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VMH Cckbr neurons

Candidate: concept label1 source documents6 linked claims
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Aliases

neurons in the ventromedial nucleus of the hypothalamus that express the cholecystokinin b receptor, VMHCckbr neurons

Extracted Explainers

What the tool is doing

This neuronal population is described as supporting physiologic glucose homeostasis and mobilizing gluconeogenic substrates during short fasts. The abstract links it to lipolysis and glycerol mobilization.

Source 1DOIPubMed

Resources required

The paper studies these neurons in mice using chronic tetanus-toxin-based silencing, acute optogenetic activation, continuous glucose monitoring, and analysis of hepatic glucose metabolism and white adipose tissue lipolysis.

Source 1DOIPubMed

What problem it solves

It provides a specific hypothalamic population for dissecting how the brain supports day-to-day glucose mobilization without conflating all VMH glucose-control neurons.

Source 1DOIPubMed

What it does not solve

The abstract does not establish a collection-worthy engineered construct or fully resolve the downstream circuit or all non-glycerol substrates involved.

Source 1DOIPubMed

Alternatives

The abstract contrasts these neurons with other glucose-mobilizing hypothalamic neuronal populations that engage distinct mechanisms in different contexts.

Source 1DOIPubMed

Evidence Snippets

neurons in the ventromedial nucleus of the hypothalamus that express the cholecystokinin b receptor (VMHCckbr neurons)
Evidence 1Source 1DOIPubMedprovenance

Supporting Sources

Linked Claims

Claim 1distinct populationsupports2025Source 1DOIPubMed

VMH Cckbr neurons are a distinct subset of glucose-mobilizing VMH neurons that support physiologic glucose homeostasis, likely through control of b23-AR-mediated gluconeogenic substrate mobilization and lipolysis.

Quoted textsource-backed
VMHCckbr neurons represent a distinct subset of glucose-mobilizing VMH neurons that support physiologic glucose homeostasis, likely through control of b23-AR-mediated gluconeogenic substrate mobilization and lipolysis.
Claim 2mechanismsupports2025Source 1DOIPubMed

VMH Cckbr neurons contribute to gluconeogenic substrate mobilization and lipolysis.

Quoted textsource-backed
and contribute to gluconeogenic substrate mobilization and lipolysis
Claim 3mechanismsupports2025Source 1DOIPubMed

VMH Cckbr neurons mobilize glucose without depleting hepatic glycogen or increasing gluconeogenic gene expression, instead mobilizing glycerol in a b23-adrenergic receptor-dependent manner.

Quoted textsource-backed
VMHCckbr neurons mobilize glucose without depleting hepatic glycogen or increasing gluconeogenic gene expression, but instead mobilize glycerol in a b23-adrenergic receptor (b23-AR)-dependent manner.
Claim 4physiologic rolesupports2025Source 1DOIPubMed

VMH Cckbr neurons support glucose homeostasis during short fasts.

Quoted textsource-backed
We found that VMHCckbr neurons support glucose homeostasis during short fasts
Claim 5rescuesupports2025Source 1DOIPubMed

Restoring glycerol availability after VMH Cckbr neuron silencing restores glucose.

Quoted textsource-backed
Restoring glycerol availability following VMHCckbr neuron silencing restores glucose.
Claim 6sufficiencysupports2025Source 1DOIPubMed

Acute activation of VMH Cckbr neurons mobilizes additional gluconeogenic substrates beyond glycerol.

Quoted textsource-backed
Finally, acute activation of VMHCckbr neurons mobilizes additional gluconeogenic substrates beyond glycerol.