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.

Slides:



Advertisements
Similar presentations
Philip J. Barter, et al. Circulation 2011;124:
Advertisements

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.
The inhibition of PI3K and Akt in human T cells selectively inhibits the proliferation of human Tregs compared with Tconvs in a dose-dependent manner.
Postprandial glucose flux in nondiabetic controls.
DNAPKcs is required for DNA repair in the presence of androgen.
Mean daily glucose concentration and frequency of hypoglycemia in long-term care residents with type 2 diabetes. Mean daily glucose concentration and frequency.
AMPK induces VEGF-A production by upregulating ERK signaling.
Hyperinsulinemic-euglycemic clamps revealed that obese TPL2KO mice have an improved insulin sensitivity compared with obese WT mice. Hyperinsulinemic-euglycemic.
Lypolytic activity (glycerol release, mg/ml) measured in adipocytes culture medium after 2 h incubation with isoproterenol or 8-Cl-cAMP. Lypolytic activity.
Central nervous system BDNF infusion fails to increase tissue glucose uptake in uncontrolled insulin-deficient diabetes. Central nervous system BDNF infusion.
Serial measurements of serum glucose, anion gap, serum carbon dioxide, and serum triglycerides throughout the patient's hospital stay. Serial measurements.
Chronic PDGFRα activation reduces sensitivity of PDGFRα-positive GBM cells to translational inhibitor–induced suppression on cell viability. Chronic PDGFRα.
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.
Glucose, insulin, and AGE levels during an OGC before and after RT
Correlation between muscle Hsp-72 mRNA expression and rates of glucose and lipid turnover, as determined in protocol 2 (n = 36). Correlation between muscle.
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.
P38 activation mediates chronic insulin-induced IRS1 and IRS2 degradation and is involved in myocardial insulin resistance in vitro. p38 activation mediates.
Rosiglitazone induces Pdk4 expression in rat and human adipose tissue ex vivo and in 3T3–F442A adipocytes. Rosiglitazone induces Pdk4 expression in rat.
Glucose infusion rate required to maintain the hyperglycemic clamp during the experimental period in sedentary and exercised dogs receiving basal or elevated.
Activation of β-adrenoceptors improves glucose tolerance in diabetic animals and increases glucose uptake in vivo, ex vivo, and in vitro. Activation of.
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.
A: The change of plasma glucose in opioid μ-receptor knockout diabetic mice and wild-type controls receiving an oral intake of metformin (100 mg/kg). A:
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.
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.
Cell proliferations, ROS production, and ATP levels in HASMCs cultured under high-glucose condition. Cell proliferations, ROS production, and ATP levels.
Left columns: Plasma glucose and serum insulin concentrations, circulating TF-PCA, and FVIIa activity before and during 24 h of selective hyperglycemia.
AGE stimulation increases MMP2 and MMP9 secretion and activation in cultured retinal endothelial cells. AGE stimulation increases MMP2 and MMP9 secretion.
Sustained activation of AMPK α2 in muscle of subjects with type 2 diabetes after an overnight withdrawal of metformin. Sustained activation of AMPK α2.
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,
The underlying physiological basis of the HOMA model.
Inhibition of GCS-derived ganglioside biosynthesis results in increased insulin sensitivity in hypothalamic cells. Inhibition of GCS-derived ganglioside.
A–E: Adiponectin secretion is stimulated via adrenergic pathways in a Ca2+-independent manner. A–E: Adiponectin secretion is stimulated via adrenergic.
DHA suppresses the translocation of NFκB and ROS generation stimulated by excess glucose and palmitate. 3T3–L1 adipocytes were cultured in 5 or 25 mmol/l.
Phosphorylation of AMPK-Thr172 before and after metformin treatment in muscle from subjects with type 2 diabetes. Phosphorylation of AMPK-Thr172 before.
Effect of blockade of the Fas receptor on glucose- and interleukin-1β–induced β-cell DNA fragmentation and proliferative activity. Effect of blockade of.
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.
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.
ATL-801 treatment increases insulin sensitivity in KKAY mice.
Adoptive transfer of purified activated G9Cα−/−
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.
Effects of N-acetyl-l-cysteine, genistein, PD98059, and SB on NF-κB stimulation by CML-HSA. Effects of N-acetyl-l-cysteine, genistein, PD98059, and.
Food intake in response to central infusion of glucose (squares) or insulin (triangles) and in response to successive central infusion of insulin, insulin.
Effect of high glucose and agents that alter mitochondrial metabolism on ROS production and expression of COX-2 mRNA in HMCs. Cells were incubated with.
Functional promoter activity of the human COX-2 gene in HMCs
Identification of divergent effects of FEN in fully differentiated adipocytes. Identification of divergent effects of FEN in fully differentiated adipocytes.
An anti-BTC neutralizing antibody and a metalloproteinase inhibitor suppress GLP-1-induced DNA synthesis in INS(832/13) cells. [3H]thymidine incorporation.
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.
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.
Effects of vinegar (□) and placebo (⧫) on plasma glucose (A–C) and insulin (D–F) responses after a standard meal in control subjects, insulin-resistant.
Clinical responses to therapy from baseline to week 24 and end point with last observation carried forward (LOCF). Clinical responses to therapy from baseline.
ALT-803 stimulates proliferation and activation of human NK cells and T cells in vitro. ALT-803 stimulates proliferation and activation of human NK cells.
FACS analyses of the inhibitory effect induced by mixed docetaxel, gefitinib, and cyclopamine on EGF plus SHHNp–stimulated PC3 cells. FACS analyses of.
Flow cytometric analysis of ROS production in oligonucleotide-treated PC3 prostate cancer cells as demonstrated by the oxidation of H2DCF → DCF and HE.
WP1066 inhibits the progression of OCIM2 cells through the cell cycle.
EGFR signaling regulates transcription of PDGFRβ gene.
A, cell number was assessed 96 hours after exposure to indicated treatment in indicated cell models. A, cell number was assessed 96 hours after exposure.
Functional SLC6A3 in ccRCC cell lines KMRC3 and SNU-349, but not in conventional cell lines. Functional SLC6A3 in ccRCC cell lines KMRC3 and SNU-349, but.
AKT activation in HCC2429 is SRC- but not Notch-dependent.
A, left: LNCaP cells were cultured in media containing complete serum, treated for 24 hours with either ethanol control (0.01%), ABT888 (2.5 mmol/L), or.
IL-1 and PGE2 mediate GRO-α, IL-6, and IL-8, but not RANTES induction in carcinoma cell–MSC coculture. IL-1 and PGE2 mediate GRO-α, IL-6, and IL-8, but.
Cumulative mean numbers of confirmed (plasma glucose ≤3
Presentation transcript:

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 glucose uptake in human muscle cells. A: Time course of glucose uptake activation in human muscle cells by CHIR 98023 (2 μmol/l), insulin (33 nmol/l), or LiCl (20 mmol/l). Results are averages ± SE, normalized against glucose uptake in untreated control cells from the same individual (n = 4). B: Muscle cells from nondiabetic (n = 5) and type 2 diabetic (n = 4) subjects were treated for 4 days with CHIR 98023 (2.5 μmol/l), CHIR 98014 (2.5 μ mol/l), inactive compound (IA, 2.5 μmol/l), or LiCl (20 mmol/l), as described in detail in research design and methods. After chronic treatment, half of the cell cultures were washed with fresh media and incubated with 33 nmol/l insulin for 2 h. Results are averages ± SE, normalized against the control and basal value for each individual. *P < 0.05 vs. untreated paired control; †P < 0.05 vs. paired basal. Svetlana E. Nikoulina et al. Diabetes 2002;51:2190-2198 ©2002 by American Diabetes Association