title: Metabolic characteristics of autoimmune diabetes mellitus in adults.
abstract: It is still a matter of debate whether patients who develop islet-cell antibody positive autoimmune diabetes during adulthood represent slowly evolving Type 1 (insulin-dependent) diabetes mellitus or a separate subgroup of Type 2 (non-insulin-dependent) diabetes. To address this question, we measured C-peptide response to a test meal, and energy metabolism in the basal state and during a euglycaemic, hyperinsulinaemic clamp in (1) 29 patients with Type 2 diabetes; (2) 10 patients with autoimmune diabetes developing after the age of 40 years; (3) 11 patients with Type 1 diabetes and (4) 15 non-diabetic control subjects. While C-peptide response to a test meal was lacking in Type 1 diabetes and nearly normal in Type 2 diabetes, the C-peptide response in autoimmune diabetes was markedly reduced. Patients with Type 2 diabetes, autoimmune diabetes and Type 1 diabetes showed a 47%, 45% and 42%, respectively, reduction in the rate of non-oxidative glucose metabolism compared with control subjects (p less than 0.05-0.01). Similarly, patients with Type 2 diabetes (+52%), autoimmune diabetes (+27%) and Type 1 diabetes (+33%) presented with an enhanced basal rate of hepatic glucose production, which was less suppressed by insulin compared with healthy control subjects (p less than 0.01). However, patients with autoimmune diabetes derived more energy from oxidation of glucose and proteins and less energy from oxidation of lipids than patients with either Type 1 or Type 2 diabetes (p less than 0.05-0.01). In conclusion, patients who develop autoimmune diabetes during adulthood share the defects in hepatic glucose production and in non-oxidative glucose metabolism with both Type 1 and Type 2 diabetes.(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: Fourth Department of Medicine, Helsinki University Hospital, Finland.
authors.forename: L C
authors.initials: LC
authors.lastname: Groop
authors.forename: J
authors.initials: J
authors.lastname: Eriksson
authors.forename: A
authors.initials: A
authors.lastname: Ekstrand
authors.forename: A
authors.initials: A
authors.lastname: Franssila-Kallunki
authors.forename: C
authors.initials: C
authors.lastname: Saloranta
authors.forename: A
authors.initials: A
authors.lastname: Miettinen
mesh_terms: D000328:Adult; D001323:Autoantibodies / Q000032:analysis; D001327:Autoimmune Diseases / Q000097:blood*; D001786:Blood Glucose / Q000378:metabolism; D002096:C-Peptide / Q000097:blood; D002784:Cholesterol / Q000097:blood; D003922:Diabetes Mellitus, Type 1 / Q000097:blood / Q000235:genetics / Q000276:immunology*; D003924:Diabetes Mellitus, Type 2 / Q000097:blood / Q000235:genetics / Q000276:immunology*; D004435:Eating; D005260:Female; D006442:Glycated Hemoglobin / Q000032:analysis; D006801:Humans; D007515:Islets of Langerhans / Q000276:immunology; D008297:Male; D008875:Middle Aged; D013961:Thyroid Gland / Q000276:immunology; D013974:Thyroxine / Q000097:blood; D014280:Triglycerides / Q000097:blood
chemical_list: D001323:Autoantibodies; D001786:Blood Glucose; D002096:C-Peptide; D002784:Cholesterol; D006442:Glycated Hemoglobin; D013974:Thyroxine; D014280:Triglycerides; C024211:islet cell antibody