Grg3 is expressed in most β-cells but less frequently in α-cells.

Slides:



Advertisements
Similar presentations
Volume 15, Issue 5, Pages (May 2016)
Advertisements

(Copyright © 1977 American Diabetes Association. Marliss EB et al
In vivo Gene Transfer to Healthy and Diabetic Canine Pancreas
Rashmi B. Prasad, Leif Groop  Cell Metabolism 
The gene encoding TP53INP1 is expressed in pancreatic endocrine cells A, B(A, B) Immunocytofluorescent staining of TP53INP1 (red) and insulin (green) in.
Nat. Rev. Neurol. doi: /nrendo
Insulin and glucagon secretion: nondiabetic and diabetic subjects.
TIE2hi/VEGFAhi TEMs are present in the TMEM
Volume 15, Issue 5, Pages (May 2016)
Volume 23, Issue 4, Pages (April 2018)
Impact of U-100 RHI administered with V-Go at OV1 (3 months after initiation) and OV2 (6 months after initiation) (n = 11) at 3 months (P = 0.32) and at.
Topisirovic et al., (2003) EMBO J,22:
Immunohistochemical analysis.
Morphological alterations in pancreatic islets demonstrate a compensatory response to HFHC diet and STZ-induced β-cell loss. Morphological alterations.
Volume 1, Issue 4, Pages (April 2005)
Zhiyu Wang, Nathaniel W. York, Colin G. Nichols, Maria S. Remedi 
Representative images of human islets infected with strains of CVB
Islet mass and β-cell proliferation is decreased in Hhip–/– embryos (Hip1 in figure). Islet mass and β-cell proliferation is decreased in Hhip–/– embryos.
INT-747 treatment showed antifibrotic, anti-inflammatory, and antioxidative effects on diabetic DBA/2J mice. INT-747 treatment showed antifibrotic, anti-inflammatory,
Cyp8b1−/− mice have improved islet insulin secretion and increased islet insulin content but unchanged β-cell mass. Cyp8b1−/− mice have improved islet.
Expression of the neural stem cell–specific marker nestin in a distinct cell population within pancreatic islets. Expression of the neural stem cell–specific.
Decreased P-IR and total FOXO1 levels in an HFS diet.
Effect of insulin on hepcidin expression in HepG2 cells.
1018-NT-β-cell clusters protect mice from STZ-induced diabetes.
WASH cKO mice display a normal pancreatic development.
Omental FFA production, calculated from the integrated lipolysis over the last 30 min of each insulin infusion period. Omental FFA production, calculated.
α-Cells mainly express SSTR2 and SSTR3
Pancreatic β-cell proliferation.
PD-1, but not PD-L1, expressed by the BDC2
Human and mouse islets express MCH and MCHR1.
Insulin promoter confers β-cell–specific GFP expression in pancreas.
Optimized STZ treatment leads to specific cytotoxicity of insulin-producing cells. Optimized STZ treatment leads to specific cytotoxicity of insulin-producing.
PMPs survive STZ cytotoxicity and produce larger colonies with a higher yield of insulin+ progeny. PMPs survive STZ cytotoxicity and produce larger colonies.
Immune cell activation detected by gene expression in representative pancreatic islets of IDDM rats after successful combination therapy with anti–TNF-α.
Fragment N expression does not affect islet morphology and cellularity
Morphometric analyses of β-cells and immune cells in IDDM rats after successful and nonsuccessful combination therapy with anti–TNF-α and anti-TCR or after.
Grg3 works with Pdx1 to repress α-cell genes and induce glucose-stimulated insulin secretion. Grg3 works with Pdx1 to repress α-cell genes and induce glucose-stimulated.
Zn2+ and NAD(P)H content in Mafa∆panc and Mafa∆panc;Mafb+/− β-cells.
ΑGLP-1R−/− mice show glucose intolerance and disturbed glucagon secretion in response to i.p. glucose administration. αGLP-1R−/− mice show glucose intolerance.
Reduced β-cell mass in MCH-KO mice on normal chow and high-fat diets.
Somatostatin released by δ-cells exerts a tonic inhibition on glucagon and insulin secretion but is not required for the glucagonostatic effect of glucose.
A-N: Immunofluorescence analysis of Bcl family genes in human islets of Langerhans. A-N: Immunofluorescence analysis of Bcl family genes in human islets.
Volume 23, Issue 4, Pages (April 2018)
Insulitis is reduced in CT-treated RIP-LCMV-GP mice.
A: Representative Western blot showing a band migrating at ∼90 kDa corresponding to neprilysin protein. A: Representative Western blot showing a band migrating.
Expression of IRS2 ameliorates the effects of ATF3 in cultured β-cells
Chop deletion preserves β-cell function in P58IPK−/− mice.
Supplementation of c-Rel–competent Treg cells reverts exacerbated diabetes in c-Rel−/− NOD mice. Supplementation of c-Rel–competent Treg cells reverts.
VIP treatment decreased the number of apoptotic cells and increased cell proliferation. VIP treatment decreased the number of apoptotic cells and increased.
Hashimoto et al. Hashimoto et al. (10) provide the data that insulin produced by β-cells is important for the maintenance of islet blood perfusion, and.
ChREBPα increases β-cell mitochondrial activity and ATP production in human islets. ChREBPα increases β-cell mitochondrial activity and ATP production.
Mean (±SE) plasma glucose concentrations before, during, and after infusions of octreotide (with growth hormone) with saline (•), with insulin replacement.
Metformin (Met) reduces membrane-associated TRPA1 levels in rat DRG neurons. Metformin (Met) reduces membrane-associated TRPA1 levels in rat DRG neurons.
Expression of VPAC2 in the pancreas at E13.
Glucose-stimulated insulin secretion, plasma glucagon levels, and pancreatic hormone contents. Glucose-stimulated insulin secretion, plasma glucagon levels,
Comparison of the percentages of ducts in the pancreas containing cells showing positive staining for the different markers between control hamster Ig–and.
Expression of PKCδ in islets and other tissues of control and PKCδKN-overexpressing mice. Expression of PKCδ in islets and other tissues of control and.
A: Photomicrograph of a fibrin gel containing ∼50 islets 2 h after polymerization of a 5-μl fibrinogen solution containing the islets with 5 μl thrombin.
Loss of Phb2 in β-cells induces development of diabetes over a 3-week period in β-Phb2−/− mice. Loss of Phb2 in β-cells induces development of diabetes.
Morphologic changes induced in immortalized human podocytes after treatment with TGF-β1 (10 ng/mL, right) for 3 days when compared with control cells (left),
Expression and function of fragment N in RIP-N mice.
Comparison of the percentages of ducts in the pancreas containing cells showing positive staining for the different markers between control patients and.
Increased pancreatic insulin content and islet size and protection against HFD- and palmitate-induced cell death in PKCδKN-overexpressing mice. Increased.
Chronic rapamycin treatment impairs β-cell mass and insulin clearance in rats. Chronic rapamycin treatment impairs β-cell mass and insulin clearance in.
IL-1R deficiency does not protect syngeneic grafts from destruction.
GFP is expressed selectively in NPY neurons.
Photomicrographs were taken at x400 final magnification.
Median (interquartile range) of sensor glucose (A) and insulin delivery (B) during closed-loop (solid red line and red shaded area) and control period.
A, GP and GR epithelial tumor cells are equally responsive to gefitinib. A, GP and GR epithelial tumor cells are equally responsive to gefitinib. Equal.
Zhiyu Wang, Nathaniel W. York, Colin G. Nichols, Maria S. Remedi 
Presentation transcript:

Grg3 is expressed in most β-cells but less frequently in α-cells. Grg3 is expressed in most β-cells but less frequently in α-cells. A: Triple immunofluorescence of E17.5 pancreas with Grg3 (green), insulin (red), and glucagon (gray) on the same section, showing that most insulin-positive cells are Grg3+ (red arrows), whereas many glucagon-positive cells are Grg3– or have low-level Grg3 expression (gray arrow). B: Immunofluorescence for Grg3, insulin, and glucagon in adult islets, showing that virtually all insulin-positive cells are Grg3+, whereas glucagon-positive cells are Grg3– (white arrows). C: The percentage of Grg3+ β-cells and α-cells was determined at E17.5 (4 animals; 588 α-cells and 932 β-cells analyzed) and adulthood (14 islets from 3 animals; 547 α-cells and 1,479 β-cells analyzed). *P < 0.0001. David E. Metzger et al. Diabetes 2014;63:1804-1816 ©2014 by American Diabetes Association