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. Author manuscript; available in PMC: 2018 Feb 7.
Published in final edited form as: Cell Metab. 2017 Feb 7;25(2):386–399. doi: 10.1016/j.cmet.2017.01.002

Figure 7. Chronic high-sugar diet increases EE number and Actβ production in the larval midgut.

Figure 7

(A–C) Confocal image (A), number of Actβ > GFP or Pros+ cells (B) (n=15, 15 larval guts), and gene expression (C) (n=4, 40 larval guts), in the larval midgut under high-sugar diet. (D–F) Midgut Actβ mRNA (D) (n=4, 40 larval guts), glycemic levels (glucose + trehalose) (E) (n=4, 40 larvae), and (F) immunoblots of fat body from Pros > Actβ-i larvae (Pros-Gal4/UAS-Actβ-RNAi) fed a chronic high-sugar diet. (G) The midgut-to-fat-body axis in glycemic control. Chronic high-sugar diet leads to an increase in Actβ production in the EEs of larval midgut and enhances the fat body AKH signaling, resulting in hyperglycemia, via Actβ/Babo signaling. Data are presented as means ± SEM. * p < 0.05.