Library

feed icon rss

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
  • 1
    ISSN: 1432-0428
    Keywords: Type 1 (insulin-dependent) diabetes ; HLA ; auto-antibodies ; islet cell antibody
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary HLA phenotypes and haplotypes in relation to organ-specific autoantibody responses were studied in 82 Japanese patients with Type 1 (insulin-dependent) diabetes. HLA-DRw9 antigen and HLA phenotype of DRw9/X (X: not DR4) were increased in patients with organ-specific autoantibodies other than islet cell antibody (CP〈0.02, RR=4.02 and p〈0.05, RR=2.30, respectively); whereas HLA-DR4 antigen and HLA phenotype of DR4/X (X: not DRw9) were increased in those without the autoantibodies (CP〈0.001, RR=3.95 and p〈0.01, RR=2.46, respectively). HLA haplotype of Bw61-DRw9 was increased in patients with the autoantibodies (p〈0.005, RR=4.94), and HLA haplotype of Bw54-DR4 was increased in those without the autoantibodies (p〈0.001, RR=5.52). The relative risk of HLA-DR4/DRw9 was the highest among all HLA-DR phenotypes or genotypes in patients either with or without the autoantibodies. No association was, however, found between the incidence of islet cell antibody and HLA-DR phenotypes. These findings suggest that Type 1 diabetes among Japanese is immunogenetically heterogeneous as is Type 1 diabetes among Caucasians; and the differences in HLA-association of Type 1 diabetes among ethnic groups might give a clue to understanding of a role of HLA-antigens in the development of Type 1 diabetes.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Diabetologia 29 (1986), S. 397-401 
    ISSN: 1432-0428
    Keywords: GLI ; glicentin-related peptide ; glucagon ; insulin ; dog pancreas
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Recent studies have demonstrated that glicentin is released during nutrient ingestion. However, the biological function of glicentin remains unclear. In order to clarify the role of glicentin in the enteroinsular axis, the effect of glicentin-related peptides was investigated using in vivo local circulation of canine pancreas. Peaks I and II of gut glucagon-like immunoreactivity, partially purified from porcine intestinal extract by affinity chromatography and gel filtration, synthesized hexadecapeptide of N-terminal glicentin (1–16) and synthesized octapeptide of C-terminal glicentin (62–69) were administered for 10 min into the pancreaticoduodenal artery of canine pancreas. Blood samples were then drawn from the pancreaticoduodenal vein. The administration of peak I of glucagon-like immunoreactivity during arginine infusion in a dosage of 20 ng reduced the glucagon secretion by 42 pmol/1 (p〈0.05), whereas peak 11 of glucagon-like immunoreactivity (20 ng) slightly increased the plasma level of insulin, although not significantly. The administration of glicentin (1–16) in a dosage of 400 ng during saline infusion did not alter the plasma insulin level, but reduced the plasma glucagon level in the pancreaticoduodenal vein by 29 pmol/1 (p〈0.05). In addition, glicentin [62–691 in a dosage of 400 ng exerted a decrease in both the plasma insulin (40 mU/1,p〈0.05) and glucagon level (27 pmol/l,p〈0.05). The present study demonstrates the suppression of pancreatic glucagon release during the infusion of peak I glucagon-like immunoreactivity and N- or C-terminal glicentin-related peptide. Therefore, it is suggested that glicentin released during nutrient intake might inhibit the secretion of glucagon.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...