Glucagon Antibody - #AF0166

Figure 6 Improvement in glucose tolerance by muscle-targeting LGP-MN and possible gastric hormone-related mechanisms. A,B) Blood glucose levels during the oral glucose tolerance test (OGTT) and analysis of area under the curve (AUC) in each treatment group at the end of the animal experiments. C) Blood insulin levels during the OGTT. D) Homeostatic model assessment of insulin resistance (HOMA-IR) results of each treatment group at the end of the animal experiments. E) Immunohistochemical (IHC) staining of ghrelin and GLP-1 in gastric wall tissues. F) Statistics of the number of GLP-1- and ghrelin-positive cells based on image analysis of the IHC stainings in (E). G) Expression levels of GLP-1 and ghrelin in the stomach on day 30. H) Plasma levels of GLP-1 and ghrelin in fasting rats on day 30. I) Plasma GLP-1 levels during the OGTT. J) Schematic diagram of the pylorus ligation model. 50% glucose was injected from the stomach or the intestine; blood samples were drawn from the gastric vein and the portal vein at each time point. K,L) Stomach- (K) and intestine-derived (L) GLP-1 levels at 0–30 min after glucose injection. M) Blood glucose levels during the OGTT with and without GLP-1 receptor antagonist, Avexitide. N) Statistical results of the OGTT AUC and body weight with and without Avexitide. O) Schematic diagram of the possible mechanisms underlying the differential therapeutic effects delivered by the gastric muscle- and submucosa-targeting LGP-MNs. Data represent mean ± SD; n = 7–8. *p < 0.05, **p < 0.01, ***p < 0.001 by Student's t-test.

Fig. 8 The effects of NaB on brain function in STZ induced diabetic mice. A Body weight, and B Fasting blood glucose in mice during the experiment. C Fasting blood glucose decrement at Week 14. D H&E staining of mice brain (black arrow indicates the atrophic and deep staining of neurons; red arrow indicates the loose structure of brain tissues; and the swollen, vacuolar neurons were indicated by green arrow). ELISA assay for concentration of E BDNF in brain tissue, and F AGEs and G IL-1β in serum. H IHC analysis of GABA and I GLP-1 in intestine tissues (red arrow indicates the GLP-1). J Expression of GABA in brain cortex or hippocampus by immunohistochemical analysis. *p < 0.05, **p < 0.01, vs. NC group; #p < 0.05, ##p < 0.01, vs. T2DM group

Fig. 3. |CUMS reduces protein levels of hippocampal GLP-1 in mice. GLP-1 protein levels in serum (A, n = 8 per group) and hippocampus (B, n = 3–4 per group).Hippocampal GLP-1R distribution (C: top, ventral hippocampus; bottom, dorsal hippocampus), gray value (D) and positive cell number (E) using IHC. Magnification 200 × , Scale bars = 50 μm. N = 3 sections per brain were analyzed, n = 3 per group. Data are presented as means ± SEM. *p < 0.05 versus Con.

Fig. 4. Effect of crocin on hippocampal GLP-1 level and expression in a rat model of CS-induced cognitive disorders. (A) GLP-1 level (pg/g tissue); n = 6, (B) western blot showing GLP-1 expression, and (C) bar graph reflecting GLP-1 expression. Protein expression level was normalized to β-actin and shown relative to that of control; n = 3. Values were expressed as means ± SD. Significant difference were presented at *p < 0.05, **p < 0.01, and ***p < 0.001; using One-way ANOVA followed by Tukey's Honestly Significant Difference (HSD) post-hoc. C: control; Cro: crocin; CS: cigarettes smoke; GLP-1: Glucagon-like peptide-1.

Fig. 2. GCG mRNA expression and GCG precursor protein are increased, but total GLP-1 and active GLP-1 levels are decreased in mice during infection. (A) GCG mRNA expression in the lungs of mock and H9N2 groups (n = 5). (B) Representative western blotting bands of the GCG precursor protein in the lungs of mock and H9N2 groups. (C) Data of GCG precursor protein expression in the lungs of mock and H9N2 groups (n = 4). (D) Representative immunohistochemistry images of GCG precursor protein expressed in the lungs of mock and H9N2 groups on 7 d.p.i. The results were similar in five mice of per group. GCG precursor protein positive cells was noted by red arrows. (E) Total GLP-1 in the lungs of mock and H9N2 groups (n = 5). (F) Total GLP-1 in the serum of mock and H9N2 groups (n = 5). (G) Active GLP- 1 in the lungs of mock and H9N2 groups (n = 5). (H) Active GLP-1 in the serum of mock and H9N2 groups (n = 5). (I) Active GLP-1/total GLP-1 in the lungs of mock and H9N2 groups on 5 and 7d.p.i. (n = 5). (J) Active GLP-1/total GLP-1 in the serum of mock and H9N2 groups on 5 and 7d.p.i. (n = 5). Data are presented as mean ± SD, analyzed using Sidak’s or Tukey’s multiple comparisons tests. * = P < 0.05, ** = P < 0.01, *** = P < 0.001, **** = P < 0.0001, NS = non-significant. GCG, glucagon. GLP-1, glucagon like peptide-1. d.p.i., days post infection.