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Publication
The neuronal (pro)renin receptor and astrocyte inflammation in the central
regulation of blood pressure and blood glucose in mice fed a high-fat diet.
Authors Worker CJ, Li W, Feng CY, Souza LAC, Gayban AJB, Cooper SG, Afrin S, Romanick S,
Ferguson BS, Feng Earley Y
Submitted By Submitted Externally on 12/3/2021
Status Published
Journal American journal of physiology. Endocrinology and metabolism
Year 2020
Date Published 5/1/2020
Volume : Pages 318 : E765 - E778
PubMed Reference 32228320
Abstract We report here that the neuronal (pro)renin receptor (PRR), a key component of
the brain renin-angiotensin system (RAS), plays a critical role in the central
regulation of high-fat-diet (HFD)-induced metabolic pathophysiology. The
neuronal PRR is known to mediate formation of the majority of angiotensin (ANG)
II, a key bioactive peptide of the RAS, in the central nervous system and to
regulate blood pressure and cardiovascular function. However, little is known
about neuronal PRR function in overnutrition-related metabolic physiology. Here,
we show that PRR deletion in neurons reduces blood pressure, neurogenic pressor
activity, and fasting blood glucose and improves glucose tolerance without
affecting food intake or body weight following a 16-wk HFD. Mechanistically, we
found that a HFD increases levels of the PRR ligand (pro)renin in the
circulation and hypothalamus and of ANG II in the hypothalamus, indicating
activation of the brain RAS. Importantly, PRR deletion in neurons reduced
astrogliosis and activation of the astrocytic NF-?B p65 (RelA) in the arcuate
nucleus and the ventromedial nucleus of the hypothalamus. Collectively, our
findings indicate that the neuronal PRR plays essential roles in
overnutrition-related metabolic pathophysiology.




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