期刊
CELL METABOLISM
卷 13, 期 6, 页码 720-728出版社
CELL PRESS
DOI: 10.1016/j.cmet.2011.03.021
关键词
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资金
- Center for Molecular Medicine (CMMC), University of Cologne [TVA1, D7]
- European Union [FP7-HEALTH-2009-241592]
- DFG [BR 1492/7-1, KL 762/2-2, KL 762/4-1]
- Federal Ministry of Education and Research [FKZ01GIO845]
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 Delta Th). 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 Delta Th 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.
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