Is this really a miracle medicine for weight loss? The study found important results that contradicted the results of previous experiments

Every sensory impulse, from anger to hunger, is regulated by hormonal or neuronal signals
.
Often, these impulses manifest as behavioral responses that are triggered
by complex biological reactions.
The building blocks of these reactions are produced in the body through the expression of certain proteins, which in turn are encoded
by certain genes.

Neuromedin U (NMU) is a neuroprotein hormone that plays a variety of physiological roles
in a variety of species, including mammals.
It is involved in metabolic processes and is responsible for energy expenditure, eating behavior, maintaining the circadian cycle in our biological clock, tumor development and immunity
.
Its "anti-hunger" (anorexia) function has been demonstrated in animal models, including mice, making it a prime target for anti-obesity drugs that work by suppressing the body's desire
to eat more than it actually needs.

In mice, drug studies have demonstrated that NMU reduces food intake and increases energy expenditure
.
A lack of NMU in mice can lead to excessive eating behavior, low body temperature, low activity, and the development of obesity
.
However, inconsistent results have been obtained in similar rat dosing experiments, and the key role of NMU energy metabolism is unclear
.

A team of researchers previously found that mRNA expression in the pituitary nodule (PT) of Nmu rats is higher in the light phase and lower in the dark phase, due to melatonin-induced inhibition
.
The team has now also investigated whether NMU in PT is related to feeding rhythm, which causes rats to eat
mainly at night.
The research was co-led by Professor Sanaka Aizawa from the Graduate School of Natural Sciences and Technology at Okayama University and Dr.
Makoto Matsuyama from the Shigenari Institute of
Medical Research.

The team wanted to study the anorexia function of NMU, a neuropeptide present or absent
in rat models.
To do this, they first bred rat NMU through Dr.
Matsuyama's recently developed rGONAD (Rat Genome Editing via Tubal Nucleic Acid Delivery) technique, where genes are silenced
.
These mice, known as NmuKO rats, cannot produce neuropeptides
.
However, unlike the NmuKO mice, the NmuKO rats did not increase their food intake and did not become obese, which surprised the team
.

Considering that NMU may be related to feeding rhythm, the researchers examined daily feeding patterns and found no difference between NmuKO and wild-type (NMU gene-containing) rats in both the light and dark phases
.
"It is likely that NMU is not critical for the regulation of feeding and energy metabolism in rats, nor is it a central regulator of food intake"
.
Professor Aizawa
explains.

Given its multiple roles, this protein is present in multiple organs and transmits signals
through receptors.
The researchers found this in the brains of mice, where the expression of Nmu pituitary PT is limited and abundant and has never been observed
in mice.
Compared to mice, NMU and its receptors in rats are rarely expressed
in brain regions involved in feed control.
This indicates that NMU has no inhibitory effect
on the feeding of rats.

Professor Aizawa explains: "What we found in rats contradicts
what we found in mice.
This difference may be due to
species differences in the expression patterns of Nmu and its receptor genes between rats and mice.
In addition, the anorexia effect of central administration may be an effect of shorter duration under specific conditions".

While NMU has been studied as a foraging-inhibiting hormone, it is now clear that it functions differently in different species, including those that are very close
.
However, more research is needed to determine whether rats or mice are better models for understanding the physiological functions and associated behavioral responses
of human NMU.

"This study expresses concerns about the application of animal experimental results to humans and provides a strong demonstration of the diversity of biological organisms"
.