Fig 2: Effect of Xiaoyaosan on glucose metabolism in hypothalamus of mice injected with 3-MA. (A) Immunofluorescence expression of GLUT4 in hypothalamus of the mice (scale bar = 20 µm). (B) Immunofluorescence intensity of GLUT4 (%) (F (3, 8) = 10.900, p = 0.0034, n = 3). (C) Serum insulin level of the mice (F (3, 16) = 9.543, p = 0.0008, n = 5). (D) The blood glucose of the mice (F (3, 56) = 22.165, p < 0.0001, n = 15). (E) Representative western blotting of GLUT4, Rab8 and Rab10 expressions. (F) Quantitative analysis of protein levels of GLUT4 (F (3, 16) = 4.001, p = 0.0266, n = 5). (G) Quantitative analysis of protein levels of Rab8 (F (3, 16) = 23.664, p < 0.0001, n = 5). (H) Quantitative analysis of protein levels of Rab10 (F (3, 16) = 6.453, p = 0.0045, n = 5). (I) The expression of GLUT4 mRNA (F (3, 12) = 5.221, p = 0.0155, n = 4). (J) The expression of Rab8 mRNA (F (3, 12) = 3.655, p = 0.0443, n = 4). (K) The expression of Rab10 mRNA (F (3, 12) = 6.112, p = 0.0091, n = 4). The values represent the mean ± SEM. ∗ p < 0.05 or ∗∗ p < 0.01 compared with the control group. &p < 0.05, &p < 0.01 compared with the 3-MA group. #p < 0.05, ##p < 0.01 compared with the 3-MA group.

Fig 3: Sleep disturbance downregulated metabolism and antioxidant genes through PGC-1α. Pregnant female mice with high blood glucose level and insulin resistance were given either 50 µL of 0.5% DMSO or ZLN005 (15 mg/kg in 50 µL of 0.5% DMSO) daily for 7 days. The mRNA (A,C) and protein (B,D) levels of PGC-1α and its target genes in gastrocnemius (A,B) and soleus (C,D) were assessed by qRT-PCR and western blot respectively. (E) PGC-1α, GLUT4, TFAM, and UCP2 protein levels of gastrocnemius were examined by IHC staining. *P<0.05 compared to control; #P<0.05 compared to Model + DMSO. DMSO, dimethyl sulfoxide; mRNA, messenger RNA; qRT-PCR, quantitative real-time polymerase chain reaction; IHC, immunohistochemical.

Fig 4: SMY regulates the key signalling pathway in rats with ISO-induced myocardial hypertrophy. (a) ADCY1, PKA, PPARγ, and Glut4 levels. (b) Relative expression of ADCY1, PKA, PPARγ, and Glut4. (c) HIF1ɑ, PPARɑ, CPT1A, and Glut1 levels. (d) Relative expression of HIF1α, PPARα, CPT1A, and Glut1. n = 3 rats per group. The data are presented as the mean ± SEM; p < 0.05 is considered significant (#p < 0.05, ##p < 0.01 and ###p < 0.001 compared with the blank group; ∗p < 0.05, ∗∗p < 0.01 and ∗∗∗p < 0.001 compared with the model group).

Fig 5: SMI regulates expression levels of CPT-1, GLUT-4, and PPAR-γ/PGC-1α through activating AMPK signaling pathway (n = 3). (A) Selection of AMPK concentration. *, compared with the blank group, # P < 0.05; compared with compound C (1 nM) group, & p < 0.05; compared with compound C (10 nM) group, P < 0.05. (B) SMI regulates protein expression levels of CPT-1, GLUT-4, and PPAR-γ/PGC-1α through activating AMPK signaling pathway. *, compared with the blank group, # P < 0.05; compared with Ang II group, & p < 0.05; compared with compound C group, ^P < 0.05; compared with SMI group, P < 0.05.