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  • 1
    Electronic Resource
    Electronic Resource
    mRNA expression of the long and short forms of uncoupling protein-3 in obese and lean humans (1998)
    Springer
    Diabetologia 41 (1998), S. 829-832 
    Details
    ISSN: 1432-0428
    Keywords: Keywords Uncoupling protein-3 ; obesity ; fasting ; skeletal muscle ; thermogenesis.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Uncoupling protein-3 (UCP3) is a mitochondrial protein expressed in skeletal muscle, an important site of thermogenesis in humans. By uncoupling respiration from ATP synthesis, UCP3 might be involved in the control of energy expenditure. Two transcripts encoding long (UCP3L) and short (UCP3S) form are generated from the human UCP3 gene. UCP3S is predicted to encode a protein which lacks the C-terminus of UCP3L, a region which contains motifs critical for uncoupling activity. We have investigated the regulation of UCP3L and UCP3S mRNAs in lean and obese humans. A specific reverse transcription-competitive polymerase chain reaction assay was developed to separately quantify the two mRNAs. Each transcript represents half of total UCP3 mRNA in 16 vastus lateralis muscle samples. The amounts of UCP3L and UCP3S mRNAs did not differ between obese and lean subjects. The effect of fasting was studied in six lean and seven obese subjects maintained on a hypocaloric diet (1045 kJ/d) for 5 days. Calorie restriction results in an approximately threefold increase of UCP3L and UCP3S mRNA levels. The induction was similar in lean and obese subjects. The data suggest that there is no major alteration of UCP3 gene expression and regulation at the level of transcription and alternative splicing in skeletal muscle of obese subjects. [Diabetologia (1998) 41: 829–832]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250050994
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  • 2
    Electronic Resource
    Electronic Resource
    Regulation of gene expression during severe caloric restriction: lack of induction of p85alpha phosphatidylinositol 3-kinase mRNA in skeletal muscle of patients with Type II (non-insulin-dependent) diabetes mellitus (2000)
    Springer
    Diabetologia 43 (2000), S. 356-363 
    Details
    ISSN: 1432-0428
    Keywords: Keywords Phosphatidylinositol-3-kinase, insulin receptor, Rad, hexokinase II, GLUT 4, lipoprotein lipase, insulin resistance.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Aims/hypothesis. Alterations in the regulation of gene expression could be involved in the development of Type II (non-insulin-dependent) diabetes mellitus.¶Methods. We compared the mRNA concentrations of eight genes encoding proteins involved in insulin action and intermediary metabolism in skeletal muscle of healthy volunteers and Type II diabetic patients. The in vivo regulation of the expression of these genes was investigated after 5 days of hypocaloric diet (1045 kJ/day).¶Results. In the basal state, diabetic muscle showed reduced insulin receptor (–38 %), hexokinase II (–73 %), glycogen synthase (–45 %) and lipoprotein lipase (–70 %) mRNA expression. There was no difference in the mRNA abundances of IRS-1, GLUT 4, p85α phosphatidylinositol-3-kinase (p85αPI3K) or Rad. In both groups, caloric restriction induced weight loss, reduced glycaemia and increased plasma ketone body concentrations. The diet also increased plasma concentrations of fatty acids and decreased whole-body insulin sensitivity in control subjects. In control subjects, the diet increased p85αPI3K ( + 146 %), insulin receptor ( + 100 %) and Rad ( + 40 %) mRNA concentrations in muscle. In Type II diabetic patients, the diet increased insulin receptor ( + 41 %) and Rad ( + 31 %) mRNAs but the expression of p85αPI3K was not modified.¶Conclusion/interpretation. The regulation of the expression of p85αPI3K is altered during caloric restriction in skeletal muscle of Type II diabetic patients. Because we have shown in an earlier study that there is also a defective regulation of p85αPI3K gene expression in response to insulin, these data support the hypothesis that alterations in the regulation of gene expression could be involved in the pathogenesis of Type II diabetes. [Diabetologia (2000) 43: 356–363]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250050054
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  • 3
    Electronic Resource
    Electronic Resource
    Defective regulation of phosphatidylinositol-3-kinase gene expression in skeletal muscle and adipose tissue of non-insulin-dependent diabetes mellitus patients (1999)
    Springer
    Diabetologia 42 (1999), S. 358-364 
    Details
    ISSN: 1432-0428
    Keywords: Keywords Hyperinsulinaemic clamp ; insulin receptor ; IRS-1 ; RT-PCR.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary We investigated the regulation of the mRNA expression of the insulin receptor, insulin receptor substrate-1 (IRS-1) and p85α-phosphatidylinositol-3-kinase (PI-3K), three major actors of insulin action, in skeletal muscle from 10 healthy lean volunteers, 13 obese patients with Type II (non-insulin-dependent) diabetes mellitus and 7 non-diabetic obese subjects. The in vivo regulation by insulin was studied using a 3-h euglycaemic, hyperinsulinaemic clamp. There were no differences in the basal concentrations of the three mRNAs in skeletal muscle between groups. Insulin infusion produced a twofold reduction in insulin receptor substrate-1 mRNA expression in the three groups (p 〈 0.02). In contrast, insulin increased p85α-phosphatidylinositol-3-kinase mRNA expression in muscle from non-diabetic subjects ( + 98 ± 22 % in lean and + 127 ± 16 % in obese, p 〈 0.02) but this effect was totally impaired in Type II diabetic patients ( + 5 ± 12 %, NS). A similar defect in insulin action on p85α-phosphatidylinositol-3-kinase mRNA expression was observed in abdominal subcutaneous adipose tissue ( + 138 ± 25 %, p 〈 0.01 in lean and + 46 ± 14 %, p 〈 0.02 in obese and + 29 ± 11 %, NS in Type II diabetic patients). The lack of action of insulin on p85α-phosphatidylinositol-3-kinase mRNA in diabetic subjects was probably not due to a deleterious effect of hyperglycaemia since improvement of the glycaemic control for 10 days did not restore the response in muscle or in adipose tissue. This study provides evidence for a defect in the regulation by insulin of PI-3K gene expression in Type II diabetic patients, thus reinforcing the concept that alterations at the gene expression might be involved in the pathogeny of Type II diabetes. [Diabetologia (1999) 42: 358–364]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250051163
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    Paper (German National Licenses)
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