Small-molecule inhibitors of FABP4/5 ameliorate dyslipidemia but not insulin resistance in mice with diet-induced obesity

J Lipid Res. 2011 Apr;52(4):646-56. doi: 10.1194/jlr.M012757. Epub 2011 Feb 4.

Abstract

Fatty acid binding protein-4 (FABP4) and FABP5 are two closely related FA binding proteins expressed primarily in adipose tissue and/or macrophages. The small-molecule FABP4 inhibitor BMS309403 was previously reported to improve insulin sensitivity in leptin-deficient Lep(ob)/Lep(ob) (ob/ob) mice. However, this compound was not extensively characterized in the more physiologically relevant animal model of mice with diet-induced obesity (DIO). Here, we report the discovery and characterization of a novel series of FABP4/5 dual inhibitors represented by Compounds 1-3. Compared with BMS309403, the compounds had significant in vitro potency toward both FABP4 and FABP5. In cell-based assays, Compounds 2 and 3 were more potent than BMS309403 to inhibit lipolysis in 3T3-L1 adipocytes and in primary human adipocytes. They also inhibited MCP-1 release from THP-1 macrophages as well as from primary human macrophages. When chronically administered to DIO mice, BMS309403 and Compound 3 reduced plasma triglyceride and free FA levels. Compound 3 reduced plasma free FAs at a lower dose level than BMS309403. However, no significant change was observed in insulin, glucose, or glucose tolerance. Our results indicate that the FABP4/5 inhibitors ameliorate dyslipidemia but not insulin resistance in DIO mice.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • 3T3-L1 Cells
  • Adipocytes / drug effects
  • Adipocytes / metabolism
  • Animals
  • Cells, Cultured
  • Chemokine CCL2 / metabolism
  • Dietary Fats / adverse effects*
  • Dyslipidemias / chemically induced
  • Dyslipidemias / drug therapy
  • Fatty Acid-Binding Proteins / antagonists & inhibitors*
  • Fatty Acids, Nonesterified / blood
  • Hypolipidemic Agents / therapeutic use*
  • Insulin Resistance
  • Lipolysis / drug effects
  • Macrophages / drug effects
  • Macrophages / metabolism
  • Mice
  • Neoplasm Proteins / antagonists & inhibitors*
  • Obesity / chemically induced
  • Obesity / drug therapy*
  • Triglycerides / blood

Substances

  • Ccl2 protein, mouse
  • Chemokine CCL2
  • Dietary Fats
  • Fabp4 protein, mouse
  • Fabp5 protein, mouse
  • Fatty Acid-Binding Proteins
  • Fatty Acids, Nonesterified
  • Hypolipidemic Agents
  • Neoplasm Proteins
  • Triglycerides