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Insulin sensitivity: modulation by nutrients and inflammation.

Simon Schenk¹, Maziyar Saberi, Jerrold M Olefsky

¹Department of Medicine, Division of Endocrinology and Metabolism, UCSD, La Jolla, California 92093, USA.

The Journal of Clinical Investigation

|September 5, 2008

Summary

Obesity and nutrient excess cause insulin resistance through distinct yet connected pathways. Understanding these mechanisms, particularly the role of macrophages in inflammation, is key to addressing metabolic diseases like type 2 diabetes.

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Area of Science:

Metabolic science
Endocrinology
Pathophysiology

Background:

Insulin resistance is a central metabolic characteristic of obesity.
It is a significant factor in the development of diseases such as type 2 diabetes.

Purpose of the Study:

To review the mechanisms linking nutrient excess and obesity to insulin resistance.
To propose that these mechanisms are distinct but interrelated.
To highlight the role of macrophages in obesity-induced inflammation and insulin resistance.

Main Methods:

Review of current literature on nutrient sensing in skeletal muscle.
Analysis of the complex interplay of factors contributing to obesity-induced insulin resistance.
Focus on the role of macrophages in inflammation and insulin resistance.

Main Results:

Nutrient sensing pathways in skeletal muscle directly regulate insulin action.
Obesity-induced insulin resistance involves systemic fatty acid excess, adipose tissue microhypoxia, ER stress, and inflammation.
Macrophages are implicated as key mediators of inflammation and insulin resistance in obesity.

Conclusions:

Brief nutrient excess and obesity induce insulin resistance through different, interconnected pathways.
Macrophages play a critical role in propagating inflammation and driving insulin resistance in the context of obesity.
An integrative perspective on nutrient-obesity interactions is crucial for understanding insulin sensitivity regulation.