title: Fasting plus prandial insulin supplements improve insulin secretory ability in NIDDM subjects.
abstract: To examine how insulin secretory ability is modified by strict glycemic control in non-insulin-dependent diabetes mellitus (NIDDM) subjects, basal and/or prandial insulin was supplemented for 4 wk in 24 diabetic subjects who were secondary failures to sulfonylurea treatment. One intermediate-acting insulin injection a day (n = 7) failed to suppress the rise in plasma C-peptide after meals and did not improve plasma C-peptide responses during a posttreatment oral glucose challenge. Continuous subcutaneous insulin infusion with a premeal bolus (n = 8) suppressed both fasting and meal-related rises in C-peptide and improved C-peptide response during the posttreatment oral glucose challenge. Daily insulin requirements during the 4 wk of treatment were reduced significantly by 52%. A short-acting insulin injection before each meal (n = 9) without basal supplementation suppressed the prandial rise in C-peptide and was associated with a significant reduction in daily insulin requirements during 4 wk of treatment by 28%. Diabetic subjects whose fasting and prandial hyperglycemia were less than 140 and less than 200 mg/dl, respectively, showed a significantly higher C-peptide response during oral glucose challenge after treatment than those whose insulin treatment only normalized (less than 200 mg/dl) prandial but not basal hyperglycemia (greater than 140 mg/dl). These results suggest that a short-term period of meal-related insulin treatment (which normalized prandial glycemia) increases residual beta-cell function in NIDDM subjects who failed long-term sulfonylurea administration. A basal insulin supplement alone was not effective. The effectiveness of a prandial insulin supplement may have been further improved by a combined basal and meal-related treatment program.
authors.affiliation: First Department of Medicine, Osaka University Medical School, Japan.
authors.forename: R
authors.initials: R
authors.lastname: Kawamori
authors.forename: K
authors.initials: K
authors.lastname: Bando
authors.forename: Y
authors.initials: Y
authors.lastname: Yamasaki
authors.forename: M
authors.initials: M
authors.lastname: Kubota
authors.forename: T
authors.initials: T
authors.lastname: Watarai
authors.forename: N
authors.initials: N
authors.lastname: Iwama
authors.forename: M
authors.initials: M
authors.lastname: Shichiri
authors.forename: T
authors.initials: T
authors.lastname: Kamada
mesh_terms: D000092:Acetohexamide / Q000627:therapeutic use; D001786:Blood Glucose / Q000378:metabolism; D002096:C-Peptide / Q000097:blood / Q000378:metabolism / Q000652:urine; D003924:Diabetes Mellitus, Type 2 / Q000097:blood / Q000188:drug therapy* / Q000503:physiopathology; D004334:Drug Administration Schedule; D004435:Eating; D005215:Fasting; D005260:Female; D005951:Glucose Tolerance Test; D005905:Glyburide / Q000627:therapeutic use; D006801:Humans; D007328:Insulin / Q000008:administration & dosage / Q000378:metabolism / Q000627:therapeutic use*; D000078790:Insulin Secretion; D007515:Islets of Langerhans / Q000187:drug effects / Q000378:metabolism*; D008297:Male; D008875:Middle Aged
chemical_list: D001786:Blood Glucose; D002096:C-Peptide; D007328:Insulin; D000092:Acetohexamide; D005905:Glyburide