Rescue of obesity-induced infertility in female mice due to a pituitary-specific knockout of the insulin receptor.
about
PI3K: An Attractive Candidate for the Central Integration of Metabolism and ReproductionGenetic Rodent Models of Obesity-Associated Ovarian Dysfunction and Subfertility: Insights into Polycystic Ovary SyndromeObesity and PCOS: implications for diagnosis and treatmentInsulin receptor signaling in the GnRH neuron plays a role in the abnormal GnRH pulsatility of obese female mice.Reduced melanocortin production causes sexual dysfunction in male mice with POMC neuronal insulin and leptin insensitivity.Kisspeptin cell-specific PI3K signaling regulates hypothalamic kisspeptin expression and participates in the regulation of female fertility.Conditional knockout of the androgen receptor in gonadotropes reveals crucial roles for androgen in gonadotropin synthesis and surge in female mice.Insulin and Leptin Signaling Interact in the Mouse Kiss1 Neuron during the Peripubertal Period.Childhood obesity and its impact on the development of adolescent PCOS.Obesity-induced infertility and hyperandrogenism are corrected by deletion of the insulin receptor in the ovarian theca cellAMP-activated protein kinase is a key intermediary in GnRH-stimulated LHβ gene transcriptionCREB binding protein (CBP) activation is required for luteinizing hormone beta expression and normal fertility in miceInsulin resistance and the polycystic ovary syndrome revisited: an update on mechanisms and implications.Selective breeding of mice for different susceptibilities to high fat diet-induced glucose intolerance: Development of two novel mouse lines, Selectively bred Diet-induced Glucose intolerance-Prone and -Resistant.Role of human pregnane X receptor in high fat diet-induced obesity in pre-menopausal female mice.Insulin action in brain regulates systemic metabolism and brain function.The regulation of reproductive neuroendocrine function by insulin and insulin-like growth factor-1 (IGF-1).Reproductive neuroendocrine dysfunction in polycystic ovary syndrome: insight from animal modelsMaternal insulin resistance causes oxidative stress and mitochondrial dysfunction in mouse oocytes.Minireview: Metabolic control of the reproductive physiology: insights from genetic mouse modelsForkhead Box O1 is present in quiescent pituitary cells during development and is increased in the absence of p27 Kip1FOXO1 is regulated by insulin and IGF1 in pituitary gonadotropes.Vaginal fold histology reduces the variability introduced by vaginal exfoliative cytology in the classification of mouse estrous cycle stagesReproductive tissues maintain insulin sensitivity in diet-induced obesity.Ablation of neurons expressing agouti-related protein, but not melanin concentrating hormone, in leptin-deficient mice restores metabolic functions and fertility.The forkhead transcription factor, FOXP3, is required for normal pituitary gonadotropin expression in miceThe hypersensitive glucocorticoid response specifically regulates period 1 and expression of circadian genesNegative regulation of human growth hormone gene expression by insulin is dependent on hypoxia-inducible factor binding in primary non-tumor pituitary cells.FOXO1 transcription factor inhibits luteinizing hormone β gene expression in pituitary gonadotrope cells.Effect of maternal obesity on estrous cyclicity, embryo development and blastocyst gene expression in a mouse modelA novel reproductive peptide, phoenixin.Integrative control of energy balance and reproduction in females.Corticosterone regulation of ovarian follicular development is dependent on the energy status of laying hens.Free fatty acids induce Lhb mRNA but suppress Fshb mRNA in pituitary LβT2 gonadotropes and diet-induced obesity reduces FSH levels in male mice and disrupts the proestrous LH/FSH surge in female mice.Disrupted kisspeptin signaling in GnRH neurons leads to hypogonadotrophic hypogonadism.Metabolic influences on neuroendocrine regulation of reproduction.Long-term consequences of obesity on female fertility and the health of the offspring.Low-Dose Dihydrotestosterone Drives Metabolic Dysfunction via Cytosolic and Nuclear Hepatic Androgen Receptor Mechanisms.Acute recapitulation of the hyperinsulinemia and hyperlipidemia characteristic of metabolic syndrome suppresses gonadotropins.Obese Neuronal PPARγ Knockout Mice Are Leptin Sensitive but Show Impaired Glucose Tolerance and Fertility.
P2860
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P2860
Rescue of obesity-induced infertility in female mice due to a pituitary-specific knockout of the insulin receptor.
description
2010 nî lūn-bûn
@nan
2010 թուականի Սեպտեմբերին հրատարակուած գիտական յօդուած
@hyw
2010 թվականի սեպտեմբերին հրատարակված գիտական հոդված
@hy
2010年の論文
@ja
2010年論文
@yue
2010年論文
@zh-hant
2010年論文
@zh-hk
2010年論文
@zh-mo
2010年論文
@zh-tw
2010年论文
@wuu
name
Rescue of obesity-induced infe ...... ckout of the insulin receptor.
@ast
Rescue of obesity-induced infe ...... ckout of the insulin receptor.
@en
type
label
Rescue of obesity-induced infe ...... ckout of the insulin receptor.
@ast
Rescue of obesity-induced infe ...... ckout of the insulin receptor.
@en
prefLabel
Rescue of obesity-induced infe ...... ckout of the insulin receptor.
@ast
Rescue of obesity-induced infe ...... ckout of the insulin receptor.
@en
P2093
P2860
P1433
P1476
Rescue of obesity-induced infe ...... ckout of the insulin receptor.
@en
P2093
Andrew Wolfe
Fredric E Wondisford
Kathryn J Brothers
Marcus R Messmer
Ryan S Miller
Sally Radovick
Sara A DiVall
P2860
P304
P356
10.1016/J.CMET.2010.06.010
P577
2010-09-01T00:00:00Z