Fig 1: Plasma levels and signaling nodes in IGFBP-1 knockdown mice. (A) Plasma was taken from IGFBP-1-KO mice and wild-type litter mate controls and there was an increase in circulating total IGF-I levels (IGFBP-1-KO 3257 ± 285.8 V Wt 2327 ± 77.61 ng/mL). N = 5 to 7 per group for plasma samples. (B) Plasma was taken from IGFBP-1-KO mice and wildtype litter mate controls and there was no difference in circulating IGFBP-2 levels (IGFBP-1-KO 1171 ± 44.09 V Wt 1292 ± 97.36 ng/mL) C: Plasma was taken from IGFBP-1-KO mice and wild-type litter mate controls and there was no difference in circulating IGFBP-3 levels (IGFBP-1-KO 557.8 ± 90.03 V Wt 495.3 ± 70.1). (D,E) There was no difference in AKT or MAPK expression in the muscle of IGFBP-1-KO mice when compared with their wild-type litter mate controls. (F,G) There was no difference in AKT or MAPK expression in the liver of IGFBP-1-KO mice when compared to their wildtype litter mate controls. N = 5 per group for blotting studies. (H) Histological examination of liver showed there was no difference in non-alcoholic fatty liver disease (NAFLD) score (Wt 1.8 ± 0.2 V IGFBP-1-KO 2 ± 0.3) (n = 4). Data are presented as mean ±SEM. (*P ≤ .05).
Fig 2: Policaptil Gel Retard affects hepatic energy storage. (a) Venn diagram of genes significantly up-regulated or down-regulatd by Policaptil Gel Retard treatment at ZT12 and ZT0 (Cyber t-test p < 0.05). (b) Volcano plot of differentially expressed genes at ZT0 and ZT12 by Policaptil Gel Retard treatment. (c) Pathway enrichment of genes decreased or induced by Policaptil Gel Retard at ZT12. (d) In silico modeling with IPA of the systemic effects of Policaptil Gel Retard administration. (e) Hepatic glycogen content in response to HFD and Policaptil Gel Retard treatment (mean ± s.e.m, n = 5; *p < 0.05; ANOVA, Holm-Sidak post hoc). (f) Hepatic triglycerides content in response to HFD and Policaptil Gel Retard treatment (mean ± s.e.m, n = 5; *p < 0.05; ANOVA, Holm-Sidak post hoc). (g) Expression of hepatic Igfbp2 in response to HFD and Policaptil Gel Retard treatment (mean ± s.e.m, n = 5; **p < 0.01; ANOVA, Holm-Sidak post hoc). (h) Serum IGFBP2 level in response to HFD and Policaptil Gel Retard treatment (mean ± s.e.m, n = 5; *p < 0.05; ANOVA, Holm-Sidak post hoc).
Fig 3: Comparison of the plasma hormone concentrations among the three groups at d3 and d5. The values are expressed as the means (SD), n = 8/group. a Plasma GH. b Plasma IGF-1. c Plasma IGFBP3. d Plasma IGFBP2. Skewed data of plasma GH are compared after log transformations among three groups by ANOVA. *P < 0.05 vs control group; # P < 0.05 vs colitis group; §P < 0.05 vs d3
Fig 4: The impact of low-carbohydrate, high-fat and high-carbohydrate, low-fat diets on IGF and IGF-binding proteins serum level. (A) IGF-1 serum level; (B) IGFBP-2 serum level; (C) IGFBP-5 serum level. Data are expressed as mean ± SD. Statistically significant if p < 0.001 ***; p < 0.0001 ****. IGF-1: Insulin growth factor-1, IGFBP-2: Insulin growth factor binding protein-2, and IGFBP-5: Insulin growth factor binding protein-5.
Fig 5: Low-carbohydrate, high-fat and high-carbohydrate, low-fat diets impact the brain’s IGF and IGF-binding protein gene expression. (A) IGF-1 gene expression; (B) IGF-1 R gene expression; (C) IGFBP-2 gene expression; (D) IGFBP-5 gene expression Data were expressed as the mean ± SD. DEX, DEX + LCHF, and DEX + HCLF groups. DEX: rats treated with dexamethasone to induce MetS; DEX + LCHF: rats treated with dexamethasone to induce MetS and fed the low-carbohydrate, high-fat diet; DEX + HCLF: rats treated with dexamethasone to induce MetS and fed the high-carbohydrate, low-fat diet (applies to all figures). Y axis (Fold expression relative to control). Statistically significant if p ≤ 0.05 *; p < 0.01 **; p < 0.0001 ****. IGF-1: Insulin growth factor-1, IGF-1 R: Insulin growth factor-1 receptors, IGFBP-2: Insulin growth factor binding protein-1, and IGFBP-5: Insulin growth factor binding protein-5.
Supplier Page from Abcam for Mouse IGFBP2 ELISA Kit