Fig. 5: AgRP neurons are not required for T1D hyperglycemia development and for leptin action in reducing T1D glucose.
From: A neural basis for brain leptin action on reducing type 1 diabetic hyperglycemia
Vgat-Cre::Ai9::AgRPDTR mice were treated with DTX/saline at P3, made STZ-T1D at 8–9-weeks old, and then implanted with i.c.v. minipump for a 2-week leptin infusion. a Representative pictures from n = 3 mice showing immunostaining for AgRP in the Arc (right panels) and PVH (left panels) of both saline-treated controls (top) and the DTX-treated group (bottom). b Comparisons in blood glucose between saline and DTX-treated groups after STZ treatment (two-tailed unpaired Student’s t tests, n = 5/each, t = 0.6019, df = 8, P = 0.5639). c Reponses in glucose levels in DTX-treated Vgat-Cre::Ai9::AgRPDTR mice that received i.c.v. treatment of saline or leptin during the 14-day leptin treatment period (two-way ANOVA, n = 5/each, F(1, 56) = 150.4, ***P < 0.0001, saline vs leptin at day 13). d Representative sections from n = 2 mice showing expression of c-Fos (green) in Arc GABA + neurons (red) in i.c.v. saline-treated (left panel) and leptin-treated mice (right panel). e, f Comparisons in glucagon (e, two-tailed unpaired Student’s t tests, n = 5/each, *P = 0.0266) and corticosterone (f, two-tailed unpaired Student’s t tests, n = 5/each, *P = 0.027) at day 13 with i.c.v. leptin treatment. 3V the third ventricle, Arc arcuate nucleus. All data presented as mean ± SEM. Scale bar: 100 µM.
