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Antimicrobial-Sensing Proteins in Obesity and Type 2 Diabetes

J. Moreno-Navarrete,J. Fernández-Real

Published 2011 in Diabetes Care

ABSTRACT

Obesity is well known to be associated with a cluster of metabolic diseases such as dyslipidemia, hypertension, insulin resistance, type 2 diabetes, and atherosclerosis (1). Alterations of the innate immune system are increasingly recognized to be intrinsically linked to metabolic pathways in humans (2). Central to metabolic diseases is insulin resistance associated with a low-grade inflammatory status (3). The mechanisms through which proinflammatory cytokines, such as tumor necrosis factor (TNF)-α, interleukin (IL)-6, and IL-1α, interact with cellular insulin signal transduction cascades have been better understood in the last few years (4–6). In vivo, a direct correlation between increased circulating proinflammatory cytokines and insulin resistance has been well demonstrated (3,7). The origin of this increased inflammatory activity in obesity and type 2 diabetes is virtually unknown. Immune system homeostasis is challenged by continuous external insults, such as saturated fatty acid–rich diets (8), pathogen-associated molecular patterns like lipopolysaccharide (LPS) (9), advanced glycation end products (AGEs) (10), burden of infection (11), and oxidative stress (12). These continuous insults could result in a chronic low level of inflammation associated with insulin resistance. Here, we review the potential significance of neutrophil dysfunction in subjects with type 2 diabetes and the consequence of altered antimicrobial-sensing protein profile in obesity-related metabolic disturbances. Given that 60–70% of blood leukocytes are granulocytes and over 90% of granulocytes are neutrophils, polymorphonuclear cells (PMNs) are the largest fraction of white blood cells. PMNs possess a variety of functions, including chemotaxis, adhesion to the endothelium and foreign agents, phagocytosis, and microbicidal activity. PMNs are able to penetrate and migrate into infected tissues and destroy invading microorganisms after internalization by producing multiple toxic agents such as reactive oxygen species (ROS), proteases (elastase), and proteins interfering with bacterial development. Chronic disease (such as type 2 diabetes), age-associated insulin resistance, nutrition, …

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