fat burning BAM 15

Highlights:

  • Researchers say a protein called BAM15 prevents weight gain and fat build-up
  • BAM15 makes ‘power plants’ of the cell less efficient so they burn more energy 
  • It could be administered as an injection or a pill for obese and overweight people
  • Current obesity treatments are few and far between and aren’t really effective 

Scientists have found a protein that prevents fat buildup and reduces blood sugar levels, it may be a solution to the most common disease obesity.

The protein, named BAM15, acts as an ‘energy uncoupler’ and could be an effective drug for treating obesity and related diseases, US researchers say.

BAM15 makes the mitochondria, the ‘powerhouse’ of living cells, less efficient, meaning they burn more energy and therefore more fat.

In lab trials using mice, scientists found mice given BAM15 were resistant to weight gain because they burned more calories than their untreated counterparts.

Bam 15

Today we leave in a world where more than 13% of the global population is suffering from obesity problem. According to data only in the USA, there are 40% of people having this issue.

It is the root cause of many common diseases including cardiovascular disease, diabetes, and fatty liver disease, which makes the disease one of the most difficult — and most crucial — to treat.

Global spending to treat obesity and obesity-related illnesses amounts to well over $150 billion (£117.3 billion) a year.

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This research holds promises for future treatment and prevention of obesity, diabetes, and especially nonalcoholic steatohepatitis (NASH), a type of fatty liver disease that is characterized by inflammation and fat accumulation in the liver. In the next few years, the condition is expected to become the leading cause of liver transplants in the United States.

The mitochondria are commonly referred to as the powerhouses of the cell. The organelle generates ATP, a molecule that serves as the energy currency of the cell, which powers body movement and other biological processes that help our body to function properly.

In order to make ATP, nutrients need to be burned and a proton motive force (PMF) needs to be established within the mitochondria. The PMF is generated from a proton gradient, where there is a higher concentration of protons outside of the inner membrane and a lower concentration of protons in the matrix, or the space within the inner membrane. The cell creates ATP whenever protons pass through an enzyme called ATP synthase, which is embedded in the membrane. Hence, nutrient oxidation, or nutrient burning, is coupled to ATP synthesis.

“So anything that decreases the PMF has the potential to increase respiration. Mitochondrial uncouplers are small molecules that go to the mitochondria to help the cells respire more. Effectively, they change metabolism in the cell so that we burn more calories without doing any exercise,”

said Santos, an affiliated member of the Fralin Life Sciences Institute and the Virginia Tech Center for Drug Discovery.

Mitochondrial uncouplers transport protons into the matrix by bypassing ATP synthase, which throws off the PMF. To reestablish the gradient, protons must be exported out of the mitochondrial matrix. As a result, the cell begins to burn fuel at higher than necessary levels.

Knowing that these molecules can change a cell’s metabolism, researchers wanted to be sure that the drug was reaching its desired targets and that it was, above all, and safe. Through a series of mouse studies, the researchers found that BAM15 is neither toxic, even at high doses, nor does it affect the satiety center in the brain, which tells our body if we are hungry or full.

In the past, many anti-fat drugs would tell your body to stop eating. But as a result, patients would rebound and eat more. In the BAM15 mouse studies, animals ate the same amount as the control group – and they still lost fat mass.

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Another side effect of previous mitochondrial uncouplers was increased body temperature. Using a rectal probe, researchers measured the body temperature of mice who were fed BAM15. They found no change in body temperature.

But one issue arises concerning the half-life of BAM15. The half-life, or the length of time that a drug is still effective, is relatively short in the mouse model. For oral dosing in humans, the optimal half-life is much longer.

Even as BAM15 has some serious potential in mouse models, the drug won’t necessarily be successful in humans – at least not this same exact molecule.

“We are essentially looking for roughly the same type of molecule, but it needs to stay in the body for longer to have an effect. We are tweaking the chemical structure of the compound. So far, we have made several hundred molecules related to this,” said Santos.

The penultimate goal of the Santos lab is to transition the anti-fat treatment from animal models to treatment for NASH in humans. The lab has used their better compounds in animal models of NASH, which have been proven to be effective as anti-NASH compounds in mice.

The penultimate goal of the Santos lab is to transition the anti-fat treatment from animal models to treatment for NASH in humans. The lab has used their better compounds in animal models of NASH, which have been proven to be effective as anti-NASH compounds in mice.

Working alongside Santos is Kyle Hoehn, an assistant professor of pharmacology from the University of Virginia and an associate professor of biotechnology and biomolecular sciences at the University of New South Wales in Australia. Hoehn is a metabolic physiology expert who is in charge of conducting animal studies. Santos and Hoehn have been collaborating for several years now and they even founded a biotech company together.

Co-founded by Santos and Hoehn in 2017, Continuum Biosciences aims to improve the ways in which our bodies burn fuel and fight back against our bodies’ ability to store excess nutrients as we age. These promising NASH treatment compounds are licensed by their company and are patented by Virginia Tech.

The company is looking to use mitochondrial uncouplers for more than just obesity and NASH. The molecules also have a unique anti-oxygen effect that can minimize the accumulation of reactive oxygen species, or oxidative stress, in our bodies, which ultimately results in neurodegeneration and ageing.

“If you just minimize ageing, you could minimize the risk of Alzheimer’s disease and Parkinson’s disease. All of these reactive oxygen species-related or inflammation-related diseases could benefit from mitochondrial uncouplers. So, we could see this heading that way,” said Santos.

The findings are published in Nature Communications on May 14, 2020,

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