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. 2017 Jan 23;127(2):657–669. doi: 10.1172/JCI88477

Figure 4. Hypercorticosteronemia drives DKA through increased lipolysis.

Figure 4

(A–C) Plasma glucose, NEFA, and βOHB concentrations in adrenalectomized T1D rats. In all panels, unless indicated otherwise, all measurements were made at the 4-hour time point. (B) *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001 between the groups indicated; §§P < 0.01 vs. adrenalectomy plus corticosterone at time zero. (D) Anion gap. (E–I) Plasma insulin, leptin, corticosterone, ACTH, and IGF-1 concentrations. (J) Whole-body glucose turnover. (K–M) Whole-body palmitate, glycerol, and βOHB turnover. (N and O) Liver acetyl and malonyl CoA concentrations. In all panels, data are the mean ± SEM of n = 8 (control), n = 11 (adrenalectomy), n = 6 (adrenalectomy plus corticosterone), or n = 6 (adrenalectomy plus sucrose water) per group. Unless otherwise specified, *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001 vs. controls; §P < 0.05, §§P < 0.01, §§§P < 0.001, §§§§P < 0.0001 vs. adrenalectomized rats; ##P < 0.01, ###P < 0.001, ####P < 0.0001 vs. adrenalectomy plus corticosterone–treated rats. Data were compared using ANOVA with Bonferroni’s multiple comparisons test.