Brain insulin controls adipose tissue lipolysis and lipogenesis.

Abstract

White adipose tissue (WAT) dysfunction plays a key role in the pathogenesis of type 2 diabetes (DM2). Unrestrained WAT lipolysis results in increased fatty acid release, leading to insulin resistance and lipotoxicity, while impaired de novo lipogenesis in WAT decreases the synthesis of insulin-sensitizing fatty acid species like palmitoleate. Here, we show that insulin infused into the mediobasal hypothalamus (MBH) of Sprague-Dawley rats increases WAT lipogenic protein expression, inactivates hormone-sensitive lipase (Hsl), and suppresses lipolysis. Conversely, mice that lack the neuronal insulin receptor exhibit unrestrained lipolysis and decreased de novo lipogenesis in WAT. Thus, brain and, in particular, hypothalamic insulin action play a pivotal role in WAT functionality.

• Authors: Thomas Scherer, James O'Hare, Kelly Diggs-Andrews, Martina Schweiger, Bob Cheng, Claudia Lindtner, Elizabeth Zielinski, Prashant Vempati, Kai Su, Shveta Dighe, Thomas Milsom, Michelle Puchowicz, Ludger Scheja, Rudolf Zechner, Simon J Fisher, Stephen F Previs, Christoph Buettner
• Journal: Cell metabolism (Cell Metab) Vol. 13 Issue 2 Pg. 183-94 (Feb 02 2011) ISSN: 1932-7420 [Electronic] United States
• PMID: 21284985 (Publication Type: Journal Article, Research Support, N.I.H., Extramural, Research Support, Non-U.S. Gov't)
• Copyright: Copyright © 2011 Elsevier Inc. All rights reserved.

Chemical References

• Insulin
• Receptor, Insulin
• Glucose

Topics

• Adipose Tissue, White (metabolism)
• Animals
• Brain (metabolism)
• Glucose (metabolism)
• Insulin (metabolism)
• Lipogenesis
• Lipolysis
• Male
• Mice
• Rats
• Rats, Sprague-Dawley
• Receptor, Insulin (metabolism)
• Signal Transduction