In the absence of SST, 20 or 30 mmol/L glucose stimulates glucagon release. In the absence of SST, 20 or 30 mmol/L glucose stimulates glucagon release.

Slides:



Advertisements
Similar presentations
Figure 1. GLP-1 induces miR-132 and miR-212 expressions in pancreatic β-cells in vitro. A, miRNA expression profiling of GLP-1-treated INS-1 832/3 cells.
Advertisements

Third-party Mesenchymal Stem Cells Improved Human Islet Transplantation in a Humanized Diabetic Mouse Model  Hao Wu, Di Wen, Ram I Mahato  Molecular Therapy 
IL-1β stimulates CXCL5 and CXCL8 gene expression and protein secretion in A549 cells in a time- and dose-dependent manner. IL-1β stimulates CXCL5 and CXCL8.
Insulin and glucagon secretion: nondiabetic and diabetic subjects.
Volume 125, Issue 4, Pages (October 2003)
Volume 17, Issue 12, Pages (December 2016)
Volume 10, Issue 3, Pages (March 2018)
Volume 127, Issue 5, Pages (November 2004)
Volume 123, Issue 1, Pages (July 2002)
Viability and function of mouse pancreatic cell line.
Glutamate Is a Positive Autocrine Signal for Glucagon Release
Glucose-stimulated insulin secretion in virus-infected human islets.
Volume 17, Issue 12, Pages (December 2016)
Hyperinsulinemic-euglycemic clamps revealed that obese TPL2KO mice have an improved insulin sensitivity compared with obese WT mice. Hyperinsulinemic-euglycemic.
Cyp8b1−/− mice have improved islet insulin secretion and increased islet insulin content but unchanged β-cell mass. Cyp8b1−/− mice have improved islet.
Decreased P-IR and total FOXO1 levels in an HFS diet.
Comparison of the protective effects of R and S isomers of LA on insulin-stimulated 2-DG uptake. Comparison of the protective effects of R and S isomers.
Liver mitochondrial protein FSR
The development of plasma (p-)C-peptide responses to an intravenous glucose (0.5 g glucose/kg body wt) and glucagon (1 mg) infusion test up to 5–7 years.
Involvement of IRS-1 in L-783,281–stimulated increases in [Ca2+]i and exocytosis. Involvement of IRS-1 in L-783,281–stimulated increases in [Ca2+]i and.
Volume 3, Issue 6, Pages (June 2006)
Decreased GLP-1 receptor expression in islets after exposure to high glucose. Decreased GLP-1 receptor expression in islets after exposure to high glucose.
1018-NT-β-cell clusters protect mice from STZ-induced diabetes.
WASH cKO mice display a normal pancreatic development.
Ion channels expression and insulin secretion in the pancreatic islets of male offspring. Ion channels expression and insulin secretion in the pancreatic.
Effect of PIs on insulin release by downstream insulin secretogogues.
α-Cells mainly express SSTR2 and SSTR3
PTx pretreatment abrogates the glucagonostatic effect of high glucose concentrations. PTx pretreatment abrogates the glucagonostatic effect of high glucose.
Models of the mechanisms by which sulfonylureas and glucose control glucagon release. Models of the mechanisms by which sulfonylureas and glucose control.
Arterial plasma glucose level and peripheral GIR in conscious dogs during the basal (−40 to 0 min) and experimental (0–240 min) periods treated with vehicle.
Gyk regulates the hepatic glycerol gluconeogenesis axis and the AKT-FOXO1-PEPCK/G6Pase pathway. Gyk regulates the hepatic glycerol gluconeogenesis axis.
Human and mouse islets express MCH and MCHR1.
Glycemia and glucose tolerance of RIP-N mice.
Nrf2−/− mice suffered greater renal damage by STZ compared with Nrf2+/+ mice. Nrf2−/− mice suffered greater renal damage by STZ compared with Nrf2+/+ mice.
Modulation of insulin sensitivity by IL-6 in mice: A lack of PTP1B prevents chronic effects of IL-6. Modulation of insulin sensitivity by IL-6 in mice:
Left columns: Plasma glucose and serum insulin concentrations, circulating TF-PCA, and FVIIa activity before and during 24 h of selective hyperglycemia.
Zn2+ and NAD(P)H content in Mafa∆panc and Mafa∆panc;Mafb+/− β-cells.
Measurement of insulin release from islets evoked by glucose, diazoxide, and high K+. Measurement of insulin release from islets evoked by glucose, diazoxide,
Effects of in vivo AICAR treatment on blood glucose and lactate concentrations. Effects of in vivo AICAR treatment on blood glucose and lactate concentrations.
A–E: Adiponectin secretion is stimulated via adrenergic pathways in a Ca2+-independent manner. A–E: Adiponectin secretion is stimulated via adrenergic.
Somatostatin released by δ-cells exerts a tonic inhibition on glucagon and insulin secretion but is not required for the glucagonostatic effect of glucose.
Effect of blockade of the Fas receptor on glucose- and interleukin-1β–induced β-cell DNA fragmentation and proliferative activity. Effect of blockade of.
MiRNA expression profiling in adipocytes from wild-type (WT) and leptin-deficient ob/ob mice. miRNA expression profiling in adipocytes from wild-type (WT)
FFAs have differential effects on NFκB translocation and ROS generation. 3T3–L1 adipocytes differentiated in 5 or 25 mmol/l glucose were cultured on glass.
Extracellular Ca2+-dependent cAMP production.
Substrate oxidation and contractile performance of Akita hearts
Inhibition of glucagon-induced glycogenolysis in human primary hepatocytes. Inhibition of glucagon-induced glycogenolysis in human primary hepatocytes.
Effect of 4 weeks of an intensive exercise program on vaspin serum concentrations in normal glucose tolerant (NGT) individuals and patients with IGT or.
Involvement of PKCα in downregulation of GLP-1 receptor by high glucose in isolated rat islets. Involvement of PKCα in downregulation of GLP-1 receptor.
Supplementation of c-Rel–competent Treg cells reverts exacerbated diabetes in c-Rel−/− NOD mice. Supplementation of c-Rel–competent Treg cells reverts.
Arterial and portal plasma glucagon levels and the portal-arterial (P-A) glucagon gradient in the control period (−40 to 0 min) and after administration.
The portal-arterial (P-A) insulin gradient and arterial plasma c-peptide levels in the control period (−40 to 0 min) and after administration of the glycogen.
ChREBPα increases β-cell mitochondrial activity and ATP production in human islets. ChREBPα increases β-cell mitochondrial activity and ATP production.
Glucose stimulates GLP-1 secretion from the perfused rat intestine by a dose- and absorption-dependent manner. Glucose stimulates GLP-1 secretion from.
The lack of effect of denatonium to stimulate insulin release in the absence of extracellular Ca2+ or in the presence of 10 μmol/l nitrendipine. The lack.
Mean (±SE) plasma glucose concentrations before, during, and after infusions of octreotide (with growth hormone) with saline (•), with insulin replacement.
A: Comparison of the glucose-dependent insulinotropic effects of efaroxan and phentolamine. A: Comparison of the glucose-dependent insulinotropic effects.
An anti-BTC neutralizing antibody and a metalloproteinase inhibitor suppress GLP-1-induced DNA synthesis in INS(832/13) cells. [3H]thymidine incorporation.
Glucose-stimulated insulin secretion, plasma glucagon levels, and pancreatic hormone contents. Glucose-stimulated insulin secretion, plasma glucagon levels,
GTTs and ITTs. A: GTTs of WT (◇), LepTg (♦), Akita (open circles), and LepTg:Akita (closed circles) mice at 8 and 16 weeks of age. GTTs and ITTs. A: GTTs.
Oral glucose tolerance testing during hospitalization and at 4 months after infarction. Oral glucose tolerance testing during hospitalization and at 4 months.
Arterial and hepatic sinusoidal plasma insulin levels in conscious dogs during the basal (−40 to 0 min) and experimental (0–240 min) periods treated with.
PKA inhibitors do not markedly affect the potentiation of glucose-induced insulin release by GLP-1. PKA inhibitors do not markedly affect the potentiation.
Chronic rapamycin treatment impairs β-cell mass and insulin clearance in rats. Chronic rapamycin treatment impairs β-cell mass and insulin clearance in.
ADCY5 targets nonmetabolic processes to alter Ca2+ responses.
Effect of GSK-3 inhibitors on basal and insulin-stimulated glucose uptake in human muscle cells. Effect of GSK-3 inhibitors on basal and insulin-stimulated.
Integrated mRNA and microRNA expression and DNA methylation clusters.
Five-day exposure to decitabine (DAC) sensitizes cells to doxorubicin (Doxo). Five-day exposure to decitabine (DAC) sensitizes cells to doxorubicin (Doxo).
NVP-BGJ398 inhibits proliferation of a subset of cancer cell lines.
Four–time point diurnal profiles of plasma glucose concentrations (A) and AUCs (B) over quintiles of HbA1c. ○, AUC1; •, AUC2; ▴, AUC2 − AUC1 (differences.
Presentation transcript:

In the absence of SST, 20 or 30 mmol/L glucose stimulates glucagon release. In the absence of SST, 20 or 30 mmol/L glucose stimulates glucagon release. A, C, and E: Islets from Sst+/+ or Sst−/− mice were perifused with MixAA 6 (A) or MixAA 2 (C and E). The glucose concentration was changed between 1 (G1), 7 (G7), 20 (G20), and 30 (G30) mmol/L as indicated. For one series of experiments shown in C, 23 mmol/L of sucrose (Suc 23) was added to a medium containing G7 when indicated. At the end of the perifusion, diazoxide (Dz; 250 µmol/L for Sst+/+ islets) or SST14 (100 nmol/L for Sst−/− islets) was added to have a basal secretion. Traces are means ± SE for three to four experiments with islets from different preparations. B, D, and F: Univariate scatter plots showing individual data and means ± SE of the average glucagon secretion calculated from the experiments shown on the left (G7, mean of 20–40 min and 120–140 min; G20, G30, or G7 + Suc 23, mean of 48–100 min). *P < 0.05 and **P < 0.01 for comparison between different conditions or islets of different mouse models. The y-axis labels for A–F are at the top of each column of panels. Bao-Khanh Lai et al. Diabetes 2018;67:2239-2253 ©2018 by American Diabetes Association