Endocrinology and Metabolism (original) (raw)

Fig. 1. In vivo assessment of β-cell glucose sensitivity using a graded insulin infusion protocol. (A) Estimation of β-cell glucose sensitivity by calculating the slope of the insulin secretion rate versus the blood glucose level. (B) Results showing that a single injection of liraglutide restored β-cell glucose sensitivity in patients with type 2 diabetes. Open triangles represent healthy control subjects. Open and closed rectangles represent type 2 diabetes subjects who received placebo or liraglutide, respectively. Adapted from Chang et al. [8], with permission from the American Diabetes Association. ISR, insulin secretion rate.

Fig. 2. In vivo assessment of β-cell incretin sensitivity using a hyperglycemic clamp with glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) infusion. (A) C-peptide responses to hyperglycemia, GLP-1 infusion, and GIP infusion in subjects with normal glucose tolerance and type 2 diabetes. (B) C-peptide response to hyperglycemia, GLP-1 infusion, and GIP infusion in subjects with type 2 diabetes before and after dapagliflozin treatment (magnified from Fig. 2A). Adapted from Ahn et al. NGT, normal glucose tolerance. aP<0.05 for comparison between NGT and predapagliflozin studies; bP<0.05 for comparison between NGT and both pre- and postdapagliflozin studies.

Fig. 3. A proposed mechanism explaining how anti-diabetic medications improve β-cell incretin sensitivity. Anti-diabetic medications including insulin, sulfonylurea, metformin, dipeptidyl peptidase-4 (DPP-4) inhibitor and sodium-glucose co-transporter 2 (SGLT2) inhibitor restores pancreatic β-cell glucose and incretin sensitivity by ameliorating hyperglycemia. GIPR, glucose-dependent insulinotropic polypeptide receptor; GLP-1R, glucagon-like peptide-1 receptor; GIP, glucose-dependent insulinotropic polypeptide; GLP-1, glucagon-like peptide-1.