Truncated glucagon-like peptide I, an insulin-releasing hormone from the distal gut

AbstractBy hydrophobic gel permeation and high pressure liquid chromatography we isolated from pig intestinal mucosa a peptide which corresponds to proglucagon 78–107 as suggested by chromatography and determination of its N-terminal sequence. Natural and synthetic proglucagon 78–107 dose dependently and potently increased insulin secretion from the isolated perfused pig pancreas. Proglucagon 78–107 also secreted by the small intestine may participate in the hormonal control of insulin secretion

Scandinavian society for the study of diabetes Abstracts Seventh Meeting

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/46039/1/125_2005_Article_BF01219478.pd

Boganmeldelser

Book review

Evidence from twins for acquired cellular immune hyperactivity in type 1 diabetes

Type 1 diabetes has been associated with an increased frequency of activated T cells and T-cell hyperactivity to non-specific and disease-specific stimuli including the islet autoantigen glutamic acid decarboxylase 65 (GAD). To address whether T-cell hyperactivity is genetic or acquired we measured whole blood cytokines in vitro in response to GAD or tetanus in 18 identical twin pairs, nine discordant for type 1 diabetes. In addition, the activity of 2′, 5′ oligoadenylate synthetase (OAS) in blood mononuclear cells was measured as a marker of viral infection. Interleukin-2 (IL-2) basally and IL-2 and interferon-γ (IFN-γ) in response to GAD, were detected more frequently and at higher levels in diabetic compared to non-diabetic twins. IL-10 was not different between groups. OAS activity was increased in diabetic compared to non-diabetic twins and showed a correlation with basal IL-2 and GAD-stimulated IFN-γ and IL-10. These findings suggest that T-cell hyperactivity in type 1 diabetes is an acquired trait and could reflect persisting virus expression