Glucose stimulation of hypothalamic MCH neurons involves K(ATP) channels, is modulated by UCP2, and regulates peripheral glucose homeostasis.
Glucose stimulation of hypothalamic MCH neurons involves K(ATP) channels, is modulated by UCP2, and regulates peripheral glucose homeostasis.
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DOI:
10.1016/j.cmet.2010.09.013
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发表时间:
2010-11-03
期刊:
影响因子:
29
通讯作者:
Lowell BB
中科院分区:
文献类型:
--
作者:
Kong D;Vong L;Parton LE;Ye C;Tong Q;Hu X;Choi B;Brüning JC;Lowell BB
Blood glucose levels are tightly controlled, a process thought to be orchestrated primarily by peripheral mechanisms (insulin secretion by β-cells, and insulin action on muscle, fat and liver). The brain also plays an important, albeit less well-defined role. Subsets of neurons in the brain are excited by glucose; in many cases this involves ATP-mediated closure of KATP channels. To understand the relevance of this, we are manipulating glucose sensing within glucose-excited neurons. In the present study, we demonstrate that glucose excitation of MCH-expressing neurons in the lateral hypothalamus is mediated by KATP channels, is negatively regulated by UCP2 (a mitochondrial protein that reduces ATP production), and that glucose sensing by MCH neurons plays an important role in regulating glucose homeostasis. Combined, the glucose-excited neurons are likely to play key, previously unexpected roles in regulating blood glucose.
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影响因子:
16.2
作者:
Dhillon, H;Zigman, JM;Lowelll, BB
通讯作者:
Lowelll, BB
DOI:
10.1111/j.1748-1716.2008.01922.x
发表时间:
2009-01
期刊:
Acta physiologica (Oxford, England)
影响因子:
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Dunn-Meynell, AA
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Ricquier, D