Biology Research News

Some curious fragments of DNA hidden within genomes across all life forms have historically been overlooked, as they appeared to have no role in survival competition—until now. Phage viruses, that used regularly to combat against antibiotic resistance, gain an advantage with the help of these curious fragments or selfish genetic elements of viruses by inhibiting a competitor’s ability to reproduce.

Date	July 4, 2024
Source	University of California – San Diego
Summary	Certain DNA segments have been identified as selfish genetic elements of viruses because they were thought not to contribute to a host organism’s survival. However, researchers have now discovered that these elements have been weaponized, playing a crucial role by inhibiting a competitor’s ability to reproduce. Published in the journal Science.

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Discovery of Selfish Genetic Elements of Viruses

• Decades ago, biologists noted the existence of selfish genetic elements but could not identify any role they played in aiding the host organism’s survival and reproduction.
• Research by scientists at the University of California San Diego has uncovered new evidence suggesting that these DNA elements might not be so selfish after all. Instead, they seem to play a significant role in the interactions between competing organisms.
• In this new study, which focused on “jumbo” phages, the researchers examined the dynamics when two phages co-infect a single bacterial cell and compete with each other.
• They closely studied endonuclease, an enzyme that acts as a DNA-cutting tool. The endonuclease from one phage’s mobile intron interferes with the genome of the competing phage.
• This enzyme cuts an essential gene in the competitor’s genome, sabotaging its ability to properly assemble its progeny and reproduce.
• This weaponized intron endonuclease gives a competitive advantage to the phage carrying it.
• “We were able to clearly delineate the mechanism that gives an advantage and how that happens at the molecular level,” said Chase Morgan, a co-first author of the paper.

Why Viruses are Not So selfish After All

• The DNA segments, known as selfish genetic elements of viruses or bacteriophages (phages) were believed to exist solely to reproduce and spread themselves, offering no apparent benefit to their host organisms.
• Scientists saw them as genetic hitchhikers, inconsequentially passed down through generations.
• The selfish genetic elements known as “mobile introns” give their virus hosts a competitive edge against other viruses: phages have weaponized mobile introns to disrupt the reproduction of competing phages.

How Bacteriophage Kills Bacteria Watch Here

Significance of This Discovery

• The selfish genetic elements are not always purely ‘selfish’ has broad implications for understanding genome evolution across all kingdoms of life.”
• The study’s results are crucial as phage viruses are increasingly used as therapeutic tools against antibiotic-resistant bacteria.
• Doctors have been using “cocktails” of phages to combat infections in this growing crisis, and the new information will likely be significant when multiple phages are deployed.
• Understanding that some phages use selfish genetic elements as weapons against others could help researchers understand why certain phage combinations may not achieve their full therapeutic potential.
• “The phages in this study can be used to treat patients with bacterial infections associated with cystic fibrosis,” said Biological Sciences Professor Joe Pogliano.

FAQ:

How cells enhance gene expression by antisense RNA? Antisense RNA plays a crucial role in gene expression by regulating the activity of specific genes. By preventing the production of certain proteins, antisense RNA helps control various cellular processes, ensuring that genes are expressed at the right levels and times. This regulation is vital for maintaining cellular function and responding to environmental changes.

Date	June 24, 2024
Source	University of Gottingen
Summary	A research team from the University of Gottingen has uncovered a crucial function of antisense RNA (asRNA). They discovered that asRNA serves as a “superhighway” for cellular transport, thereby speeding up gene expression. Their findings were published in Nature.

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Role of RNA in Gene Expression:

• RNA (ribonucleic acid) is essential for converting DNA information into proteins. There are various types of RNA, including messenger RNA (mRNA).
• Just visit types of RNA here
• As a type of coding RNA, mRNA’s function is to carry the genetic instructions for protein synthesis from the DNA in the cell nucleus to the cytoplasm, where these instructions are used by other cellular components to produce proteins.
• In addition to coding RNA, cells produce large quantities of non-coding RNA. A significant portion of this non-coding RNA is complementary to mRNA and is known as antisense RNA (asRNA). The role of asRNA has long been a mystery.

How Cells Enhance Gene Expression:

• The research team team discovered that antisense RNA binds with mRNA, facilitating its transport from the cell nucleus to the cytoplasm.
• This results in faster translation of mRNA into proteins compared to when antisense RNA is absent.
• Thus, antisense RNA acts as a “booster” for gene expression, which is crucial for cells, especially when facing harmful environmental conditions or stress.

Prospect of This Research:

• This new research builds on the team’s previous work, also published in Nature, which demonstrated that mRNAs activated under stress bypass quality control.
• The recent findings clarify why cells produce large amounts of antisense RNA (asRNA), given the significant energy investment involved.
• The newly identified mechanism explains how cells rapidly respond to external stimuli by producing essential proteins in large quantities, allowing them to adapt to environmental changes or enter specific developmental stages.
• This new understanding positions asRNAs at the forefront of research into disease development and potential treatments.

To explain how cells enhance gene expression Professor Heike Krebber from Gottingen University’s Institute of Microbiology and Genetics said “I couldn’t believe that cells would generate RNAs without a purpose. This goes against natural principles.”

FAQ:

Traditionally, proteins are studied at low temperatures to maintain stability. Yet, a recent study illustrates that specific proteins exhibit high sensitivity to temperature and undergo structural changes when observed at body temperature. So heating proteins to body temperature uncovers new drug targets these findings, published today in Nature.

Date	May 15, 2024
Source	Van Andel Research Institute
Summary	A novel method for studying proteins at body temperature reveals that some proteins significantly change their structures when heated, creating new opportunities for structure-guided drug development. The study focused on a protein called TRPM4.

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About TRPM4 Protein:

• Certain proteins alter their shape when exposed to different temperatures and reveal previously unknown binding sites for medications. These findings could transform various areas of biology by fundamentally changing the study of protein structures and their use in drug design.
• The research centered on TRPM4, a protein essential for heart function and metabolism, including insulin release. Consequently, TRPM4 is associated with various health conditions such as stroke, heart disease, and diabetes.
• TRPM4 is a type of protein known as a transient receptor potential (TRP) channel. It plays a crucial role in various physiological processes within the body.
• The TRPM4 protein is a transmembrane protein, meaning it spans the cell membrane. It consists of multiple domains, including transmembrane domains that form the channel pore and regulatory domains that control its activity.
• The TRPM4 protein is involved in regulating the flow of ions, particularly calcium ions, across cell membranes. It helps control cell signaling, which is essential for numerous functions, including heart function, metabolism, and insulin release.

How Drugs Enter into the Cell Membrane Watch Here

Experiment of How Heating Proteins to Body Temperature Uncovers New Drug Targets:

Experiment	Observation	Conclusion
To detect TRPM4 at body temperature, the team utilized VAI’s advanced cryo-electron microscopes (cryo-EM). These instruments enable scientists to flash-freeze proteins and create detailed images of their structures, instead of using a low-temperature sample.	This approach revealed that ligands—molecules that bind to proteins—interact with entirely different sites on TRPM4 at body temperature compared to lower temperatures.	The findings of this study have extensive implications and underscore the significance of examining proteins at body temperature to accurately identify physiologically relevant drug binding sites.

Proteins serve as the molecular engines of the body, with their shape dictating their interactions with other molecules to carry out their functions. By unraveling protein structures, scientists can craft templates that steer the development of more potent medications and thus heating proteins to body temperature uncovers new drug targets.

FAQ:

A recent study published in the Journal of Virology, a publication of the American Society for Microbiology, found that a small number of wild birds in New York City carry highly pathogenic H5N1 avian influenza and this is a highly infectious bird flu virus.

Date	May 15, 2024
Source	American Society for Microbiology
Summary	A recent study found that a small number of wild birds in New York City are carriers of highly pathogenic H5N1 avian influenza.

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About H5N1:

The H5N1 virus, commonly known as avian influenza or bird flu, is a type of influenza virus that primarily affects birds but can also infect humans and other animals. It is highly pathogenic, meaning it can cause severe disease and death in poultry and has significant implications for public health and agriculture.

Transmission

H5N1 is primarily spread through direct contact with infected birds, their droppings, or contaminated environments. Human infections are rare but can occur, typically through close interaction with infected poultry. There is a concern among scientists about the potential for the virus to mutate and gain the ability to spread easily between humans, which could lead to a global pandemic.

Symptoms in Humans

In humans, H5N1 infection can cause a range of symptoms, from mild respiratory issues to severe respiratory distress and pneumonia. Common symptoms include fever, cough, sore throat, muscle aches, and in severe cases, difficulty breathing and acute respiratory distress syndrome (ARDS). The virus has a high mortality rate in humans, making it a serious public health concern.

Another Viral Infection is Here

How Highly Infectious Bird Flu Virus Detected in New York City:

Case	Observation	Conclusion
In the study, the researchers collected and screened 1,927 samples between January 2022 and November 2023, detecting H5N1 in six city birds from four different species. All positive samples came from urban wildlife rehabilitation centers, highlighting their crucial role in viral surveillance.	Genetic comparison of these samples with other H5N1 viruses in a public database revealed slight differences, showing they belonged to two different genotypes. These genotypes are a mix of Eurasian H5N1 2.3.4.4.b clade virus and local North American avian influenza viruses. New York City is a key stopover for migrating wild birds	H5N1 in city birds does not indicate the onset of a human influenza pandemic. H5N1 has been present in New York City for about two years, and no human cases have been reported

According to the expert, it’s wise to stay vigilant and avoid contact with wildlife, including preventing pets from interacting with wild animals. If handling wildlife is necessary, it is crucial to always use safe practices when dealing with sick or injured birds or other animals because they may carry the highly infectious bird flu virus H5N1.

FAQ:

In the wake of the alarming decline of numerous animal and plant species towards endangerment and extinction, a scientist from the University of Michigan stresses the pressing need for chemists and pharmacists to actively engage in species conservation endeavors because pharmacists and chemists can become the key players in species conservation.

Date	April 30, 2024
Source	University of Michigan
Summary	In light of the imminent threat of losing numerous animal and plant species to endangerment and extinction, a scientist emphasizes the critical role of chemists and pharmacists in conservation initiatives.

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Why Pharmacists and Chemists Can Become The Key Players in Species Conservation:

• Timothy Cernak, assistant professor of medicinal chemistry at the U-M College of Pharmacy, emphasizes the critical need for medicinal chemistry expertise on the forefront of extinction becausepharmacists and chemists can become the key players in species conservation.
• He highlights that while animals are facing alarming rates of mortality, there is hope through the application of modern bioscience breakthroughs, originally developed for human disease treatment, in wildlife conservation efforts so pharmacists and chemists can become the key players in species conservation.
• He emphasized that they are currently experiencing a widespread extinction event, with mass mortality events occurring globally. From lowland gorillas to Argentinian penguins, and the akikiki bird in Hawaii to loggerhead turtles in Florida, the list is extensive, with numerous precious plant species also teetering on the brink.
• With deadly fungus devastating Panamanian golden frogs, cancerous tumors afflicting loggerhead turtles, and a multitude of pests and diseases plaguing plants like the hemlock tree, conservation medicine faces a plethora of challenges to address.

Watch The Video of An Extinct Animal Here

Causes of Extinction:

According to Cernak, the ongoing mass extinction is propelled by factors such as habitat destruction, climate change, and excessive harvesting. However, one particular underlying issue is wildlife diseases, which presents a promising opportunity for intervention. Medicinal chemistry stands as that intervention and pharmacists and chemists can become the key players in species conservation.

Research	Observation	Conclusion
In one of his numerous roles and research endeavors, Cernak receives specimens of deceased and ailing species from various regions worldwide. Employing methodologies and models akin to those utilized in identifying compounds effective against human diseases, his laboratory at U-M, recently augmented by the addition of a veterinarian, assesses chemical compounds’ efficacy on these samples to identify those that combat disease-causing organisms. A significant emphasis is placed on addressing fungus, which stands as the primary threat to amphibians, causing widespread mortality	They suggest that while a lasting solution to mass extinction lies in addressing climate change and habitat loss through innovative technologies and policies, there is an immediate need for chemistry to aid endangered species as a short-term measure.	Medicinal chemists invested in extinction prevention are urged to engage in discussions with a range of professionals, including zookeepers, foresters, veterinarians, entomologists, wildlife rehabilitators, and conservationists.

Cernak’s laboratory has pioneered the application of artificial intelligence and other technologies to accelerate the drug discovery process. He emphasized that this advancement not only enhances the potential to assist animals and plants but also expedites the timeframe for providing such aid because pharmacists and chemists can become the key players in species conservation.

FAQ:

The researchers began their experiment by identifying mice that lacked a functional olfactory system, rendering them unable to perceive smells. These mice served as the subjects for the experiment, providing a unique opportunity to investigate the restoration of sensory function. This marks the first successful integration of sensory apparatus from one species into another. Thus researchers proves that hybrid brains help mice to smell like a rat.

Date	April 25, 2024
Source	Columbia University Irving Medical Center
Summary	Scientists have achieved a breakthrough by restoring the sense of smell in mice that were previously without an olfactory system, using neurons from rats these hybrid brains help mice to smell like a rat

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Experiment: Hybrid Brains Help Mice To Smell Like A Rat:

Research	Observation	Conclusion
The research team implanted rat stem cells into mouse blastocysts, a developmental stage that occurs shortly after fertilization. This allowed the rat and mouse cells to coalesce and naturally integrate with each other.	In their initial hybrid experiments, the team investigated the distribution of rat neurons within the mouse brain. Despite rats typically having larger brains and a slower developmental pace, the rat cells conformed to the developmental cues of the mouse, speeding up their maturation process and forming analogous connections to those observed in native mouse cells. They observed rat cells spread across nearly the entirety of the mouse brain was quite unexpected	This indicates that there are minimal obstacles to integration, indicating that various types of mouse neurons could potentially be substituted by equivalent rat neurons. The researchers then assessed whether the rat neurons had been incorporated into a functional neural circuit, specifically within the olfactory system, crucial for mice to locate food and evade predators. By manipulating the mouse embryo to eliminate or deactivate its own olfactory neurons, the researchers could easily determine if the rat neurons had reinstated the animals’ sense of smell.

Watch The Video of Mice Here

Result of The Experiments:

They placed a cookie in each mouse cage and observed their ability to locate it using the rat neurons. However, some mice performed better than others in finding the cookie. That is hybrid brains help mice to smell like a rat.

The researchers discovered that mice retaining their own silenced olfactory neurons were less adept at finding hidden cookies compared to those whose olfactory neurons were engineered to vanish during development.

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The hybrid brains help mice to smell like a rat. This indicates that adding replacement neurons isn’t a simple plug-and-play process. For functional replacement, it may be necessary to clear out dysfunctional neurons that are inactive, which could be relevant in certain neurodegenerative diseases as well as neurodevelopmental disorders like autism and schizophrenia.

FAQ:

A team of researchers has advanced our understanding of a crucial enzyme governing cell migration. Their recent publication in the journal Nature Communications highlights that the PI3K enzyme has both accelerator and brake functions.

Date	April 24, 2024
Source	Tohoku University’s Frontier Research Institute for Interdisciplinary Sciences (FRIS)
Summary	The enzyme PI3K is crucial for cell migration, a function long recognized by scientists. However, recent findings reveal that a subunit of this enzyme can also act as a brake, halting this process.

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About PI3K:

The phosphoinositide 3-kinase (PI3K) is a significant signaling enzyme extensively studied for over three decades due to its pivotal roles in essential cellular functions such as growth, survival, movement, and metabolism. It also plays a crucial role in cell migration and invasion, processes whose dysregulation can lead to various pathologies.

PI3K Enzyme Has Both Accelerator And Brake Functions:

Research	Observation	Conclusion
Employing a blend of bioinformatics, molecular modeling, biochemical binding assays, and live-cell imaging, researchers disordered segment within the inter-SH2 domain of p85β directly interacts with the endocytic protein AP2. This segment of PI3K can trigger a cellular process that draws specific molecules into the cell, independent of the enzyme’s usual lipid-modification function.	Disrupting this binding resulted in the mutated p85β failing to function properly. Instead of modulating cell movement through its brake mechanism, it accumulated in specific cellular locations. Instead of modulating cell movement through its brake mechanism, it accumulated in specific cellular locations.	This led to heightened and sustained cell movement, indicating a loss of control over cell migration by the brake mechanism. Significantly, this single PI3K enzyme has both accelerator and brake functions within its molecular structure. The endocytic mechanism plays a pivotal role in regulating PI3K’s activity, ensuring that cell movement is appropriately controlled during critical biological processes.

Watch The Enzyme Action Here

Relation of PI3K Enzyme With Cancer:

1. Instead, the scientists reveal PI3K enzyme has both accelerator and brake functions but the braking function was identified as unique to the p85β subunit alone.
2. The p85β subunit of PI3K is associated with cancer-promoting characteristics, gaining a deeper comprehension of PI3K regulation and its isoform specificity could pave the way for innovative therapeutic approaches.
3. These strategies could selectively target and inhibit the cancer-promoting attributes of PI3K while safeguarding the normal functions of PI3K in healthy cells.

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While the PI3K enzyme has both accelerator and brake functions, the ongoing research on PI3K aims to deepen our understanding of PI3K signaling and develop more effective and safer therapies. Combining PI3K inhibitors with other cancer treatments shows promise in overcoming drug resistance and improving patient outcomes.

FAQ:

T. rex was not as smart as previously claimed is in top science news because the latest research, released today in The Anatomical Record, conducted by a collaborative team including the University of Bristol, delves into the methodologies for predicting brain size and neuron counts in dinosaur brains. The findings highlight the unreliability of previous assumptions regarding the brain size and neuron count in dinosaurs.

Date	April 29, 2024
Source	University of Bristol
Summary	Previous research suggests that dinosaurs possessed intelligence comparable to reptiles but fell short of the level seen in monkeys.

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About T. rex:

• Tyrannosaurus rex (T. rex) lived approximately 68 to 66 million years ago, during the Late Cretaceous period, in what is now North America.
• With its massive size, powerful jaws, and distinctive appearance, it belonged to a group of carnivorous dinosaurs known as theropods, characterized by their bipedal stance, sharp teeth, and predatory behavior.
• T. rex stood tall, reaching heights of up to 20 feet at the hips and lengths of around 40 feet from head to tail.
• Estimates suggest that it weighed between 9 and 14 metric tons, making it one of the largest land predators ever known.

Previous Research:

• A study published last year asserted that dinosaurs such as T. rex possessed an unusually large number of neurons, indicating higher intelligence than previously believed.
• This research suggested that these elevated neuron counts could offer insights into intelligence, metabolism, and life history, portraying T. rex as exhibiting behaviors reminiscent of primates.
• Additionally, the study suggested that T. rex might have displayed cognitive abilities such as cultural transmission of knowledge and potential tool use.

Watch The Video of The Dinosaur Here

Research: Why T. rex Was Not As Smart As Previously Claimed:

Research	Observation	Conclusion
This study builds upon decades of analysis conducted by paleontologists and biologists who have scrutinized the size and anatomy of dinosaur brains. These researchers have utilized data from mineral infillings within brain cavities, known as endocasts, as well as the shapes of these cavities, to glean insights into dinosaur behavior and lifestyle.	The team observed that the estimated brain size, particularly that of the forebrain, had been exaggerated, consequently affecting neuron counts. Furthermore, they demonstrated that using neuron count estimates as a gauge for intelligence is not dependable.	The team asserts that to accurately reconstruct the biology of extinct species, and concluded that researchers should consider various lines of evidence, such as skeletal anatomy, bone histology, the behavior of modern relatives, and trace fossils.

The recent scientific research that is T. rex was not as smart as previously claimed has challenged the long-standing perception of Tyrannosaurus rex as a highly intelligent predator. Studies comparing the brain structure of T. rex to other dinosaurs and modern-day birds, its closest living relatives, indicate that its brain-to-body ratio was relatively low.

FAQ on T. rex Was Not As Smart As Previously Claimed

The study was published on April 16 in Nature Structural & Molecular Biology revealed that one key factor responsible for bacterial defense against viral infection is when phages invade bacteria and exploit their cellular mechanisms for replication. Recent advancements in technology have facilitated the identification of the proteins engaged in these defense mechanisms. However, researchers are still delving further into the functions of these proteins.

Date	April 26, 2024
Source	Ohio State University
Summary	Scientists document the molecular formation of a prevalent anti-phage system, belonging to the protein family known as Gabija, which is believed to be employed by approximately 8.5% to 18% of bacterial species worldwide.

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About Bacteriophages:

Bacteriophages are viruses composed of genetic material, either DNA or RNA, encased in a protein coat. They come in various shapes and sizes, ranging from simple structures to complex arrangements resembling lunar landers. Despite their diversity, all bacteriophages share a common mission: to infect bacterial cells and hijack their cellular machinery to replicate and produce more phages.

Experiment: Bacterial Defense Against Viral Infection

Research	Observation	Conclusion
The components of this bacterial defense against viral infection are referred to as Gabija A and Gabija B, abbreviated as GajA and GajB, respectively. Using cryo-electron microscopy, scientists employed a method to discern the biochemical architectures of GajA and GajB separately, as well as of a supramolecular complex termed GajAB. This complex arises when the two proteins combine, forming a cluster composed of four molecules from each protein.	Scientists observed that while one protein alone dictate the ability to repel a phage, its effectiveness significantly amplifies when it interacts with another protein. This combined complex exhibits remarkable proficiency in cleaving the genome of an invading phage, rendering it incapable of replication.	Researchers hypothesize that the formation of the complex between the two proteins is essential for their involvement in phage prevention. However, they also suggest that one protein on its own possesses some anti-phage capabilities.

Future Application of The Experiment:

Watch The Application of Bacteria Here

These discoveries of bacterial defense against viral infection contribute to our comprehension of microorganisms’ evolutionary tactics and hold potential for future biomedical applications, according to researchers.

If you want to read more such biology news: Why Fasting is Not Always Good for Your Health, Cell Membrane Damage Promotes Cellular Senescence.

Bacteria employ sophisticated defense mechanisms to combat viral infections. Recent research has unveiled intricate molecular assemblies, such as the Gabija protein complex, which play pivotal roles in bacterial defense against viral infection. Understanding these defense strategies enhances our grasp of microbial biology and may pave the way for innovative biomedical interventions in the future.

FAQ on Bacterial Defense Against Viral Infection:

Intermittent fasting provides defense against liver inflammation and liver cancer because an approved drug for these diseases can partially imitate the effects of intermittent fasting. Fatty liver disease frequently progresses to chronic liver inflammation and may result in liver cancer. Recent studies in mice demonstrate that intermittent fasting, following a 5:2 schedule, can effectively arrest this progression. This fasting regimen diminishes the incidence of liver cancer in mice already afflicted with liver inflammation.

Date	May 7, 2024
Source	German Cancer Research Center (Deutsches Krebsforschungszentrum, DKFZ)
Summary	Researchers have pinpointed two proteins within liver cells that collaborate to engender the protective benefits of fasting. Furthermore, an approved medication exhibits the capacity to emulate this effect to some extent.

If you want to know recent biology news like Intermittent Fasting Provides Defense Against Liver Inflammation and Liver Cancer, then read here: Why Fasting is Not Always Good for Your Health, Specific Genomic Changes in the Monkeypox Virus Associated with Their Transmissibility, Better View of Living Bacteria with New Mid-Infrared Nanoscopy.

About The Liver Diseases:

The most prevalent chronic liver condition is non-alcoholic fatty liver disease (NAFLD), which can have severe implications. If left unaddressed, NAFLD can progress to liver inflammation, known as metabolic dysfunction-associated steatohepatitis (MASH), liver cirrhosis, and potentially liver cancer. Fatty liver disease is predominantly perceived as a direct consequence of obesity.

Experiment: Intermittent Fasting Provides Defense Against Liver Inflammation and Liver Cancer

Watch Here: What does the liver do?

Experiment	Observation	Conclusion
The animals(mice) were provided with a diet high in both sugar and fat, resembling the typical Western diet.	One set of mice had unrestricted access to this diet. As anticipated, these mice experienced weight gain, increased body fat, and developed chronic liver inflammation.	During the exploration of various intermittent fasting regimens, it became evident that several factors such as the frequency and duration of fasting cycles, along with the timing of the fasting phase initiation, influence the safeguarding against liver inflammation.
On the other hand, the mice in the alternate group underwent a dietary regimen where they fasted for two days a week for 5:2, while being allowed to eat huge on the remaining days.	Despite consuming a high-calorie diet, these mice did not exhibit weight gain, displayed fewer indications of liver disease, and demonstrated reduced levels of biomarkers associated with liver damage.	From this analysis, two key components driving the protective response to fasting were identified: the transcription factor PPARα and the enzyme PCK1. These molecular entities collaborate to enhance the breakdown of fatty acids and gluconeogenesis while impeding the accumulation of fats

Role of Approved Drug:

The medication pemafibrate emulates the actions of PPARα within the cell. Is it possible for this substance to replicate the protective benefits of fasting as well? To address this inquiry, researchers conducted experiments in mice. Pemafibrate prompted certain beneficial metabolic alterations akin to those observed during 5:2 fasting so the researchers can say that the intermittent fasting provides defense against liver inflammation and liver cancer

Intermittent fasting provides defense against liver inflammation and liver cancer through controlled periods of fasting, the body undergoes metabolic shifts that contribute to the reduction of liver inflammation and the inhibition of cancerous growth.

FAQ on Intermittent Fasting Provides Defense Against Liver Inflammation and Liver Cancer: