Glut 4 Antibody - #AF5386

Fig. 1. Heart damage in MI mice. (a) Echocardiogram, EF, and FS measurements of sham and MI mice (n  =  5). **P  <  0.01, compared with sham, mean ± SEM. (b) H&E staining of cross‐sectional slices derived from sham and MI hearts (n  = 3). The blue arrow indicates the larger intercellular space, and the yellow stars indicate inflammatory cell infiltration. (c) Representative transmission electron microscopy (TEM) micrograph of sham and MI hearts; the blue arrow indicates karyopyknosis, and the green arrow indicates mitochondrial swelling (n  = 4). (d) ATP levels in the homogenate of heart tissue from sham and MI (n  = 3; *P  < 0.05). (e, f) The expression of GLUT4, HK1, and CD36 at the mRNA and protein levels in the infarct border zones of the left ventricular from each group at 24 h after the MI operation, respectively (*P  < 0.05, **P  < 0.01, compared with the sham group; n  = 3 to n  = 4; mean ± SEM).

Figure S15, Related to Figure 7. GLUTs and SGLT1/2 expression. (A and B) Western blot and quantitation for TRPC6, GLUT1, GLUT2, GLUT4, GLUT5, SGLT1 and SGLT2 expression in PC12 cells. Lv-Con, the recombinant lentiviral vector; Lv-TRPC6, the recombinant lentiviral vector with TRPC6 over-expression. The data are expressed as the mean ± SEM. Statistical significance was assessed using unpaired student’s t test. *P＜0.05; NS, no significant difference.

Figure 5 RH reduced brain GLUT3-mediated glucose uptake in STZ-induced APP/PS1-DM mice. (A) Representative PET/CT images showing in vivo brain 18F-FDG uptake (coronal, sagittal, and transaxial sections, n = 6 mice for each group). Cor, Cortex; Hip, hippocampus; Mid, midbrain; HPOA, hypothalamus; BS, brain stem; Cer, cerebellum; OB, Olfactory Bulb; BF, basal forebrain; Tha, thalamus; SC, superior colliculi; CG, central gray; Str, striatum. (B) Quantification for SUV of 18F-FDG in brain region (n = 6 for mice for each group). (C) Western blot and quantitation for GLUT1, GLUT2, GLUT3, GLUT4, GLUT5, SGLT1, and SGLT2 in hippocampal homogenates (n = 3 mice for each group). The data are expressed as the mean ± SEM. Statistical significance was assessed using unpaired Student’s t test. *P < 0.05 and **P < 0.01, APP/PS1-DM versus APP/PS1; #P < 0.05 and ##P < 0.01, APP/PS1-DM-RH versus APP/PS1-DM; WT versus APP/PS1; NS, no significant difference.

Figure 5 Effect of djulis hull crude extract on the expression of proteins involved in glucose transportation in (A) epididymal white adipose tissue (eWAT) and (B) the liver of high-fat diet-induced hyperglycaemia. ND: normal diet; HFD: high-fat diet; HCE: high dosage of crude extract. Values represent the mean ± SEM (n = 6). The statistical methods used one-way ANOVA, and the values with different letters are significantly different at p < 0.05.

FIGURE 5 Polyethylene glycol loxenatide (PEG-Loxe) regulates the expressions of the Sirt1-AMPK pathway-, insulin PI3K/AKT pathway- and apoptosis-related proteins. Protein expression levels were normalized to the levels of β-actin. Data are presented as the mean ± SD; n = 3; ### p < 0.001 compared to the normal control group; * p < 0.05, ** p < 0.01, and *** p < 0.001 compared to the T2DM group.

Fig. 5. Identification of Exo in co-culture system supernatant, establishment of IR model and influence of GSY on it. A. TEM identification of Exo morphology and size-concentration distribution of Exo in the supernatant. B. Expression levels of Exo marker proteins CD9, CD63 and TSG101 in the supernatant of the co-culture system. C. Expression levels of PPARγ, GLUT4 and FABP4 genes in Exo supernatant of co-culture system. D. Glucose consumption in supernatant during the establishment of IR model in co-culture system. E. Glucose consumption rate in supernatant during the establishment of IR model in co-culture system. F. Glucose consumption rate after the establishment of IR model of co-culture system. J. Glucose consumption in the supernatant of each experimental group in the co-culture system. H. TG content in supernatant of each experimental group of co-culture system. I. Expression levels of PPARγ, GLUT4 and FABP4 proteins in the supernatant Exo of co-culture system after GSY intervention. J. Expression levels of PPARγ, GLUT4 and FABP4 genes in Exo after GSY intervention. *p < 0.05; **p < 0.01; ***p < 0.001. NC: Negative control; MOD: Model (60 mmol/L glucose). All experiments were repeated three times.

Fig. 6. Effects of MOTS-c treatment and exercise intervention on lean mice. (A, B) The wild-type C57BL/6 mice were assigned into exercise and sedentary groups, (C–I) and then intraperitoneally injected with 0.5 mg/kg MOTS-c or saline daily for eight weeks. (C, D) The skeletal muscle and plasma concentrations of MOTS-c were detected by ELISA kits after normalizing to total protein content. (E-I) Protein expression of PGC-1α and GLUT4 as well as phosphorylation levels of AMPK and ACC in mouse muscle (n = 6–8 in each group) were determined by immunoblotting. Each bar represents mean ± SD of triplicates. *P < 0.05, **P < 0.01, remarkably different from control mice.

Fig. 4. The effects of GO-CURSD on IGF1/Insulin-Akt-mTOR activities in middle-aged rat’s muscles. Western blots of (A) Insulin receptor substrate 1 (IRS-1), (B) the phosphorylated Akt (p-Akt) /total Akt, (C) the phosphorylated mTOR/total mTOR, (D) Glucose transporter type 4 (GLUT4). The total protein expressions are normalized to β-actin and presented as the fold differences compared to the YC group which was set as one (n = 3). (E) Muscular glucose uptake activity and (F) glycogen content. Data are expressed as means ± SD for each group. The letters were significantly different compared with the YC group (a p < 0.05, aa p < 0.01, and aaa p < 0.001), MC groups (b p < 0.05, bb p < 0.01, and bbb p < 0.001), CURSD groups (c p < 0.05, and ccc p < 0.001). # is significantly different between without insulin vs Insulin.