Glucose stimulation of hypothalamic MCH neurons involves K(ATP) channels, is modulated by UCP2, and regulates peripheral glucose homeostasis.
Kong
Dong
D
Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215, USA.
Vong
Linh
L
Parton
Laura E
LE
Ye
Chianping
C
Tong
Qingchun
Q
Hu
Xiaoxia
X
Choi
Brian
B
Brüning
Jens C
JC
Lowell
Bradford B
BB
D000818:Animals; D002478:Cells, Cultured; D015870:Gene Expression; D005947:Glucose / Q000378:metabolism*; D007028:Hypothalamic Hormones / Q000378:metabolism*; D007031:Hypothalamus / Q000166:cytology*; D007473:Ion Channels / Q000235:genetics / Q000378:metabolism*; D054086:KATP Channels / Q000235:genetics / Q000378:metabolism*; D008543:Melanins / Q000378:metabolism*; D051379:Mice; D008822:Mice, Transgenic; D024101:Mitochondrial Proteins / Q000235:genetics / Q000378:metabolism*; D009154:Mutation; D009474:Neurons / Q000378:metabolism*; D010907:Pituitary Hormones / Q000378:metabolism*; D000071246:Uncoupling Protein 2
D007028:Hypothalamic Hormones; D007473:Ion Channels; D054086:KATP Channels; D008543:Melanins; D024101:Mitochondrial Proteins; D010907:Pituitary Hormones; C000604390:Ucp2 protein, mouse; D000071246:Uncoupling Protein 2; C019463:melanin-concentrating hormone; D005947:Glucose