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. 2022 Jan 8;298(2):101572. doi: 10.1016/j.jbc.2022.101572

Figure 5.

Figure 5

Peroxisomal β-oxidation increased cytosolic acetyl-CoA formation in the STZ-induced diabetic mice.A, liver cytosolic acetyl-CoA was significantly higher in diabetic mice compared to the normal group, which was further elevated after treatment with C22:1 or HRO and reduced by pretreatment of TDYA. B, liver citrate content was significantly lower in the STZ-induced diabetic mice compared to the normal group, whereas there was no alteration after treatment with C22:1, OO, HRO, or TDYA. C and D, citrate lyase (C) and acetyl-CoA carboxylase (ACC) activities (D) in liver homogenate were reduced in the STZ-induced diabetic mice compared to the normal group, whereas there was no alteration after the treatment with OO, HRO, C22:1, or TDYA. E, liver malonyl-CoA was significantly lower in diabetic mice compared to the normal group, while no significant changes in the diabetic mice treated with C22:1, OO, HRO, or TDYA. Mean ± SEM, n = 8, ∗p < 0.05 by t test between paired conditions. HRO, high erucic acid rapeseed oil; OO, olive oil; STZ, streptozotocin; TDYA, 10,12-tricosadiynoic acid.