The paper studies brain SIRT1 as an NAD-dependent deacetylase whose expression and regulation may link energy availability to neural control of metabolism.
First-pass extracted concept
Brain SIRT1
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Sirt1, SIRT1
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Hypothalamic fasting-induced SIRT1 regulation is altered in leptin-deficient obese mice.
Quoted textsource-backed
we found that this hypothalamic-specific, fasting-induced SIRT1 regulation is altered in leptin-deficient, obese mice
Sirt1 mRNA is expressed in pro-opiomelanocortin neurons.
Quoted textsource-backed
our single-cell reverse transcription-PCR analyses revealed that Sirt1 mRNA is expressed in pro-opiomelanocortin neurons
Sirt1 mRNA is highly expressed in metabolically relevant brain sites including hypothalamic arcuate, ventromedial, dorsomedial, and paraventricular nuclei, as well as the area postrema and nucleus of the solitary tract.
Quoted textsource-backed
we performed in situ hybridization histochemistry analyses and found that Sirt1 mRNA is highly expressed in metabolically relevant sites. These include, but are not limited to, the hypothalamic arcuate, ventromedial, dorsomedial, and paraventricular nuclei and the area postrema and the nucleus of the solitary tract in the hindbrain.
The findings suggest a previously unrecognized role of brain SIRT1 in regulating energy homeostasis.
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Collectively, our findings establish the distribution of Sirt1 mRNA throughout the neuraxis and suggest a previously unrecognized role of brain SIRT1 in regulating energy homeostasis.
SIRT1 protein levels are selectively increased in the hypothalamus in the fasted brain.
Quoted textsource-backed
We also found that SIRT1 protein levels are restrictedly increased in the hypothalamus in the fasted brain.