Role for Insulin Signaling in Catecholaminergic Neurons in Control of Energy Homeostasis

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• 作者：A.  ; Christine Kö ; nner¹ ; ³ ; ⁴ ; Simon Hess² ; Sulay Tovar¹ ; ³ ; Andrea Mesaros¹ ; Carmen Sá ; nchez-Lasheras¹ ; ³ ; Nadine Evers¹ ; ³ ; Linda  ; A.W. Verhagen¹ ; ³ ; Hella  ; S. Brö ; nneke⁵ ; André ; Kleinridders¹ ; Brigitte Hampel¹ ; ³ ; Peter Kloppenburg² ; Jens  ; C. Brü ; ning¹ ; ³ ; ⁴ ; ^{bruening@nf-mpg.de"" rel=""nofollow}
• 刊名：Cell Metabolism
• 出版年：2011
• 出版时间：8 June 2011
• 年：2011
• 卷：13
• 期：6
• 页码：720-728
• 全文大小：1120 K

文摘

Summary

Dopaminergic midbrain neurons integrate signals on food palatability and food-associated reward into the complex control of energy homeostasis. To define the role of insulin receptor (IR) signaling in this circuitry, we inactivated IR signaling in tyrosine hydroxylase (Th)-expressing cells of mice (IR^ΔTh). IR inactivation in Th-expressing cells of mice resulted in increased body weight, increased fat mass, and hyperphagia. While insulin acutely stimulated firing frequency in 50 % of dopaminergic VTA/SN neurons, this response was abolished in IR^ΔTh mice. Moreover, these mice exhibited an altered response to cocaine under food-restricted conditions. Taken together, these data provide in vivo evidence for a critical role of insulin signaling in catecholaminergic neurons to control food intake and energy homeostasis.