Summary: A recent study has revealed that obesity disrupts the precise timing of biochemical responses, despite the chemical structure of the liver’s metabolism remaining alive during starvation. Important “hub” molecules, such as ATP and AMP, quickly and effectively responded to malnutrition in good mice.
Even though the chemical network appeared architecturally sound, this historical cooperation was lost in obese mice. This discovery demonstrates the significance of timing in biochemical rules and provides a novel method for studying genetic networks over period.
Important Information
- Temporal Breakdown: Big mice exhibit a dysfunctional liver metabolism during starvation that is based on structure rather than timing.
- Hub Molecule Shift: Fat stomachs did not use ATP/AMP as key regulators, but good stomachs did.
- New Method: Mixes architectural and historical data to gain a deeper understanding of digestion.
University of Tokyo supply
Despite not causing any significant structural changes in the chemical system, experts led by Keigo Morita and Shinya Kuroda of the University of Tokyo have discovered a historical change in big mice’s respiration when they adapt to starvation.
This is a discovery discovery because studies of the historical dimension in biology have been extremely tedious and it has been challenging to get systematic information from big data.
This study opens the door for further investigation into more general biochemical processes, such as food consumption and disease development.
The results were reported in Science Signaling, a journal.
Living things must constantly remove energy from “food” and spread it within the body to maintain life, i .e. keep their physiology high so that their bodies are in the ideal range known as “homeostasis.”
One of the most significant disruptions to this method is starvation. The heart, which is essential to digestion, coordinates not just when substances need to take action, but also when they adapt to starvation.
According to Kuroda, the lead researcher, “molecules inside cells form a huge network” that includes a small number of molecules known as hotspot molecules that regulate a variety of physiological reactions.”
Due to the lack of thorough time-series data during hunger, it had been difficult to get a comprehensive understanding of the historical coordination of the liver’s molecules.
By comparing the stomachs of good and fat rabbits, the researchers attempted to bridge the gap. Their tests revealed a clear distinction between the gateway molecules of healthier and overweight liver cells. The original contained the energy-related substances ATP and AMP, but the latter did no.
The atomic network may have been structurally altered by such a glaring difference between hub molecules. The researchers examined the historical sizing because they could not find such disruptions.
We thoroughly examined the moment programs of several molecules,” says Kuroda,” and found that gateway molecules in good livers responded to starvation more quickly than other molecules.
This suggested a well-controlled chronological order of the atomic networks in healthful livers when they are starved. On the other hand, this cooperation disappeared in obese mice’s livers.
In other words, the molecular network became dynamically vulnerable to obesity even though the structure remained stable during starvation.
The technique that combined architectural and historical analysis of the cellular chemical system can be applied to various studies that include data sets from various “omes” like the genome or the microbiome, opening up new avenues for research. How their upcoming project is described by Kuroda.
The complex biological phenomenon adaptation to starvation was successfully described in our approach. We would like to apply our knowledge of the metabolic network during food consumption or disease progression to the metabolic network during starvation.
About this research on obesity and metabolism
Author: Emese Berta
Source: University of Tokyo
Contact: Emese Berta – University of Tokyo
Image: The image is credited to Neuroscience News
Original Research: Disclosed access.
Keigo Morita and colleagues ‘ study” The starvation-responsive metabolic network in healthy and obese mouse livers has structural robustness and temporal vulnerability..” Science Signaling
Abstract
The starvation-responsive metabolic network in healthy and obese mouse livers has structural robustness and temporal vulnerability.
Adaptation to starvation is a multimolecular and chronological process. We investigated how obesity interferes with the healthy liver’s ability to regulate various molecules in a temporally ordered manner during starvation.
We used multiomic data from wild-type and obese ( ob/ob ) mice at various point points during starvation to create a starvation-responsive metabolic network that included responsive molecules and their regulatory relationships.
The key molecules for energy homeostasis, ATP and AMP, served as hub molecules to regulate various metabolic reactions in the network in wild-type mice, according to analysis of the network structure. The network’s structural characteristics were maintained despite the fact that neither ATP nor AMP were sensitive to starvation in mice.
The molecules in the network were positively or negatively coregulated in wild-type mice by their metabolic processes, which included ATP and AMP, coordinated by hub molecules. In contrast, mice with   and ob/ob dysregulation both experienced temporal order and coregulation.
These findings suggest that the hub molecules ‘ obesity-associated loss of responsiveness caused the metabolic network to be structurally robust but temporally damaged.
We also discuss how intermittent fasting is affected by obesity.
