• Home
  • Search Results
  • Effect of extracellular vesicles of human adipose tissue on insulin signaling in liver and muscle cells.

Effect of extracellular vesicles of human adipose tissue on insulin signaling in liver and muscle cells.

Obesity (Silver Spring, Md.) (2014-07-22)
Mariëtte E G Kranendonk, Frank L J Visseren, Joost A van Herwaarden, Esther N M Nolte-'t Hoen, Wilco de Jager, Marca H M Wauben, Eric Kalkhoven
ABSTRACT

Insulin resistance (IR) is a key mechanism in obesity-induced cardiovascular disease. To unravel mechanisms whereby human adipose tissue (AT) contributes to systemic IR, the effect of human AT-extracellular vesicles (EVs) on insulin signaling in liver and muscle cells was determined. EVs released from human subcutaneous (SAT) and omental AT (OAT)-explants ex vivo were used for stimulation of hepatocytes and myotubes in vitro. Subsequently, insulin-induced Akt phosphorylation and expression of gluconeogenic genes (G6P, PEPCK) was determined. AT-EV adipokine levels were measured by multiplex immunoassay, and AT-EVs were quantified by high-resolution flow cytometry. In hepatocytes, AT-EVs from the majority of patients inhibited insulin-induced Akt phosphorylation, while EVs from some patients stimulated insulin-induced Akt phosphorylation. In myotubes AT-EVs exerted an ambiguous effect on insulin signaling. Hepatic Akt phosphorylation related negatively to G6P-expression by both SAT-EVs (r = -0.60, P = 0.01) and OAT-EVs (r = -0.74, P = 0.001). MCP-1, IL-6, and MIF concentrations were higher in OAT-EVs compared to SAT-EVs and differently related to lower Akt phosphorylation in hepatocytes. Finally, the number of OAT-EVs correlated positively with liver enzymes indicative for liver dysfunction. Human AT-EVs can stimulate or inhibit insulin signaling in hepatocytes- possibly depending on their adipokine content- and may thereby contribute to systemic IR.

MATERIALS
Product Number
Brand
Product Description

Sigma-Aldrich
Anti-AKT antibody produced in rabbit, affinity isolated antibody
Sigma-Aldrich
Anti-AKT1 antibody produced in rabbit, Prestige Antibodies® Powered by Atlas Antibodies, affinity isolated antibody, buffered aqueous glycerol solution
Sigma-Aldrich
Anti-AKT1 antibody produced in rabbit, affinity isolated antibody
Sigma-Aldrich
Anti-AKT antibody produced in rabbit, affinity isolated antibody
Sigma-Aldrich
Anti-AKT antibody produced in rabbit, affinity isolated antibody
Sigma-Aldrich
Anti-AKT antibody produced in rabbit, affinity isolated antibody
Sigma-Aldrich
Anti-Akt1 antibody produced in rabbit, affinity isolated antibody, buffered aqueous solution
Sigma-Aldrich
Anti-AKT1 (Ab-473) antibody produced in rabbit, affinity isolated antibody
Sigma-Aldrich
Anti-AKT1 (Ab-450) antibody produced in rabbit, affinity isolated antibody
Sigma-Aldrich
Anti-AKT1 (Ab-308) antibody produced in rabbit, affinity isolated antibody
Sigma-Aldrich
Monoclonal Anti-AKT1 antibody produced in mouse, clone 6D6, purified immunoglobulin, buffered aqueous solution
Sigma-Aldrich
Monoclonal Anti-AKT1 antibody produced in mouse, clone 2H1, purified immunoglobulin, buffered aqueous solution
Sigma-Aldrich
Monoclonal Anti-AKT1 antibody produced in mouse, clone 4B9, purified immunoglobulin, buffered aqueous solution
Sigma-Aldrich
Monoclonal Anti-AKT1 antibody produced in mouse, clone 6G6, purified immunoglobulin, buffered aqueous solution
Sigma-Aldrich
Anti-AKT1 antibody produced in rabbit, affinity isolated antibody
Sigma-Aldrich
Anti-AKT1 (ab1) antibody produced in chicken, affinity isolated antibody, buffered aqueous solution
Sigma-Aldrich
Monoclonal Anti-AKT1 antibody produced in mouse, clone 2E11, purified immunoglobulin, buffered aqueous solution
Sigma-Aldrich
Monoclonal Anti-Rac antibody produced in mouse, clone 23A8, purified immunoglobulin, buffered aqueous solution
Sigma-Aldrich
Rabbit anti-AKT1 Antibody, Affinity Purified, Powered by Bethyl Laboratories, Inc.