Skip to main content
. Author manuscript; available in PMC: 2020 May 15.
Published in final edited form as: Endocrinology. 2015 Dec 22;157(2):536–547. doi: 10.1210/en.2015-1725

Figure 7. Insulin treatment of STZ-induced diabetic mice partially corrects α-cell function.

Figure 7

Data corresponding to control chow-diet (CTRL), diabetic mice (STZ) and treated diabetic mice with insulin implant (STZ+Insulin implant) are illustrated respectively by black, white and grey colors. Black arrow indicates the begining of insulin treatment (insulin implant input). Weight (A) and random glycemia (B) were monitored during 28 days whereas glycated hemoglobin (HbA1c; C) was measured at the end of treatment. OGTT was performed in insulin-treated STZ-induced diabetic mice and evaluated for glycemia (D) and glucagonemia before and 15min after glucose loading (E). Due to the fact that insulin-treated STZ-induced diabetic mice do not tolerate fasting, glucose (1mg/kg of D-glucose) was administered during the fasting period when glycemia reached 5 to 6mM (T0). α-cell secretion was evaluated from Facs-sorted Venus+ α cells of control (CTRL, black), STZ-diabetic (STZ, white) and insulin-treated STZ (STZ+Insulin implant, grey) mice (F-G). Acute glucagon secretion was evaluated during 30min periods in 5.6 and 1mM glucose solutions and expressed relative to glucagon content in each condition (F). The effect of glucose was evaluated by the ratio of glucagon secretion measured at 1mM and 5.6mM glucose (G). Each parameter was evaluated from 11 mice except for ex vivo secretion assays which included Facs-sorted α cells from 5 mice.

* indicate statistical significance compared to control. $ significance compared to STZ group. & significance compared to 5.6mM conditions