Language
English
Publication Date
5-13-2026
Journal
Nature Communications
DOI
10.1038/s41467-026-73102-3
PMID
42129178
PMCID
PMC13376941
PubMedCentral® Posted Date
5-13-2026
PubMedCentral® Full Text Version
Post-print
Abstract
Stress and diet are known to synergistically promote risks of obesity but the underlying neural basis remains elusive. Corticotropin-releasing hormone neurons in the paraventricular hypothalamus (PVHCRH) are stress responsive and release both CRH and glutamate. Here we generated a mouse model with gain or loss of release in CRH or glutamate from PVHCRH neurons. While these models showed no changes in body weight when fed chow, they exhibited contrasting effects when fed high-fat high-caloric diets (HFD). Whereas disrupting glutamate release from PVHCRH neurons led to diet-induced obesity (DIO), that of CRH caused no impact. Conversely, augmented CRH release led to DIO while that of glutamate caused no impact. The observed DIO in both cases was associated with an increased drive for HFD, but without obvious changes in behavioral signs of anxiety. Our results suggest PVHCRH neurons as a key mediator for the exerbated DIO induced by maladaptive stress responses.
Keywords
Animals, Obesity, Corticotropin-Releasing Hormone, Paraventricular Hypothalamic Nucleus, Diet, High-Fat, Mice, Neurons, Glutamic Acid, Neurotransmitter Agents, Male, Mice, Inbred C57BL, Body Weight, Neurotransmitters, Obesity
Published Open-Access
yes
Recommended Citation
Jiang, Zhiying; Cao, Yuhan; He, Michelle; et al., "Selective and Differential Roles of PVHCRH Neurotransmitters in Diet-Induced Obesity in Mice" (2026). The Brown Foundation: Institute of Molecular Medicine. 136.
https://digitalcommons.library.tmc.edu/molecular_med/136