Figure 6

Stim dysfunction in the fat body exerts systemic control of hyperphagia and obesity possibly via Akh secretion from neuroendocrine cells. (A) Akh mRNA expression levels are unresponsive to Stim-TRiPI On as compared to Stim-TRiPI Off flies in adult male flies at day 1 and 10 after RNAi induction (n = 3–6). (B) Reduced Akh peptide storage in corpora cardiaca cells (red) visualized by immunohistochemistry on adult male flies at day 10 under control condition (Stim-TRiPI Off; B”’) or at day 10 after Stim-TRiPI On (B””). Note that anti-Bruchpilot antibody NC82 was used to counterstain the corpora cardiaca cells (B’ and B”). Scale bars in B represent 50 μm. (C) Quantification of Akh reduction in corpora cardiaca cells of day 10 Stim- TRiPI On adult male flies as compared to corresponding control adult male Stim-TRiPI Off flies (n = 7–12). (D) Stim-DRiPI On causes progressive obesity in heterozygous but not in homozygous Akh mutant males. Relative (rel.) fat content is represented as fold change normalized with respect to the value of day 1 Stim-DRiPI Off flies in Akh heterozygous (n = 6). (E) Loss-of-Akh suppresses the hyperphagia of Stim-DRiPI On male flies. No difference between average daily food intake from day 1 to day 8 in Akh mutant male flies with (Stim-DRiPI Off) or without (Stim-DRiPI Off) Stim dysfunction in the fat body (n = 32). Data are presented as means ± standard deviations. All data were analyzed by the two-tailed unpaired Student’s t-test. No *p ≥ 0.05, *p < 0.05, **p < 0.01, ***p < 0.001.