Abstract:
BACKGROUND:Overconsumption of calorically dense foods contributes substantially to the current obesity epidemic. The adiposity hormone leptin has been identified as a potential modulator of reward-induced feeding. The current study asked whether leptin signaling within the lateral hypothalamus (LH) and midbrain is involved in effort-based responding for food rewards and/or the modulation of mesolimbic dopamine. METHODS:The contribution of endogenous leptin signaling for food motivation and mesolimbic dopamine tone was examined after viral-mediated reduction of the leptin receptor within LH and midbrain neurons in male rats. RESULTS:Knockdown of leptin receptors selectively in the LH caused increased body weight, caloric consumption, and body fat in rats maintained on a calorically dense diet. Knockdown of leptin receptors selectively in midbrain augmented progressive ratio responding for sucrose and restored high-fat, diet-induced suppression of dopamine content in the nucleus accumbens. CONCLUSIONS:In summary, endogenous leptin signaling in the hypothalamus restrains the overconsumption of calorically dense foods and the consequent increase in body mass, whereas leptin action in the midbrain regulates effort-based responding for food rewards and mesolimbic dopamine tone. These data highlight the ability of leptin to regulate overconsumption of palatable foods and food motivation through pathways that mediate energy homeostasis and reward, respectively.
journal_name
Biol Psychiatryjournal_title
Biological psychiatryauthors
Davis JF,Choi DL,Schurdak JD,Fitzgerald MF,Clegg DJ,Lipton JW,Figlewicz DP,Benoit SCdoi
10.1016/j.biopsych.2010.08.028subject
Has Abstractpub_date
2011-04-01 00:00:00pages
668-74issue
7eissn
0006-3223issn
1873-2402pii
S0006-3223(10)00912-1journal_volume
69pub_type
杂志文章abstract::Disturbances in dopaminergic transmission have been implicated in the etiology of psychotic disorders. Interindividual differences in deoxyribonucleic acid (DNA) sequences coding for dopamine receptor proteins might contribute to the genetic background of these diseases. We have identified a variation in exon 1 of the...
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journal_title:Biological psychiatry
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pub_type: 临床试验,杂志文章
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journal_title:Biological psychiatry
pub_type: 临床试验,杂志文章
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更新日期:1998-03-01 00:00:00
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pub_type: 杂志文章
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更新日期:1989-04-01 00:00:00
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pub_type: 杂志文章
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更新日期:1997-07-01 00:00:00
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journal_title:Biological psychiatry
pub_type: 临床试验,杂志文章
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更新日期:1998-06-15 00:00:00
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pub_type: 杂志文章
doi:10.1016/j.biopsych.2010.05.016
更新日期:2010-10-01 00:00:00
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journal_title:Biological psychiatry
pub_type: 临床试验,杂志文章
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更新日期:1996-10-15 00:00:00
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pub_type: 杂志文章
doi:10.1016/j.biopsych.2010.02.008
更新日期:2010-06-15 00:00:00
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pub_type: 杂志文章
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journal_title:Biological psychiatry
pub_type: 杂志文章
doi:10.1016/j.biopsych.2010.09.005
更新日期:2011-02-15 00:00:00
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pub_type: 杂志文章
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更新日期:2020-04-15 00:00:00
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pub_type: 杂志文章
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更新日期:2007-07-01 00:00:00
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pub_type: 杂志文章
doi:10.1016/j.biopsych.2015.03.014
更新日期:2016-02-15 00:00:00
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journal_title:Biological psychiatry
pub_type: 杂志文章,评审
doi:10.1016/s0006-3223(00)01003-9
更新日期:2000-12-15 00:00:00
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journal_title:Biological psychiatry
pub_type: 杂志文章
doi:10.1016/j.biopsych.2016.12.010
更新日期:2017-06-15 00:00:00
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journal_title:Biological psychiatry
pub_type: 杂志文章
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更新日期:1987-12-01 00:00:00
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journal_title:Biological psychiatry
pub_type: 杂志文章
doi:10.1016/0006-3223(90)90485-k
更新日期:1990-09-15 00:00:00
abstract::The addition of lithium to perphenazine altered the pattern of plasma homovanillic acid (HVA) during the course of treatment for acute psychosis. In the perphenazine-treated group plasma HVA declined significantly by days 7-9 of treatment, whereas in the perphenazine-plus-lithium group plasma HVA tended to increase. T...
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pub_type: 杂志文章
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更新日期:1992-12-15 00:00:00