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iNature
Obesity caused by a high-fat diet (HFD) is an increasingly epidemic and a major health problem
.
While excessive daytime sleepiness (EDS) is a common symptom of HFD-induced obesity, preliminary research suggests that sleep deprivation can be improved
by time-restricted feeding (TRF).
However, the underlying neural mechanisms remain largely unclear
.
On October 16, 2022, Li Haohong of Zhejiang University and Luoying Zhang of Huazhong University of Science and Technology jointly published a joint communication entitled "Time-Restricted Feeding Is an Intervention against Excessive Dark-phase" online in National Science Review (IF=23).
Sleepiness Induced by Obesogenic Diet", which shows that time-restricted eating is an intervention for
excessive nighttime sleepiness caused by an obese diet.
The parathalamic ventricular nucleus (PVT) plays a role
in maintaining wakefulness.
The study found that chronic HFD impairs the activity
of PVT neurons.
Notably, the inactivation of PVT was sufficient to reduce and split the awake state during the active phase of emaciated mice, similar to the sleep/wake changes observed in HFD-induced obese mice.
On the other hand, enhancing PVT neuronal activity consolidated the arousal capacity
of HFD-induced obese mice.
The study observed that fragmented sobriety can be eliminated and reversed
by TRF.
TRF prevents disruption
of synaptic transmission in HFD-induced PVT in a feeding duration-dependent manner.
Overall, the study suggests that random intake of HFD leads to PVT inactivation, which is essential for impaired nocturnal awakenings and increased sleep, while TRF can prevent and reverse diet-induced PVT dysfunction and excessive sleepiness
.
The study established a link between TRF and neural activity, through which TRF could serve as a lifestyle intervention
for diet/obesity-related EDS.
in many adults and children.
Excessive daytime sleepiness (EDS) is common in obese patients, which seriously affects vigilance, attention, and quality of life
.
Excessive sleepiness during the active phase of the circadian cycle has also been reported in obese rodents, including genetic and HFD-induced obesity models
.
Time-restricted feeding (TRF) can alleviate metabolic disorders in obese mice, restore clock gene oscillations in peripheral tissues, and also improve the irregularities
of obesity-induced sleep-wake cycles.
However, the underlying mechanisms remain largely unclear
.
PVT spans the length of the beak across the midline of the thalamus and exhibits different functions
on the anterior and posterior axes.
It is associated
with saliency, arousal, and regulation of emotional and motivated behaviors.
PVT is also involved in regulating feeding behavior, further regulating food intake
through complex interactions of energy homeostatic cyclic signals.
Previous studies have found that PVT is very sensitive
to energy balance.
Hypoglycemia induces increased activity of PVT-NAc projection neurons, leading to rectal effects
.
Conversely, administration of glucagon-like peptide-1 receptor (GLP-1R) agonists in PVT reduces the activity of these neurons, leading to anorexia effects
.
In PVT, the discharges associated with the sleep-wake transition are disturbed by AL-HFD feeding (Figure from National Science Review) Early studies in rats have shown an increase
in c-Fos (markers of neuronal activity) in PVT in the dark (active) phase compared to the light phase.
PVT belongs to the thalamic cortical arousal system
.
PVT receives dense peptidolic fiber nerves from the sleep-wake regulatory network, including noradrenergic and serotonergic fibers from the brainstem, as well as histaminergic, orexic, and neurotensionin-containing fibers
from the hypothalamus.
Extensive excitatory input into PVT activates the cerebral cortex to cause arousal
.
However, in humans and rodents, lesions can impair the integrity of the waking state and induce drowsiness
.
In addition, recent studies have shown that PVT is also associated
with arousal that does not depend on the light and dark cycles.
In constant darkness, c-Fos levels in PVT increase
when delicious food is preserved.
In addition, food entrainment alters the peak daily oscillation of
PER1 in PVT.
Therefore, the researchers hypothesized that the activity of PVT neurons is essential for maintaining wakefulness during the active phase of the circadian cycle, which may be regulated
by daily feeding schedules.
The study was able to reproduce the EDS phenotype
in HFD-induced obese mice.
Chronic free consumption of HFD shortens waking time and increases awake fragmentation
during activity.
The AL pathway HFD reduces neuronal excitability, disrupts synaptic transmission of PVT, and remodels the excitation/inhibition (E/I) ratio
.
Consistently, PVT inactivation in lean mice reduced and dispersed arousal, similar to HFD treatment, while the restoration of PVT neuronal activity consolidated arousal
in obese mice.
In addition, active/nocturnal TRFs can prevent this fragmented arousal
.
The study found that active-phase TRF also eliminated HFD-induced PVT synaptic activity damage, while treatment effectiveness depended on feeding/starvation time
.
In addition, TRF not only prevents and reverses the effects
of HFD-induced obesity on PVT and arousal.
These results highlight the underlying pathological mechanisms of obesity-related EDS and provide non-pharmacological interventions for
it.
Original link: https://doi.
org/10.
1093/nsr/nwac222—END—The content is [iNature].
