variation. The FOXC2 -512C > T polymorphism was genotyped by a restriction fragment length polymorphism PCR assay. RESULTS: FOXC2 -512C > T allele and genotype distribution did not differ between patients with type 2 diabetes and control subjects, but the C/C genotype was associated with increased body mass index (BMI, kg/m(2)) (P-a = 0.03) among type 2 diabetic patients. The FOXC2 -512C > T polymorphism was a significant independent predictor of BMI (P = 0.001) in a multiple regression model including age, gender and affection status. We found no significant association with type 2 diabetes-related metabolic parameters but that the C-allele (P = 0.01) and C/C and C/T genotypes (P = 0.03) were significantly over-represented in type 2 diabetic males with a concomitant diagnosis of dysmetabolic syndrome. CONCLUSION: We conclude that FOXC2 is associated with obesity and metabolic deterioration but does not contribute to an increased risk for type 2 diabetes.
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24.
  • Nilsson, Emma, et al. (författare)
  • Regulation of skeletal muscle PPAR delta mRNA expression in twins
  • 2007
  • Ingår i: Journal of Physiology. - : Wiley. - 1469-7793 .- 0022-3751. ; 584:3, s. 1011-1017
  • Tidskriftsartikel (refereegranskat)abstract
    • Peroxisome proliferator-activated receptors (PPARs) are nuclear receptors regulating the expression of genes involved in lipid and glucose metabolism in a complex and to some extent unknown manner. Our aim was to study the impact of different factors on PPAR delta mRNA expression in human skeletal muscle on one side, and the impact of PPAR delta mRNA expression on these factors, including glucose and lipid metabolism, aerobic capacity, fibre type composition and lipid profile, on the other side. PPAR delta mRNA levels were quantified by real-time PCR in muscle biopsies from 176 young and elderly monozygotic and dizygotic twins. Young twins had significantly increased PPAR delta mRNA levels compared with elderly twins. A 2 h hyperinsulinaemic euglycaemic clamp had no significant effect on PPAR delta mRNA levels. Biometric models were calculated for basal PPAR delta mRNA expression to estimate the degree of genetic versus environmental influence. In both young and elderly twins there was a substantial genetic component influencing basal PPAR delta mRNA levels. In a regression model, the muscle PPAR delta mRNA expression was correlated to birth weight, central adiposity and age. The level of PPAR delta mRNA was also positively correlated with markers for oxidative muscle fibres. However, in this apparently healthy study population, we found no correlations between PPAR delta mRNA expression and aerobic capacity, lipid profile or glucose and lipid metabolism. In conclusion, we provide evidence that mRNA expression of PPAR delta in human skeletal muscle is under genetic control but also influenced by factors such as age, birth weight and central adiposity.
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25.
  • Orho-Melander, Marju, et al. (författare)
  • Variants in the calpain-10 gene predispose to insulin resistance and elevated free fatty acid levels.
  • 2002
  • Ingår i: Diabetes. - : American Diabetes Association. - 1939-327X .- 0012-1797. ; 51:8, s. 2658-2664
  • Tidskriftsartikel (refereegranskat)abstract
    • The calpain-10 gene (CAPN10) has been associated with type 2 diabetes, but information on molecular and physiological mechanisms explaining this association is limited. Here we addressed this question by studying the role of CAPN10 for phenotypes associated with type 2 diabetes and free fatty acid (FFA) metabolism. Among 395 type 2 diabetic patients and 298 nondiabetic control subjects from Finland, the SNP-43 allele 1 (P = 0.011), SNP-63 allele 2 (P = 0.010), and the haplotype combination SNP-44/43/19/63 1121/1121 (P = 0.028) were associated with type 2 diabetes. The SNP-43 genotypes 11 and 12 were associated with higher fasting insulin and homeostasis model assessment (HOMA) insulin resistance index among control subjects (P = 0.021 and P = 0.0076) and with elevated FFA among both control subjects (P = 0.0040) and type 2 diabetic patients (P = 0.0025). Multiple regression analysis further indicated that SNP-43 is an independent predictor of FFA levels (P = 0.0037). Among 80 genotype discordant sibling pairs, the SNP-43 allele 1 was associated with elevated fasting serum insulin and HOMA index (P = 0.013 and P = 0.0068). None of the four SNPs showed distorted transmission of alleles to patients with type 2 diabetes in a qualitative transmission disequilibrium test, including 108 trios. Because FFA and insulin resistance are known to predict type 2 diabetes, the finding that variation in the CAPN10 gene influences FFA levels and insulin resistance may provide an explanation for how the CAPN10 gene increases susceptibility to type 2 diabetes.
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27.
  • Ridderstråle, Martin, et al. (författare)
  • Differential phosphorylation of Janus kinase 2, Stat5A and Stat5B in response to growth hormone in primary rat adipocytes
  • 2001
  • Ingår i: Molecular and Cellular Endocrinology. - 1872-8057. ; 183:1-2, s. 49-54
  • Tidskriftsartikel (refereegranskat)abstract
    • In vitro growth hormone (GH) stimulation of Janus kinase 2 (Jak2) tyrosine phosphorylation and activation has been detected in rat adipocytes where GH exerts both chronic diabetogenic and acute insulin-like effects but not in adipocytes where only chronic diabetogenic effects are exerted. The 95 kDa transcription factor Stat5, which is tyrosine phosphorylated in response to GH in both cases, is here identified as the 5A-isoform. Stat5B was not tyrosine phosphorylated in response to GH in adipocytes but subject to a gel supershift indicating regulation by serine and/or threonine phosphorylation. The differential tyrosine phosphorylation of these proteins suggests involvement of a kinase other than Jak2 in Stat5A activation. However, in adipocytes where GH exerts both diabetogenic and insulin-like effects, and both Jak2 and Stat5A were activated, their phosphorylation kinetics and downregulation of tyrosine phosphorylation were almost identical. We conclude that Stat5A is important for the diabetogenic actions of GH and that Jak2 still is the most probable candidate kinase for Stat5A in primary adipocytes.
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28.
  • Ridderstråle, Martin, et al. (författare)
  • Fallbeskrivning. Rosiglitazonbehandling gav kraftfull effekt, men fick ändå avbrytas
  • 2002
  • Ingår i: Läkartidningen. - 0023-7205. ; 99:5, s. 407-410
  • Tidskriftsartikel (refereegranskat)abstract
    • The thiazolidinediones were introduced as oral hypoglycemic drugs in Sweden during the fall of 2000. A case is reported in which a woman with insulin-dependent type-2 diabetes and both macro- and microangiopathy and pronounced insulin resistance was treated with rosiglitazone (Avandia). Within three months insulin doses could be reduced by 36% (from 176 to 112 units insulin daily) and concomitantly Ery-HbA1c was reduced from 8.4 to 5.3%. In spite of this dramatic effect on glucose homeostasis administration of the drug had to be discontinued due to critical congestive heart failure.
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29.
  • Ridderstråle, Martin, et al. (författare)
  • FOXC2 mRNA Expression and a 5' Untranslated Region Polymorphism of the Gene Are Associated With Insulin Resistance.
  • 2002
  • Ingår i: Diabetes. - : American Diabetes Association. - 1939-327X .- 0012-1797. ; 51:12, s. 3554-3560
  • Tidskriftsartikel (refereegranskat)abstract
    • The human transcription factor FOXC2 has recently been shown to protect against diet-induced insulin resistance in transgenic mice. We investigated the expression of FOXC2 in fat and muscle and performed a genetic analysis in human subjects. FOXC2 mRNA levels were increased in visceral compared with subcutaneous fat from obese subjects (12 ± 4-fold; P = 0.0001), and there was a correlation between whole-body insulin sensitivity and FOXC2 mRNA levels in visceral fat (fS-insulin R = −0.64, P = 0.01, and homeostasis model assessment of insulin resistance [HOMA-IR] R = −0.68, P = 0.007) and skeletal muscle (fS-insulin R = −0.57, P = 0.03, and HOMA-IR R = −0.55, P = 0.04). Mutation screening of the FOXC2 gene identified a common polymorphism in the 5′ untranslated region (C-512T). The T allele was associated with enhanced insulin sensitivity (HOMA-IR P = 0.007) and lower plasma triglyceride levels in females (P = 0.007). Also, the higher expression of FOXC2 in visceral than in subcutaneous fat was restricted to subjects homozygous for the T allele (P = 0.03 vs. P = 0.7). Our data suggest that increased FOXC2 expression may protect against insulin resistance in human subjects and that genetic variability in the gene may influence features associated with the metabolic syndrome.
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30.
  • Ridderstråle, Martin, et al. (författare)
  • Genetic dissection of type 2 diabetes.
  • 2009
  • Ingår i: Molecular and Cellular Endocrinology. - : Elsevier BV. - 1872-8057 .- 0303-7207. ; 2008:Oct 19, s. 10-17
  • Tidskriftsartikel (refereegranskat)abstract
    • Compared to the successful probing of genetic causes of monogenic disorders, dissecting the genetics of complex polygenic diseases has until recently been a fairly slow and cumbersome process. With the introduction of whole genome wide association studies (WGAS) the situation dramatically changed in 2007. The results from several recent WGAS on type 2 diabetes (T2D) and obesity have identified at least eighteen genes consistently associated with T2D. Many of the genes implicate pancreatic beta-cell function in the pathogenesis of T2D whereas only one clearly associate with insulin resistance. The identified genes most likely merely represent the tip of the iceberg in the explanation behind T2D. Refined tools will have to provide a more complete picture of the genetic complexity of T2D over the next few years. In addition to common variants increasing susceptibility for the disease, rare variants with stronger effects, copy number variations, and epigenetic effects like DNA methylation and histone acetylation will become important. Nevertheless, today we are able for the first time to anticipate that the genetics of a complex disease like T2D really can be dissected.
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