title: [Significance of the regulation of hyperglucagonemia in type 2 diabetes mellitus].
abstract: Abstract Generally, pancreatic β-cell dysfunction and hypoinsulinemia have been known as the cause of development of hyperglycemia in diabetes mellitus. Pancreatic α-cell dysfunction, particularly hyperglucagonemia is also serious problem to increase hepatic glucose production in type 2 diabetes mellitus (T2DM). β-cell mass decrement and α-cell mass increment in T2DM have been reported in many reports inclusive of our study. Those might be the background to the pancreatic cells dysfunction in T2DM. Glucagon secretion from α-cells could not be suppressed by insufficient insulin, and hyperglucagonemia has been worsening in T2DM. Incretin, particularly glucagon like peptide-1 (GLP-1) could control both α- and β-cell dysfunction, via the decrease of glucagon and the increase of insulin respectively. We believe that incretin therapy(GLP-1 receptor agonists and DPP-4 inhibitors) is the best strategy to control hyperglucagonemia caused by α-cell dysfunction in T2DM.
authors.forename: Masayuki
authors.initials: M
authors.lastname: Miuchi
authors.forename: Jun-ichiro
authors.initials: J
authors.lastname: Miyagawa
authors.forename: Mitsuyoshi
authors.initials: M
authors.lastname: Namba
mesh_terms: D000818:Animals; D003924:Diabetes Mellitus, Type 2 / Q000178:diet therapy / Q000188:drug therapy* / Q000378:metabolism*; D018819:Dipeptidyl Peptidase 4 / Q000378:metabolism; D005934:Glucagon / Q000037:antagonists & inhibitors* / Q000378:metabolism*; D006801:Humans; D007328:Insulin / Q000378:metabolism; D000078790:Insulin Secretion; D010179:Pancreas / Q000378:metabolism
chemical_list: D007328:Insulin; D005934:Glucagon; C042807:DPP4 protein, human; D018819:Dipeptidyl Peptidase 4