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  • 1.
    Björkman, Frida
    et al.
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences.
    Holm, Karin
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences.
    Fysisk status hos pojkar med typ 1 diabetes2008Independent thesis Basic level (degree of Bachelor), 10 credits / 15 HE creditsStudent thesis
    Abstract [en]

    Aim

    The aim of this study was to survey the physical fitness in boys with type 1 diabetes (IDDM). The results were compared to a control group with healthy boys that have preformed the same tests in other studies. Our questions were:

    1. How does BMI relate between IDDM-children and healthy peers?

    2. How does physical activity level relate between IDDM-children and healthy peers?

    3. How does aerobic fitness (VO2max), grip strength and balance relate between IDDM-children and healthy peers?

    Method

    Subjects were recruited in cooperation with Astrid Lindgrens Barnsjukhus. Height, body mass, VO2max, grip strength, balance and measurement of physical activity level with accelerometry were data collected from five boys with type 1 diabetes. The results were compared to data found in healthy subjects. The collected data were presented as z scores.

    Results

    Two subjects showed a main difference in their test results compared to the mean value of healthy boys. The subjects that were deviated from mean values performed poor results in some or all of the tests. Only two subjects provided sufficiently registration of physical activity level for comparison with the control group. Data showed a lower activity level in one subject compared to healthy controls and a higher activity level in the other subject.

    Conclusions

    The examined group cannot be proven to be a representative selection, and no general conclusion regarding children with type 1 diabetes and their physical status could be drawn. No statistic significant differences could be found based on the data of this study. One notable tendency was that the subjects that differs a lot from mean values in some test also show the same discrepancy in the other tests.

  • 2. Fakhrai-Rad, H
    et al.
    Nikoshkov, A
    Kamel, A
    Fernström, Maria
    Karolinska institutet.
    Zierath, J R
    Norgren, S
    Luthman, H
    Galli, J
    Insulin-degrading enzyme identified as a candidate diabetes susceptibility gene in GK rats.2000In: Human Molecular Genetics, ISSN 0964-6906, E-ISSN 1460-2083, Vol. 9, no 14, p. 2149-58Article in journal (Refereed)
    Abstract [en]

    Genetic analysis of the diabetic GK rat has revealed several diabetes susceptibility loci. Congenic strains have been established for the major diabetes locus, Niddm1, by transfer of GK alleles onto the genome of the normoglycemic F344 rat. Niddm1 was dissected into two subloci, physically separated in the congenic strains Niddm1b and Niddm1i, each with at least one disease susceptibility gene. Here we have mapped Niddm1b to 1 cM by genetic and pathophysiological characterization of new congenic substrains for the locus. The gene encoding insulin-degrading enzyme (IDE:) was located to this 1 cM region, and the two amino acid substitutions (H18R and A890V) identified in the GK allele reduced insulin-degrading activity by 31% in transfected cells. However, when the H18R and A890V variants were studied separately, no effects were observed, demonstrating a synergistic effect of the two variants on insulin degradation. No effect on insulin degradation was observed in cell lysates, indicating that the effect is coupled to receptor-mediated internalization of insulin. Congenic rats with the IDE: GK allele displayed post-prandial hyperglycemia, reduced lipogenesis in fat cells, blunted insulin-stimulated glucose transmembrane uptake and reduced insulin degradation in isolated muscle. Analysis of additional rat strains demonstrated that the dysfunctional IDE: allele was unique to GK. These data point to an important role for IDE: in the diabetic phenotype in GK.

  • 3.
    Fernström, Maria
    et al.
    Karolinska institutet.
    Song, Xiao Mei
    Karolinska institutet.
    Galuska, Dana
    Karolinska institutet.
    Fiedler, Maj
    Pharmacia & UpJohn.
    Rincon, Jorge
    Karolinska institutet.
    Ryder, Jeffrey W
    Karolinska institutet.
    Liang, Yin
    Pharmacia & UpJohn.
    Krook, Anna
    Karolinska institutet.
    Zierath, Juleen R
    Karolinska institutet.
    AICAR-treatment improves glucose homeostasis in ob/ob mice2000In: Diabetes Research and Clinical Practice, ISSN 0168-8227, E-ISSN 1872-8227, Vol. 50, no Suppl 1, p. 396-396Article in journal (Refereed)
  • 4.
    Fiedler, Maj
    et al.
    Pharmacia.
    Liang, Yin
    Pharmacia.
    Song, Xiao Mei
    Karolinska institutet.
    Fernström, Maria
    Karolinska institutet.
    Zierath, Juleen R
    Karolinska institutet.
    Selén, Göran
    Pharmacia.
    Klingström, Gunnel
    Pharmacia.
    Sakariassen, Kjell S
    Pharmacia.
    AICAR (5-aminoimidazole-4-carboxamide ribonucleoside) ameliorates hyperglycemia and hyperinsulinemia in type 2 diabetic mice2000In: Diabetes Research and Clinical Practice, ISSN 0168-8227, E-ISSN 1872-8227, Vol. 50, no Suppl 1, p. 397-397Article in journal (Refereed)
  • 5. Haglind, Charlotte
    et al.
    Ask, Sara
    von Döbeln, Ulrika
    Ekblom, Örjan
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Åstrand Laboratory of Work Physiology, Björn Ekblom's and Mats Börjesson's research group.
    Stenlid, Maria
    Nordenström, Anna
    Energy expenditure and lipid metabolism in very long-chain Acyl-CoA dehydrogenase (VLCAD) deficiency2015In: Molecular Genetics and Metabolism (ISSN 1096-7192), 2015, Vol. 114, no 3, p. 333-333Conference paper (Refereed)
  • 6. Hey-Mogensen, M
    et al.
    Højlund, K
    Vind, B F
    Wang, Li
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Åstrand Laboratory of Work Physiology, Research group for Mitokondriell funktion och metabolisk kontroll.
    Dela, F
    Beck-Nielsen, H
    Fernström, Maria
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Åstrand Laboratory of Work Physiology.
    Sahlin, Kent
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Åstrand Laboratory of Work Physiology, Research group for Mitokondriell funktion och metabolisk kontroll.
    Effect of physical training on mitochondrial respiration and reactive oxygen species release in skeletal muscle in patients with obesity and type 2 diabetes.2010In: Diabetologia, ISSN 0012-186X, E-ISSN 1432-0428, Vol. 53, no 9, p. 1976-85Article in journal (Refereed)
    Abstract [en]

    AIM/HYPOTHESIS: Studies have suggested a link between insulin resistance and mitochondrial dysfunction in skeletal muscles. Our primary aim was to investigate the effect of aerobic training on mitochondrial respiration and mitochondrial reactive oxygen species (ROS) release in skeletal muscle of obese participants with and without type 2 diabetes. METHODS: Type 2 diabetic men (n = 13) and control (n = 14) participants matched for age, BMI and physical activity completed 10 weeks of aerobic training. Pre- and post-training muscle biopsies were obtained before a euglycaemic-hyperinsulinaemic clamp and used for measurement of respiratory function and ROS release in isolated mitochondria. RESULTS: Training significantly increased insulin sensitivity, maximal oxygen consumption and muscle mitochondrial respiration with no difference between groups. When expressed in relation to a marker of mitochondrial density (intrinsic mitochondrial respiration), training resulted in increased mitochondrial ADP-stimulated respiration (with NADH-generating substrates) and decreased respiration without ADP. Intrinsic mitochondrial respiration was not different between groups despite lower insulin sensitivity in type 2 diabetic participants. Mitochondrial ROS release tended to be higher in participants with type 2 diabetes. CONCLUSIONS/INTERPRETATION: Aerobic training improves muscle respiration and intrinsic mitochondrial respiration in untrained obese participants with and without type 2 diabetes. These adaptations demonstrate an increased metabolic fitness, but do not seem to be directly related to training-induced changes in insulin sensitivity.

  • 7. Mogensen, M
    et al.
    Vind, B F
    Højlund, K
    Beck-Nielsen, H
    Sahlin, Kent
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Research group for Mitokondriell funktion och metabolisk kontroll.
    Maximal lipid oxidation in patients with type 2 diabetes is normal and shows an adequate increase in response to aerobic training.2009In: Diabetes, obesity and metabolism, ISSN 1462-8902, E-ISSN 1463-1326, Vol. 11, no 9, p. 874-83Article in journal (Refereed)
    Abstract [en]

    AIM: Insulin resistance in subjects with type 2 diabetes (T2D) and obesity is associated with an imbalance between the availability and the oxidation of lipids. We hypothesized that maximal whole-body lipid oxidation during exercise (FATmax) is reduced and that training-induced metabolic adaptation is attenuated in T2D. METHODS: Obese T2D (n = 12) and control (n = 11) subjects matched for age, sex, physical activity and body mass index completed 10 weeks of aerobic training. Subjects were investigated before and after training with maximal and submaximal exercise tests and euglycaemic-hyperinsulinaemic clamps combined with muscle biopsies. RESULTS: Training increased maximal oxygen consumption (VO(2max)) and muscle citrate synthase activity and decreased blood lactate concentrations during submaximal exercise in both groups (all p < 0.01). FATmax increased markedly (40-50%) in both T2D and control subjects after training (all p < 0.001). There were no significant differences in these variables and lactate threshold (%VO(2max)) between groups before or after training. Insulin-stimulated glucose disappearance rate (Rd) was lower in T2D vs. control subjects both before and after training. Rd increased in response to training in both groups (all p < 0.01). There was no correlation between Rd and measures of oxidative capacity or lipid oxidation during exercise or the training-induced changes in these parameters. CONCLUSIONS: FATmax was not reduced in T2D, and muscle oxidative capacity increased adequately in response to aerobic training in obese subjects with and without T2D. These metabolic adaptations to training seem to be unrelated to changes in insulin sensitivity and indicate that an impaired capacity for lipid oxidation is not a major cause of insulin resistance in T2D.

  • 8.
    Mogensen, Martin
    et al.
    University of Southern Denmark, Odense, Denmark.
    Sahlin, Kent
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Åstrand Laboratory of Work Physiology, Research group for Mitokondriell funktion och metabolisk kontroll. University of Southern Denmark, Odense, Denmark.
    Fernström, Maria
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Åstrand Laboratory of Work Physiology. Karolinska institutet.
    Glintborg, Dorte
    Odense University Hospital, Odense, Denmark.
    Vind, Birgitte F
    Odense University Hospital, Odense, Denmark.
    Beck-Nielsen, Henning
    Odense University Hospital, Odense, Denmark.
    Højlund, Kurt
    Odense University Hospital, Odense, Denmark.
    Mitochondrial respiration is decreased in skeletal muscle of patients with type 2 diabetes.2007In: Diabetes, ISSN 0012-1797, E-ISSN 1939-327X, Vol. 56, no 6, p. 1592-9Article in journal (Refereed)
    Abstract [en]

    We tested the hypothesis of a lower respiratory capacity per mitochondrion in skeletal muscle of type 2 diabetic patients compared with obese subjects. Muscle biopsies obtained from 10 obese type 2 diabetic and 8 obese nondiabetic male subjects were used for assessment of 3-hydroxy-Acyl-CoA-dehydrogenase (HAD) and citrate synthase activity, uncoupling protein (UCP)3 content, oxidative stress measured as 4-hydroxy-2-nonenal (HNE), fiber type distribution, and respiration in isolated mitochondria. Respiration was normalized to citrate synthase activity (mitochondrial content) in isolated mitochondria. Maximal ADP-stimulated respiration (state 3) with pyruvate plus malate and respiration through the electron transport chain (ETC) were reduced in type 2 diabetic patients, and the proportion of type 2X fibers were higher in type 2 diabetic patients compared with obese subjects (all P < 0.05). There were no differences in respiration with palmitoyl-l-carnitine plus malate, citrate synthase activity, HAD activity, UCP3 content, or oxidative stress measured as HNE between the groups. In the whole group, state 3 respiration with pyruvate plus malate and respiration through ETC were negatively associated with A1C, and the proportion of type 2X fibers correlated with markers of insulin resistance (P < 0.05). In conclusion, we provide evidence for a functional impairment in mitochondrial respiration and increased amount of type 2X fibers in muscle of type 2 diabetic patients. These alterations may contribute to the development of type 2 diabetes in humans with obesity.

  • 9. Song, X M
    et al.
    Fiedler, M
    Galuska, D
    Ryder, J W
    Fernström, Maria
    Karolinska institutet.
    Chibalin, A V
    Wallberg-Henriksson, H
    Zierath, J R
    5-Aminoimidazole-4-carboxamide ribonucleoside treatment improves glucose homeostasis in insulin-resistant diabetic (ob/ob) mice.2002In: Diabetologia, ISSN 0012-186X, E-ISSN 1432-0428, Vol. 45, no 1, p. 56-65Article in journal (Refereed)
    Abstract [en]

    AIMS/HYPOTHESIS: The 5'AMP-activated protein kinase is an important mediator of muscle contraction-induced glucose transport and a target for pharmacological treatment of Type II (non-insulin-dependent) diabetes mellitus. The 5'AMP-activated protein kinase can be activated by 5-aminoimidazole-4-carboxamide ribonucleoside. We hypothesised that 5-aminoimidazole-4-carboxamide ribonucleoside treatment could restore glucose homeostasis in ob/ob mice.

    METHODS: Lean and ob/ob mice were given 5-aminoimidazole-4-carboxamide ribonucleoside (1 mg.g body wt(-1).day(-1) s.c) or 0.9 % NaCl (vehicle) for 1-7 days.

    RESULTS: Short-term 5-aminoimidazole-4-carboxamide ribonucleoside treatment normalised glucose concentrations in ob/ob mice within 1 h, with effects persisting over 4 h. After 1 week of daily injections, 5-aminoimidazole-4-carboxamide ribonucleoside treatment corrected hyperglycaemia, improved glucose tolerance, and increased GLUT4 and hexokinase II protein expression in skeletal muscle, but had deleterious effects on plasma non-esterified fatty acids and triglycerides. Treatment with 5-aminoimidazole-4-carboxamide ribonucleoside increased liver glycogen in fasted and fed ob/ob mice and muscle glycogen in fasted, but not fed ob/ob and lean mice. Defects in insulin-stimulated phosphatidylinositol 3-kinase and glucose transport in skeletal muscle from ob/ob mice were not corrected by 5-aminoimidazole-4-carboxamide ribonucleoside treatment. While ex vivo insulin-stimulated glucose transport was reduced in isolated muscle from ob/ob mice, the 5-aminoimidazole-4-carboxamide ribonucleoside stimulated response was normal.

    CONCLUSION/INTERPRETATION: The 5-aminoimidazole-4-carboxamide ribonucleoside mediated improvements in glucose homeostasis in ob/ob mice can be explained by effects in skeletal muscle and liver. Due to the apparently deleterious effects of 5-aminoimidazole-4-carboxamide ribonucleoside on the blood lipid profile, strategies to develop tissue-specific and pathway-specific activators of 5'AMP-activated protein kinase should be considered in order to improve glucose homeostasis.

  • 10. Tsuchida, Hiroki
    et al.
    Björnholm, Marie
    Fernström, Maria
    Karolinska institutet.
    Galuska, Dana
    Johansson, Per
    Wallberg-Henriksson, Harriet
    Zierath, Juleen R
    Lake, Staffan
    Krook, Anna
    Gene expression of the p85alpha regulatory subunit of phosphatidylinositol 3-kinase in skeletal muscle from type 2 diabetic subjects.2002In: Pflügers Archiv: European Journal of Physiology, ISSN 0031-6768, E-ISSN 1432-2013, Vol. 445, no 1, p. 25-31Article in journal (Refereed)
    Abstract [en]

    The gene of the p85alpha regulatory subunit of phosphatidylinositol (PI) 3-kinase gives rise to several splice variants. We hypothesized that the expression of p85alpha splice variants may be altered in skeletal muscle from subjects with type 2 diabetes mellitus. Skeletal muscle biopsies were obtained from nine type 2 diabetic and eight healthy men, matched for age, body mass index (BMI) and physical fitness. PI 3-kinase activity in skeletal muscle following in vitro insulin stimulation was reduced in subjects with type 2 diabetes. p85alpha mRNA was elevated fourfold in type 2 diabetic as compared to healthy control subjects ( P<0.05). p85alpha mRNA abundance was positively correlated with plasma insulin concentration ( P<0.01) and serum glucose concentration ( P<0.01). Despite this, protein levels of p85alpha, p55alpha, and the novel human p50alpha were not altered in type 2 diabetic subjects. Thus, although gene expression of full-length p85alpha is increased in skeletal muscle from type 2 diabetics, this is not reflected by increased protein levels. Therefore, defects in PI 3-kinase activity are likely due to impaired activation of the enzyme rather than changes in protein expression of the isoforms of the regulatory subunit.

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