Treatment of diabetes and atherosclerosis by inhibiting fatty-acid-binding protein aP2

By M. Furuhashi, Gurol Tuncman, Cem Z. Görgün, L. Makowski, G. Atsumi, Éric Vaillancourt, K. Kono, V. Babaev, S. Fazio, M. Linton and 4 more. Nature, 2007

706 citations recorded by the source corpus.

Subfields: Cancer Research, Epidemiology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/cd6ea78a19f9ee036253ffdc86a39de6874d0221

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cancer Research

1. Herbert Tilg
2. A. Moschen
3. A. Chawla
4. G. Hotamışlıgil

In Epidemiology

1. A. Chawla
2. Herbert Tilg
3. A. Moschen
4. J. Odegaard
5. Ping Li
6. Suneng Fu
7. Ling Yang
8. M. Wymann

In Molecular Biology

1. A. Chawla
2. M. Wymann
3. Herbert Tilg
4. R. Schneiter
5. A. Moschen
6. G. Hotamışlıgil

Citations in the corpus

• Defective Hepatic Autophagy in Obesity Promotes ER Stress and Causes Insulin Resistance (2010, methodology): “Western Blot Analysis Proteins were extracted from tissues and subjected to SDS-polyacrylamide gel electrophoresis, as previously described (Furuhashi et al., 2007).”
• Inflammatory Mechanisms in the Regulation of Insulin Resistance (2008, background): “(103) have recently demonstrated that an orally active smallmolecule inhibitor of aP2 is an effective therapeutic agent against severe atherosclerosis and T2DM in various mouse models.”
• Alternative M2 activation of Kupffer cells by PPARdelta ameliorates obesity-induced insulin resistance. (2008, background): “In support of this notion, deletion or inhibition of cytosolic fatty acid-binding proteins improves insulin sensitivity (Furuhashi et al., 2007; Hotamisligil et al., 1996); however, the potential involvement of fatty acid-binding proteins in alternative macrophage activation will require further inv”
• Lipid signalling in disease (2008, background): “Remarkably, mice lacking FABP4 or FABP5, or animals treated with a small-molecule inhibitor of FABP4, are protected against almost every aspect of the metabolic syndrome, including visceral obesity, insulin resistance, hepatosteatosis and atherosclerosi”