Activation of corticotropin-releasing factor receptors in the rostral ventrolateral medulla is required for glucose-induced sympathoexcitation.
Level 5 - mechanism / opinion, no new human data
Animal mechanistic and neurophysiological study
PubMed 25269482 · doi:10.1152/ajpendo.00291.2014
What was done
Researchers investigated the central neural mechanisms mediating glucose-driven sympathetic nerve activity (SNA) in male rats. Intravenous glucose (150 mg/kg, 10 min) was administered to achieve physiological postprandial levels. In conscious rats, c-Fos immunofluorescence was measured in corticotropin-releasing factor (CRF)-containing paraventricular nucleus (PVN) neurons and tyrosine hydroxylase (TH)-containing rostral ventrolateral medulla (RVLM) neurons. In α-chloralose/urethane-anesthetized rats, lumbar and splanchnic SNA were measured during glucose infusion following RVLM microinjection of the CRF receptor antagonist astressin (10 pmol/50 nl) or during PVN inhibition with the GABA-A receptor agonist muscimol (100 pmol/50 nl).
What was found
Glucose infusion activated CRF-positive PVN neurons and TH-positive RVLM neurons in conscious rats. In anesthetized rats, glucose infusion elevated lumbar and splanchnic SNA. Microinjection of astressin into the RVLM nearly prevented this glucose-induced SNA increase without affecting responses to sciatic afferent stimulation. PVN inhibition with muscimol largely reversed glucose-stimulated sympathoexcitation. Pretreatment with astressin in the RVLM prevented both the initial glucose-induced SNA rise and the subsequent decrease in SNA normally caused by PVN inhibition. The abstract does not report specific numerical values or baseline statistics.
Why it matters
This study defines a specific central pathway—linking hypothalamic PVN activation to RVLM CRF receptor signaling—that mediates glucose-induced sympathetic excitation and metabolic thermogenesis.
Limits
The study was conducted in male rats, limiting direct extrapolation to females and human metabolic regulation. Sample sizes for each experimental group are not reported in the abstract. Key autonomic measurements required general anesthesia (α-chloralose/urethane), which can alter physiological autonomic reflexes.
Cited by
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