TY - JOUR
T1 - Brain insulin controls adipose tissue lipolysis and lipogenesis
AU - Scherer, Thomas
AU - OHare, James
AU - Diggs-Andrews, Kelly
AU - Schweiger, Martina
AU - Cheng, Bob
AU - Lindtner, Claudia
AU - Zielinski, Elizabeth
AU - Vempati, Prashant
AU - Su, Kai
AU - Dighe, Shveta
AU - Milsom, Thomas
AU - Puchowicz, Michelle
AU - Scheja, Ludger
AU - Zechner, Rudolf
AU - Fisher, Simon J.
AU - Previs, Stephen F.
AU - Buettner, Christoph
PY - 2011/2/2
Y1 - 2011/2/2
N2 - 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.
AB - 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.
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U2 - 10.1016/j.cmet.2011.01.008
DO - 10.1016/j.cmet.2011.01.008
M3 - Article
C2 - 21284985
AN - SCOPUS:79551506567
SN - 1550-4131
VL - 13
SP - 183
EP - 194
JO - Cell Metabolism
JF - Cell Metabolism
IS - 2
ER -