Diet-derived nutrients mediate the inhibition of hypothalamic NPY neurons in the arcuate nucleus of mice during refeeding.

@article{Becskei2009DietderivedNM,
  title={Diet-derived nutrients mediate the inhibition of hypothalamic NPY neurons in the arcuate nucleus of mice during refeeding.},
  author={Csilla Becskei and Thomas A. Lutz and Thomas Riediger},
  journal={American journal of physiology. Regulatory, integrative and comparative physiology},
  year={2009},
  volume={297 1},
  pages={
          R100-10
        }
}
  • C. Becskei, T. Lutz, T. Riediger
  • Published 1 July 2009
  • Biology, Medicine
  • American journal of physiology. Regulatory, integrative and comparative physiology
Fasting activates orexigenic neuropeptide Y neurons in the hypothalamic arcuate nucleus (ARC) of mice, which is reversed by 2 h refeeding with standard chow. Here, we investigated the contribution of diet-derived macronutrients and anorectic hormones to the reversal of the fasting-induced ARC activation during 2 h refeeding. Refeeding of 12-h-fasted mice with a cellulose-based, noncaloric mash induced only a small reduction in c-Fos expression. Refeeding with diets, containing carbohydrates… 
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Reduced fasting-induced activation of hypothalamic arcuate neurons is associated with hyperleptinemia and increased leptin sensitivity in obese mice.
TLDR
It is indicated that high leptin levels prevent the fasting-induced activation of ARC neurons in mice, and fasting seems to interfere with the responsiveness of the ARC to signals related to the status of energy intake.
The receptive function of hypothalamic and brainstem centres to hormonal and nutrient signals affecting energy balance
  • T. Riediger
  • Biology, Medicine
    Proceedings of the Nutrition Society
  • 2012
TLDR
There is consistency between the neurophysiological actions of these stimuli and their effects on energy homoeostasis under experimental conditions and their interactions might hold the potential to develop poly-mechanistic therapeutic strategies against obesity.
Ghrelin agonists impact on Fos protein expression in brain areas related to food intake regulation in male C57BL/6 mice
Actions of NPY, and Its Y1 and Y2 Receptors on Pulsatile Growth Hormone Secretion during the Fed and Fasted State
TLDR
An integrated neural circuit that modulates GH release relative to food intake is demonstrated, and essential information is provided to address the differential roles of Y1 and Y2 receptors in regulating the release of GH under fed and fasting states.
PNS1200077 463..477
TLDR
There is consistency between the neurophysiological actions of these stimuli and their effects on energy homoeostasis under experimental conditions and their interactions might hold the potential to develop poly-mechanistic therapeutic strategies against obesity.
Differential gene regulation of GHSR signaling pathway in the arcuate nucleus and NPY neurons by fasting, diet-induced obesity, and 17β-estradiol
Short-term fasting decreases excitatory synaptic inputs to ventromedial tuberoinfundibular dopaminergic neurons and attenuates their activity in male mice
The role of neuropeptide Y in energy homeostasis.
TLDR
Evidence from diverse types of experiments suggests that rather than initiating behavioral eating per se, endogenous NPY elicits autonomic responses that prepare the individual to better cope with consuming a calorically large meal.
Central apelin controls glucose homeostasis via a nitric oxide-dependent pathway in mice.
TLDR
These data provide compelling evidence that central apelin participates in the regulation of glucose homeostasis and suggest a novel pathophysiological mechanism involved in the transition from normal to diabetic state.
Nutritional regulation of central fat mass and obesity-associated (FTO) expression, and its association with the central melanocortin signaling in the regulation of energy homeostasis
TLDR
The hypothesis that central melanocortin signaling regulates hepatic lipid metabolism in part by regulating de novo lipogenesis is supported, and the hypothesis that Fto is expressed in the hypothalamic melanOCortinergic neurons and is regulated by metabolic signals involving changes in CNS glucose availability and/or glucose action is supported.
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TLDR
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