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. 2021 Apr 1;134(18):2246–2248. doi: 10.1097/CM9.0000000000001408

Figure 1.

Figure 1

ALDH2 deficiency contributed to the development of type 2 diabetes in both mice and humans. IPGTTs of WT and ALDH2-KO mice with or without HFD at 6 weeks (A) and 32 weeks (D). IPGTT AUC at 6 weeks (B) and 32 weeks (E). Fasting serum glucose levels at 6 weeks (C) and 32 weeks (F). n = 6, ∗P < 0.05. (G) Representative Western blotting images of GLUT-1, GLUT-4, p-Akt, Akt, p-AMPK, AMPK, p-mTOR, mTOR, and p62. (H–P) Quantitative analysis of GLUT-1, GLUT-4, p-Akt, p-Akt/Akt, p-AMPK, p-AMPK/AMPK, p-mTOR, p-mTOR/mTOR, and p62. n = 3–4, ∗P < 0.05. (Q) Diabetes prevalence in male and female study participants with the ALDH2 GG, GA, or AA genotypes. Chi-square test, P < 0.05. ALDH2: Aldehyde dehydrogenase; ALDH2-KO: ALDH2-knockout; AUC: Area under the curve; HFD: High-fat diet; IPGTTs: Intraperitoneal glucose tolerance tests; WT: Wild type.