PKA inhibitors do not markedly affect the potentiation of glucose-induced insulin release by GLP-1. PKA inhibitors do not markedly affect the potentiation.

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

Plasma insulin concentrations (A) and insulin secretion rates (B) in response to molar increments of plasma glucose concentration during the graded glucose.
Dynamic Modulation of Interendothelial Gap Junctional Communication by 11,12-Epoxyeicosatrienoic Acid by Rüdiger Popp, Ralf P. Brandes, Gregor Ott, Rudi.
Choosing glucose-lowering medication in those with established ASCVD, HF, and CKD. CV, cardiovascular; DPP-4i, dipeptidyl peptidase 4 inhibitor; GLP-1.
Nat. Rev. Endocrinol. doi: /nrendo
Insulin and glucagon secretion: nondiabetic and diabetic subjects.
Glucose homeostasis: roles of insulin, glucagon, amylin, and GLP-1.
The means and SDs of the data from all Glucommander runs from 1984 to 1998 are graphed. The means and SDs of the data from all Glucommander runs from 1984.
Respondents’ perceptions on (A) the potential of IDegLira compared with basal-bolus therapy to improve patient motivation to reach their target blood glucose.
Glucose-stimulated insulin secretion in virus-infected human islets.
Lypolytic activity (glycerol release, mg/ml) measured in adipocytes culture medium after 2 h incubation with isoproterenol or 8-Cl-cAMP. Lypolytic activity.
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.
NOx ASR (in mmol/day), arginine Ra (in µmol/kg × min), the fraction of arginine flux converted to NOx (%), and the insulin-mediated glucose disposal (M)
Hyperinsulinemic-euglycemic clamp–derived insulin sensitivity (glucose disposal), model-derived insulin secretion parameters (sensitivity first-phase insulin.
Effect of insulin on hepcidin expression in HepG2 cells.
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.
Changes (mean +SEM) in glucose, insulin, glucagon-like peptide (GLP)-1 and ghrelin from the baseline values after administration of placebo (broken lines.
Decreased GLP-1 receptor expression in islets after exposure to high glucose. Decreased GLP-1 receptor expression in islets after exposure to high glucose.
Effect of palmitate and oleate preincubation on fatty acid oxidation, triglyceride content, glycerol release, and HSL mRNA. Effect of palmitate and oleate.
1018-NT-β-cell clusters protect mice from STZ-induced diabetes.
P38 activation mediates chronic insulin-induced IRS1 and IRS2 degradation and is involved in myocardial insulin resistance in vitro. p38 activation mediates.
Plasma glucose (A) and glucose specific activity (B) during euglycemic clamp experiments. Plasma glucose (A) and glucose specific activity (B) during euglycemic.
GSIS. GSIS. In vivo: serum insulin levels at fasting state and 30 min after glucose injection (A) and the fold change in serum insulin after glucose loading.
Glucose infusion rate required to maintain the hyperglycemic clamp during the experimental period in sedentary and exercised dogs receiving basal or elevated.
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.
PTx pretreatment abrogates the glucagonostatic effect of high glucose concentrations. PTx pretreatment abrogates the glucagonostatic effect of high glucose.
Influence of insulin on AdipoR1 mRNA expression in murine C2C12 myotubes. Influence of insulin on AdipoR1 mRNA expression in murine C2C12 myotubes. Data.
Time-dependent effects of IL-6 on tyrosine phosphorylation of IRS-1.
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.
Glycemia and glucose tolerance of RIP-N mice.
Correlation of myotube AdipoR1 (A) and AdipoR2 (B) mRNA expression with insulin secretion (n = 40). Correlation of myotube AdipoR1 (A) and AdipoR2 (B)
IL-6 inhibits insulin-induced formation of p85/IRS-1 complexes.
Zn2+ and NAD(P)H content in Mafa∆panc and Mafa∆panc;Mafb+/− β-cells.
IRS-1 and -2 expression in four mesangial cell lines from different D-NOD (A and B) and ND-NOD (C and D) mice. IRS-1 and -2 expression in four mesangial.
Measurement of insulin release from islets evoked by glucose, diazoxide, and high K+. Measurement of insulin release from islets evoked by glucose, diazoxide,
A: QTL analysis of genotyping data on chromosome 12 revealed a locus linked to glucose levels in F2 mice at 6 months of age at marker D12Mit231 with a.
Somatostatin released by δ-cells exerts a tonic inhibition on glucagon and insulin secretion but is not required for the glucagonostatic effect of glucose.
Extracellular Ca2+-dependent cAMP production.
The effects of various fatty acids on the activity of the human ABCA1 promoter in RAW264.7 cells. The effects of various fatty acids on the activity of.
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.
GLP-1 and gastrin combination therapy increases pancreatic insulin content (A) and β-cell mass (B) in NOD mice. GLP-1 and gastrin combination therapy increases.
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.
EPA treatment rescued LPL RNAi–induced suppression of MTCOI protein expression. EPA treatment rescued LPL RNAi–induced suppression of MTCOI protein expression.
GLP-1 and gastrin combination therapy induces immunoregulatory cell activity in NOD mice. GLP-1 and gastrin combination therapy induces immunoregulatory.
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.
Fig. 2 The glucose binding and charge-switch study.
Fig. 3 Glucose- and structure-dependent insulin release.
Mean (±SE) plasma glucose concentrations before, during, and after infusions of octreotide (with growth hormone) with saline (•), with insulin replacement.
Npas4 is a stress-induced factor in pancreatic β-cells.
Src kinases mediate TSP-1 inhibition of AC and PKA activity.
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.
Effect of IBMP and PKG on cAMP levels
The activity of transcription factor CREBP downstream of MEK signaling is markedly reduced in insulin-resistant macrophages. The activity of transcription.
Chronic rapamycin treatment impairs β-cell mass and insulin clearance in rats. Chronic rapamycin treatment impairs β-cell mass and insulin clearance in.
DPP-4 enhances M1 polarization and inhibits M2 polarization in macrophages in an ROS-dependent manner. DPP-4 enhances M1 polarization and inhibits M2 polarization.
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.
Effects of vinegar (□) and placebo (⧫) on plasma glucose (A–C) and insulin (D–F) responses after a standard meal in control subjects, insulin-resistant.
Effects of receptor antagonists, Ca2+ channel blocker, Ca2+depletion, and protein kinase inhibitors on CREB phosphorylation in cultured hippocampal neurons.
Plasma glucose (A), serum insulin (B), serum C peptide (C) and plasma GLP-1 level (D) during the 2-hour OGTT among subjects with normal glucose tolerance.
Distribution of daily frequency of BGM
Postprandial glucose, insulin and glucagon-like peptide-1 (GLP-1) levels following carbohydrate-first (CF), carbohydrate-last (CL) and sandwich (S) meal.
FACS analyses of the inhibitory effect induced by mixed docetaxel, gefitinib, and cyclopamine on EGF plus SHHNp–stimulated PC3 cells. FACS analyses of.
Effects of metformin on GLP-1(7–36)amide degradation in vitro shown by GLP-1(7–36)amide concentrations (% variation from time 0) after a 30-min incubation.
(A) Twenty-four-hour plasma profiles of insulin and amylin in healthy subjects. (A) Twenty-four-hour plasma profiles of insulin and amylin in healthy subjects.
Presentation transcript:

PKA inhibitors do not markedly affect the potentiation of glucose-induced insulin release by GLP-1. PKA inhibitors do not markedly affect the potentiation of glucose-induced insulin release by GLP-1. Insulin secretion from isolated islets was determined as described in Fig. 1. Islets were incubated with or without 10 nmol/l GLP-1. H-89 and KT5720 were used at 5 μmol/l, Rp-cAMP (Rp-c) was used at 100 μmol/l, and nifedipine (Nif) was used at 1 μmol/l. The data are the means ± SD from four independent experiments. Mitsuhiro Nakazaki et al. Diabetes 2002;51:3440-3449 ©2002 by American Diabetes Association