Journal: Molecular Metabolism

Article Title: The regulator of G-protein signaling RGS16 promotes insulin secretion and β-cell proliferation in rodent and human islets

doi: 10.1016/j.molmet.2016.08.010

Figure Lengend Snippet: RGS16 knockdown inhibits insulin secretion and is sensitive to PTX and SSTR antagonism . (A–D) Isolated mouse islets were infected with Adv–shRGS16 or Adv-shCTL (scrambled) as a control. Insulin secretion was assessed in 1-h static incubations in response to glucose without or with GLP-1 (100 nM) or carbachol (Carb; 0.5 mM) in control islets ( n = 6–12) (A), after 16 h pretreatment with pertussis toxin (PTX; 100 ng/ml; n = 6) (B), or in the presence of cyclosomatostatin (cSST) at 1 μM ( n = 3) (C) or increasing cSST concentrations ( n = 4) (D). (E) MIN6 cells were infected with Adv–RGS16 or Adv-GFP as a control and insulin secretion was assessed in 1-h static incubations in response to glucose with or without 100 nM SST-14 ( n = 4). Insulin levels are expressed as % of total islet insulin content and are mean ± SEM. * p < 0.05, *** p < 0.001, as compared to the corresponding control.

Article Snippet: Cyclosomatostatin and 8-Bromo-cAMP were from Tocris (Minneapolis, MN, USA).

Techniques: Knockdown, Isolation, Infection, Control

Journal: Molecular metabolism

Article Title: Inhibition of somatostatin enhances the long-term metabolic outcomes of sleeve gastrectomy in mice.

doi: 10.1016/j.molmet.2024.101979

Figure Lengend Snippet: Figure 4: Long-term response of obese mice to SG followed by inhibition of somatostatin signaling. A. Change in weight of SG-cSst mice (purple triangles) and SG-saline mice (black triangles), sham-cSst mice (green circles) and sham-saline mice (black squares). p < 0.01 by treatment and by treatment surgery interaction by 3-way repeated measurement ANOVA. Error bars denote SEM. n ¼ 7,7,9,9. B. Glucose levels following an oral mixed meal tolerance test. Colors as in A. p < 0.01 by treatment 3-way repeated measurement ANOVA. Error bars denote SEM. n ¼ 7,7,9,9. C. Area under the curve (AUC) for the mixed meals tolerance test. D. Fasting plasma insulin levels at the end of the experiment. E,F. Fasting (E) and post-prandial (F) plasma GLP-1 levels at the end of the experiment. G. Post-prandial total cholesterol, HDL-cholesterol, and LDL-cholesterol in the plasma at the end of the experiment. H. Quantification of hepatic steatosis by percent of the area covered by lipid droplets in a hematoxylin and eosin staining. *,**p < 0.05, p < 0.01 by Tukey post-hoc test (A,F,G,H). ##p < 0.01 by surgery in 2-way ANOVA.

Article Snippet: Cyclosomatostatin treatment Cyclosomatostatin (cSst) was purchased from Tocris (Cat. No. 3493) and dissolved to a final concentration of 0.08% EtOH and saline. cSst was injected subcutaneously at 30 mg/kg body weight every evening from 7 days after the surgery until the end of the experiment.

Techniques: Inhibition, Saline, Clinical Proteomics, Staining

Journal: Biological psychiatry

Article Title: Disengagement of somatostatin neurons from lateral septum circuitry by oxytocin and vasopressin restores social-fear extinction and suppresses aggression outbursts in Prader-Willi syndrome model

doi: 10.1016/j.biopsych.2023.10.016

Figure Lengend Snippet: (A) Diffusion area in dLS of a fluorescent tracer injected through a cannula. (B) Injection of the SSTR pan-antagonist cyclosomatostatin (2 μg/side (62,63)) in LS improved social-fear extinction deficits of Magel2KO mice. Arrows indicate the onset of injection. Bold lines are means±SEM, light line individual subjects (N). Two-way ANOVA: time × SSTR antagonism F(4,55)=2.7 p=0.03 post-hoc Sidak test. (C) Discrimination between stimulus mice during extinction increased with cyclosomatostatin compared to NaCl-injected KO-controls (Chi2 p=0.001). (D) Cumulated time of attacks on the 6 stimulus mice not affected by cyclosomatostatin in LS (means±SEM). Mann Whitney test comparing antagonist and vehicle groups p=0.3. (E) Injection of the SSTR agonist SST14 (1 ng/side, (64,65)) in LS impaired social-fear extinction of Magel2WT mice. Arrows indicate the onset of injection. Bold lines are means±SEM, light line individual subjects (N). Two-way ANOVA: time × SST F(4,50)=4 p=0.006 post-hoc Sidak test. (F) Discrimination between stimulus mice decreased with SST14 compared to NaCl-injected WT-controls (Chi2 p=0.002). (G) Cumulated time of attacks on the 6 stimulus mice not affected by SST14 in LS (means±SEM). Mann Whitney test comparing SST14 and NaCl groups p=0.06 (non-significant trend).

Article Snippet: Two-way ANOVA: time × SSTR antagonism F (4,55) =2.7 p =0.03 post-hoc Sidak test. (C) Discrimination between stimulus mice during extinction increased with cyclosomatostatin compared to NaCl-injected KO-controls (Chi 2 p =0.001). (D) Cumulated time of attacks on the 6 stimulus mice not affected by cyclosomatostatin in LS (means±SEM).

Techniques: Diffusion-based Assay, Injection, MANN-WHITNEY