A new experimental drug was able to protect mice’s livers and prevent them from gaining weight after they had been fed a diet rich in sugars and fats for the majority of their lives.
You can also find out more about the following: Small-molecule drugThe University of Texas Health Science Center, San Antonio (UT Health San Antonio), led a group that developed this tool. KKnown by its chemical abbreviation CPACC, this substance works by limiting entry of magnesium into mitochondria, which are the parts in the cell that are responsible for generating energy and calorie burning.
Abnormal mitochondrial function has been linked to a variety of diseases, such as obesity. DiabetesHeart disease is a serious condition.
These findings are the culmination of years of research.” You can find out more about this by clicking here.Madesh Muniswamy of UT Health San Antonio is a molecular biochemist and senior author. Publication of paperReporting the results
Magnesium is one of the major positively charged ions, which contributes in many ways to the cellular functions of the body. In fact, magnesium is essential for maintaining good health. It regulates blood sugar and blood tension and helps to build strong bones. Magnesium is important for energy production, but too much can cause mitochondria to slow down.
“It slows down, but it doesn’t stop,” You can find out more about this by clicking here.Travis Madaris is a biologist from UT Health San Antonio. He is the co-author and lead author of this paper.
Researchers found the drug by studying the effect on deleting MRS2, an encoded gene. magnesium transporterThis protein is called Mrs2. This protein is called Mrs2. It acts as a conduit for magnesiumThe mitochondrial membrane is a thin layer of membrane that runs across the cell.
They compared normal mice to mice with the MRS2 gene deleted in order to determine if a high fat, high sugar, and high calorie Western diet would have any effect on them.
MRS2 deletion led to healthier, leaner mice, who had improved sugar and lipid metabolism in their mitochondria. This was despite the fact that they were fed a Western diet for a period of up to a full year, starting at age 14 weeks.
The liver controls the sugar and fat metabolism as a response to fasting and eating. Although a A robust organThere are limits to it. It was telling that there were no indications of Fatty liver diseaseMRS2 deletion can lead to fat tissue or liver in MRS2 deleted mice. unbalanced dietObesity, type 2 diabetes, or both.
“Lowering of mitochondrial magnesium ameliorated the adverse effects from prolonged dietary stress,” You can find out more about this by clicking here.Manigandan Venkatesan, a biologist from UT Health San Antonio and the third co-author.
The team also reported that CPACC administration had the same effect as deletion of MRS2 gene. The drug blocks the magnesium channels for which the gene codes. It also resulted again in healthy, lean mice by reducing magnesium transport into the mitochondria.
It’s a given. Results in mice may not necessarily be applicable to humansThe study has limitations, as the authors note. To mimic Metabolic SyndromeIn humans, they use long-term dietary stresses. The main effects of MRS2 loss could be clarified by putting the system under short-term nutritional stress.
The researchers also point out that a method of deletion for MRS2 is not able to determine how the metabolic regulation in each tissue. MRS2 is widely expressed, so they stress the importance of more research on its effects in various organs including the brain and heart.
Researchers have filed a patent on CPACC.
“A drug which can reduce the risk for cardiometabolic disease such as heart attacks and strokes, and also reduces the incidence of liver diseases.” CancerMuniswamy You can find out more about this by clicking here..
We will continue the development of this product.
The research was published in Cell Reports.
