Brain Insulin Controls Adipose Tissue Lipolysis and Lipogenesis

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• 作者：Thomas Scherer¹ ; ² ; James O'Hare¹ ; ² ; Kelly Diggs-Andrews³ ; Martina Schweiger⁴ ; Bob Cheng¹ ; ² ; Claudia Lindtner¹ ; ² ; Elizabeth Zielinski¹ ; ² ; Prashant Vempati¹ ; ² ; Kai Su¹ ; ² ; Shveta Dighe¹ ; ² ; Thomas Milsom¹ ; ² ; Michelle Puchowicz⁵ ; ⁶ ; Ludger Scheja⁷ ; Rudolf Zechner⁴ ; Simon J. Fisher³ ; Stephen F. Previs⁵ ; ⁶ ; ⁸ ; Christoph Buettner¹ ; ² ; ^{christoph.buettner@mssm.edu}
• 刊名：Cell Metabolism
• 出版年：2011
• 出版时间：2 February 2011
• 年：2011
• 卷：13
• 期：2
• 页码：183-194
• 全文大小：878 K

文摘

Summary

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.