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Differentiated Mouse Adipocytes in Primary Culture: A Model of Insulin Resistance

Differentiated Mouse Adipocytes in Primary Culture: A Model of Insulin Resistance

Published on: February 17, 2023

Insulin inhibits tissue factor expression in monocytes.

A J Gerrits¹, C A Koekman, C Yildirim

¹Department of Clinical Chemistry and Haematology, University Medical Center Utrecht, Utrecht, The Netherlands.

Journal of Thrombosis and Haemostasis : JTH

|November 6, 2008

Summary

Insulin inhibits tissue factor (TF) expression in monocytes, even in type 2 diabetes mellitus. This insulin effect on monocytes may counteract hyperactivity and reduce clotting risk.

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Area of Science:

Immunology
Endocrinology
Vascular Biology

Background:

Platelets in type 2 diabetes mellitus (T2DM) exhibit insulin resistance and hyperactivity.
Investigating insulin's effect on monocytes is crucial for understanding T2DM-related vascular complications.

Purpose of the Study:

To determine if monocytes are responsive to insulin.
To elucidate the mechanism by which insulin affects monocyte function.

Main Methods:

Assessed LPS-induced tissue factor (TF) upregulation in human monocytes and THP-1 cells.
Measured TF inhibition by varying insulin concentrations.
Investigated insulin receptor (INS-R) phosphorylation and complex formation with G(i)alpha(2).
Analyzed the impact of insulin on cAMP levels and Ca(2+) mobilization.

Main Results:

Insulin dose-dependently inhibited TF upregulation in monocytes and THP-1 cells.
Insulin reduced cytosolic, membrane-bound, and microparticle TF expression.
Insulin interfered with LPS-induced cAMP suppression via INS-R and G(i)alpha(2) complex formation.
Insulin modulated Ca(2+) signaling pathways involved in TF synthesis.

Conclusions:

Insulin effectively inhibits TF expression in monocytes and their microparticles.
This inhibition occurs through interference with G(i)alpha(2)-mediated cAMP suppression.
Insulin's action attenuates Ca(2+)-mediated TF synthesis, potentially mitigating T2DM-related hypercoagulability.