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. 2019 Feb 8;22:71–83. doi: 10.1016/j.molmet.2019.02.001

Figure 7.

Figure 7

Loss of PEX5 in β-cells causes mitochondrial deterioration and massive vacuole overload. Representative electron micrographs of (A) HFD-fed control β-cells showing normal (white arrow) and slightly damaged mitochondria (yellow arrow) and numerous electron dense insulin granules (black arrow), whereas (B) HFD-fed Rip-Pex5−/− mice showed marked changes in β-cells represented by damaged mitochondria (blue arrow), reduced numbers of mature secretory granules, and cytoplasmic vacuolization (red arrow). n = 3–4 per group; Scale bars, 1 μm. (C) Stacked box plot showing the proportion of β-cells having vacuole-like structures (along with the number of vacuoles per β-cell) in HFD-fed Rip-Pex5−/− and control mice. (D) Graph showing the percentage of altered mitochondria in β-cells from HFD-fed control and Rip-Pex5−/− mice. (E) Relative complex I activity in islets isolated from HFD-fed control and Rip-Pex5−/− mice (n = 6 per genotype). (F, G) Representative electron micrographs of chow-fed control and Rip-Pex5−/− β-cells showing reduced numbers of mature secretory granules and cytoplasmic vacuolization (red arrow, more pronounced in HFD-fed Rip-Pex5−/− mice (B)). n = 3 per group; Scale bars, 1 μm. Data are expressed as mean ± SEM. p < 0.05: *; p < 0.01: **; Rip-Pex5−/− versus control mice.