Skip to main content
. 2015 Jan 13;11(1):145–154. doi: 10.1080/15548627.2014.998917

Figure 2.

Figure 2.

Effects of POMC-specific Atg12 and Atg5 deletion on body weight in mice fed a normal chow diet. (A) Accumulation of SQSTM1 (red) in POMC (ACTH, green) positive neurons confirms defective autophagy in hypothalamic POMC neurons of Atg12ckoPomc-Cre+ and Atg5ckoPomc-Cre+ mice. Bar = 500 μm Right: Quantification of the percentage of POMC neurons positive for SQSTM1 accumulation (n=4 for each genotype). (B) Accumulation of ubiquitin (green) in POMC (ACTH, red) positive neurons in hypothalamic POMC neurons of Atg12ckoPomc-Cre+ and Atg5ckoPomc-Cre+ mice. Bar = 500 μm Right: Quantification of the percentage of POMC neurons positive for ubiquitin accumulation (n=4 for each genotype). (C) POMC neuron quantification in Atg12+/+ vs. Atg12ckoPomc-Cre+ mice (n=5 for each genotype), and Atg5+/+ vs. Atg5ckoPomc-Cre+ mice (n=6 for each genotype). Sections from the arcuate nucleus of 15-wk-old mice were quantified. (D) Body weight curves for Atg12+/+ (n=14 ) vs. Atg12ckoPomc-Cre+ mice (n=10 ), and Atg5+/+ (n=10 ) vs. Atg5ckoPomc-Cre+ mice (n=8 ) maintained on normal chow. For all experiments, control mice are Pomc-Cre-expressing wild-type littermates (Atg12+/+ or Atg5+/+). n.s., nonsignificant. Data represent the means ± SEM.