Related Experiment Video
Updated: Jun 16, 2026

Isolation, Characterization, and Purification of Macrophages from Tissues Affected by Obesity-related Inflammation
Published on: April 3, 2017
Macrophages, inflammation, and insulin resistance
Jerrold M Olefsky1, Christopher K Glass
1Department of Medicine, University of California-San Diego, La Jolla, CA 92093-0651, USA. jolefsky@ucsd.edu
Abstract:
Obesity induces an insulin-resistant state in adipose tissue, liver, and muscle and is a strong risk factor for the development of type 2 diabetes mellitus. Insulin resistance in the setting of obesity results from a combination of altered functions of insulin target cells and the accumulation of macrophages that secrete proinflammatory mediators. At the molecular level, insulin resistance is promoted by a transition in macrophage polarization from an alternative M2 activation state maintained by STAT6 and PPARs to a classical M1 activation state driven by NF-kappaB, AP1, and other signal-dependent transcription factors that play crucial roles in innate immunity. Strategies focused on inhibiting the inflammation/insulin resistance axis that otherwise preserve essential innate immune functions may hold promise for therapeutic intervention.
Related Concept Videos
Type I Diabetes II: Pathophysiology
Type II Diabetes II: Pathophysiology
Inflammation
Chronic Inflammation: Introduction
Type II Diabetes I: Introduction
Insulin: The Receptor and Signaling Pathways

