ArticleDiabetologia2009
Endosomal proteolysis of internalised [ArgA0]-human insulin at neutral pH generates the mature insulin peptide in rat liver in vivo.
Article in Diabetologia, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed, 8 citations in OpenAlex.
- Modulation of Insulin Sensitivity by Insulin-Degrading Enzyme.Biomedicines · 2021Review
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Authors and funding
3 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aims/hypothesisA proteolysis study of human monoarginyl-insulin ([Arg(A0)]-HI) and diarginyl-insulin ([Arg(B31)-Arg(B32)]-HI) within hepatic endosomes was undertaken to determine whether the endosomal compartment represents a physiological site for the removal of Arg residues and conversion of Arg-extended insulins into fully processed human insulin.
methodsThe metabolic fate of arginyl-insulins has been studied using the in situ rat liver model system following ligand administration to rats and cell-free hepatic endosomes.
resultsWhile the kinetics of insulin receptor endocytosis after the administration of arginyl-insulins were similar to those observed using human insulin, a more prolonged concentration of endosomal insulin receptor was observed in response to [Arg(A0)]-HI. [Arg(A0)]-HI induced a marked increase in the phosphotyrosine content of endosomal insulin receptor, coinciding with a more sustained endosomal association of growth factor receptor-bound protein 14 (GRB14), and a higher and prolonged activation of mitogen-activated protein kinase pathways. At acidic pH, the endosomal cathepsin D rapidly degraded insulin peptides with similar binding affinity, and generated comparable intermediates for both arginyl-insulins without affecting amino and carboxyl arginyl-peptide bonds. At neutral pH, hepatic endosomes fully processed [Arg(A0)]-HI into mature human insulin while no conversion was observed with [Arg(B31)-Arg(B32)]-HI. The neutral endosomal Arg-convertase was sensitive to bestatin, immunologically distinct from insulin-degrading enzyme, nardilysin or furin, and was potentially related to aminopeptidase-B-type enzyme. CONCLUSIONS/
interpretationThe data describe a unique processing pathway for the endosomal proteolysis of [Arg(A0)]-HI which involves the removal of Arg(A0) and subsequent generation of mature human insulin through an uncovered neutral Arg-aminopeptidase activity. The endosomal conversion of [Arg(A0)]-HI into human insulin might extend the insulin receptor signalling at this locus.
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