Adipocyte/macrophage fatty acid binding proteins in metabolic syndrome.
The link between inflammation and the development of insulin resistance, type 2 diabetes, and atherosclerosis has been uncovered in the past decade. Although the molecular mechanisms underlying the co-occurrence of these metabolic and inflammatory diseases are not fully understood, several molecular players, integrating stress and inflammatory responses with metabolic homeostasis, were discovered recently. One of these molecular integration sites is through the action of cytosolic lipid chaperones or fatty acid binding proteins (FABPs), which are common to adipocytes and macrophages. Furthermore, studies in a variety of genetic models demonstrated that the FABPs aP2 and mal1 are critical mediators of many components of metabolic syndrome in mice. These exciting findings raise the possibility that FABPs represent desirable therapeutic targets for metabolic syndrome. In this review, we describe the findings demonstrating FABP's role in metabolic and inflammatory diseases and highlight recent advances in understanding the mechanisms of FABP function at the cellular and molecular level.
Erbay
Ebru
E
Department of Genetics and Complex Diseases, Harvard School of Public Health, Boston, MA 02115, USA.
Cao
Haiming
H
Hotamisligil
Gökhan S
GS
D017667:Adipocytes / Q000502:physiology; D000818:Animals; D001249:Asthma / Q000503:physiopathology; D050197:Atherosclerosis / Q000503:physiopathology; D003920:Diabetes Mellitus / Q000503:physiopathology; D050556:Fatty Acid-Binding Proteins / Q000502:physiology*; D022781:Hepatocytes / Q000502:physiology; D006801:Humans; D007249:Inflammation / Q000503:physiopathology; D007333:Insulin Resistance / Q000502:physiology; D008264:Macrophages / Q000502:physiology; D024821:Metabolic Syndrome / Q000378:metabolism; D009765:Obesity / Q000503:physiopathology
D050556:Fatty Acid-Binding Proteins