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  • IPF1  (1)
  • Peritoneal  (1)
  • closed-loop insulin therapy  (1)
  • 1
    Electronic Resource
    Electronic Resource
    Determination of peritoneal glucose kinetics in rats: implications for the peritoneal implantation of closed-loop insulin delivery systems (1989)
    Springer
    Diabetologia 32 (1989), S. 331-336 
    Details
    ISSN: 1432-0428
    Keywords: Peritoneal ; rat ; glucose kinetics ; closed-loop insulin therapy ; glucose sensor ; bioartificial pancreas
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Peritoneal glucose kinetics were evaluated in the anaesthetized rat, to assess whether the peritoneal cavity would be a suitable site for the implantation of membrane-protected islets of Langerhans (bioartificial pancreas) or the glucose sensor of an artificial B cell. Glucose was measured in peritoneal fluid samples aspirated by needle puncture. Basal peritoneal and blood glucose concentrations were identical in 16 h fasted (n=4) and non fasted (n=3) animals. After 10 min of an i.v. glucose infusion (n=15) the increment in peritoneal glucose concentration was 63±3% of the increment in blood glucose concentration and both values were significantly correlated (r=0.92; p〈0.001). After 10 min of glucose clamping (12.6±0.8 mmol/l), the increment in peritoneal glucose concentration was 69±3% (n=5; p〈0.05) of the increment in blood glucose concentration. In three additional experiments it was 93±3% of the increment in blood glucose concentration (NS), after 30 min of glucose clamping (8.0±0.5 mmol/l). Peritoneal glucose concentration monitored by a glucose sensor: (a) followed blood glucose sluggishly during a glucose clamp (n=5), confirming the data shown above, (b) followed blood glucose with a 5 min delay and reached the same plateau after the intravenous injection of 1U insulin (n=3; NS). We conclude that peritoneal glucose reflects blood glucose at basal state and during variations of glycaemia, nevertheless, presenting heterogeneous kinetics. These kinetics might be appropriate for a bioartificial pancreas but not for an in vivo calibration procedure, of a peritoneally implanted glucose sensor.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00277254
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Mutation screening in 18 Caucasian families suggest the existence of other MODY genes (1998)
    Springer
    Diabetologia 41 (1998), S. 1017-1023 
    Details
    ISSN: 1432-0428
    Keywords: Keywords Genetics ; MODY ; glucokinase gene ; HNF-1α ; HNF-4α ; HNF-1β ; IPF1 ; transcription factors
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Maturity-onset diabetes of the young (MODY) is a heterogeneous subtype of non-insulin-dependent diabetes mellitus characterised by early onset, autosomal dominant inheritance and a primary defect in insulin secretion. To date five MODY genes have been identified: hepatocyte nuclear factor-4 alpha (HNF-4 α/MODY1/TCF14) on chromosome 20 q, glucokinase (GCK/MODY2) on chromosome 7 p, hepatocyte nuclear factor-1 alpha (HNF-1 α/MODY3/TCF1) on chromosome 12 q, insulin promoter factor-1 (IPF1/MODY4) on chromosome 13 q and hepatocyte nuclear factor-1 beta (HNF-1 β/MODY5/TCF2) on chromosome 17cen-q. We have screened the HNF-4 α, HNF-1 α and HNF-1 β genes in members of 18 MODY kindreds who tested negative for glucokinase mutations. Five missense (G31D, R159W, A161T, R200W, R271W), one substitution at the splice donor site of intron 5 (IVS5nt + 2T→A) and one deletion mutation (P379fsdelT) were found in the HNF-1 α gene, but no MODY-associated mutations were found in the HNF-4 α and HNF-1 β genes. Of 67 French MODY families that we have now studied, 42 (63 %) have mutations in the glucokinase gene, 14 (21 %) have mutations in the HNF-1 α gene, and 11 (16 %) have no mutations in the HNF-4 α, IPF1 and HNF-1 β genes. Eleven families do not have mutations in the five known MODY genes suggesting that there is at least one additionnal locus that can cause MODY. [Diabetologia (1998) 41: 1017–1023]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250051025
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    Paper (German National Licenses)
    Fulltext
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