about
Postnatal Sim1 deficiency causes hyperphagic obesity and reduced Mc4r and oxytocin expressionOxytocin deficiency mediates hyperphagic obesity of Sim1 haploinsufficient miceA Novel Letrozole Model Recapitulates Both the Reproductive and Metabolic Phenotypes of Polycystic Ovary Syndrome in Female Mice.Absent Progesterone Signaling in Kisspeptin Neurons Disrupts the LH Surge and Impairs Fertility in Female MiceDevelopmental GnRH signaling is not required for sexual differentiation of kisspeptin neurons but is needed for maximal Kiss1 gene expression in adult femalesInducible neuronal inactivation of Sim1 in adult mice causes hyperphagic obesity.Impaired kisspeptin signaling decreases metabolism and promotes glucose intolerance and obesity.Effects of Selective Deletion of Tyrosine Hydroxylase from Kisspeptin Cells on Puberty and Reproduction in Male and Female Mice.SIM1 overexpression partially rescues agouti yellow and diet-induced obesity by normalizing food intake.The development of kisspeptin circuits in the Mammalian brain.The Changes They are A-Timed: Metabolism, Endogenous Clocks, and the Timing of Puberty.Metabolism and Energy Expenditure, But Not Feeding or Glucose Tolerance, Are Impaired in Young Kiss1r KO Female Mice.Unaltered Hypothalamic Metabolic Gene Expression in Kiss1r Knockout Mice Despite Obesity and Reduced Energy Expenditure
P50
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P50
description
researcher
@en
wetenschapper
@nl
հետազոտող
@hy
name
Kristen P Tolson
@ast
Kristen P Tolson
@en
Kristen P Tolson
@es
Kristen P Tolson
@nl
type
label
Kristen P Tolson
@ast
Kristen P Tolson
@en
Kristen P Tolson
@es
Kristen P Tolson
@nl
prefLabel
Kristen P Tolson
@ast
Kristen P Tolson
@en
Kristen P Tolson
@es
Kristen P Tolson
@nl
P108
P106
P31
P496
0000-0002-0729-8554