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. 2012 Apr 3;26(6):967–976. doi: 10.1210/me.2011-1306

Fig. 1.

Fig. 1.

Islets lacking leptin receptor exhibit greater GLP-1 effects on glucose-stimulated [Ca2+]i increase and insulin release. A, B, D, and E, Representative traces of intracellular Ca2+ flux (A and B) and insulin release (D and E) measured in primary size-matched islets isolated from 6-month-old male ObRlox (A and D) and ObR-KO (B and E) mice in different glucose concentrations with or without 10 nm GLP-1(7–36) amide or 10 nm leptin. C, Percent changes in [Ca2+]i from basal glucose (3 mm) in response to 8 mm glucose treated as indicated (mean ± sem; *, P < 0.05; **, P < 0.01; n = 5). F, Percent changes in insulin secretion in response to glucose (8 mm) from basal glucose (3 mm) treated as indicated (mean ± sem; *, P < 0.05; **, P < 0.01; n = 5). G, Islet insulin content was measured in acid-ethanol extracts from 5-month-old ObRlox and ObR-KO mice by RIA. Values are expressed as means ± sem in picograms/islet (n = 3; P = 0.222). H, Expression of GLP-1 receptor gene in size-matched ObRlox and ObR-KO islets assessed by quantitative real-time PCR (P = 0.766; n = 3). Data are obtained from islet samples from 6-month-old mice and are shown as mean ± sem.