Scientists create a drug that allows you to eat junk food without gaining weight

Scientists in Texas have tested a new drug in mice that allowed them to stay slim even while eating a sugary, fatty junk-food diet. The drug, called CPACC, changes how magnesium moves inside cells. In mice, it stopped both weight gain and liver damage.

The work, led by Dr. Madesh Muniswamy at The University of Texas Health Center at San Antonio (UTHCSA), used mice fed a Western-style diet for most of their lives, similar in calories to fast-food meals.

Obesity and metabolism matter

Around the world, obesity is climbing. It brings a higher risk of heart disease, stroke, and type 2 diabetes – a pattern doctors often group as cardiometabolic disease, a mix of heart and metabolic problems.

In the United States, a large national survey found that about 40 percent of adults had obesity between 2021 and 2023.

Extra body fat strains the heart and can cause nonalcoholic fatty liver disease – fat buildup in the liver not caused by drinking alcohol.

Inside almost every cell sit mitochondria, tiny structures in cells that make most of our usable energy. When these power stations fail, the body struggles to burn sugar and fat, and weight gain and high blood sugar become more likely.

Magnesium’s role in energy

The mineral magnesium, a charged mineral that helps many enzymes work, is essential for life. It supports muscle function and takes part in hundreds of reactions that turn food into cellular fuel.

To move magnesium in and out, mitochondria use a special ion channel, a protein tunnel that lets charged atoms cross a membrane.

The main channel that pulls magnesium into mitochondria is called MRS2. It sets how much of this ion enters the organelle.

When too much magnesium collects inside mitochondria, their energy output can slow down instead of speeding up.

Over time, this slowdown can feed into metabolic syndrome. That’s a cluster of high blood sugar, unhealthy cholesterol, and raised blood pressure.

Some body fat is especially active. So-called brown fat, a type of fat that burns energy to make heat, can help protect against weight gain.

How CPACC controls weight

In the new mouse study, researchers blocked MRS2 so that less magnesium entered the mitochondria. Mice that lacked this protein or had it blocked burned sugar and fat more efficiently, even though they ate the same rich food.

The team then designed CPACC, a lab-made, cobalt-based molecule that blocks MRS2. Animals given CPACC showed reduced weight and white adipose tissue – the usual body fat under the skin – that resembled heat-producing fat.

Researchers noted that giving the drug to mice for a short period led to quick weight loss and a slimmer appearance. Such a treatment could cut cardiometabolic risks and lower liver cancer odds, creating a major health impact.

CPACC is not a junk-food pass

All of these experiments are preclinical – early lab and animal research done before human testing – and they were carried out only in mice.

Mice share many metabolic features with humans. But drugs that work well in mice often fail when researchers test them in people.

CPACC contains cobalt, and certain inorganic cobalt salts can be toxic at high exposures. Any future human version will need very careful safety checks to make sure it does not harm the heart, nerves, or other organs.

For people, no pill can replace healthy food and regular movement. Even if a magnesium-targeting drug eventually reaches clinical trial, it would likely treat severe obesity or liver disease, not excuse junk food.

The mouse results are still important because they reveal a new way to regulate metabolism. By tuning how magnesium flows into mitochondria, scientists may be able to shift the body from storing energy toward burning it.

CPACC and weight control

Future work will test different doses and schedules of CPACC and related molecules and explore how they affect weight, heart, kidney, and brain health in animals.

Researchers also want to see whether similar strategies can protect against insulin resistance, the state when the body stops responding well to insulin.

In time, magnesium handling inside mitochondria could become a target for personalized medicine, tailoring treatments to a person’s unique biology.

For example, some people might have variants in the MRS2 gene or related pathways that make them respond better to this kind of drug.

The same pathway could also matter for people at high risk of heart attack, stroke, and liver cancer because of long-standing obesity.

If safe blockers of mitochondrial magnesium uptake can be designed, they may one day sit alongside diet and exercise to reduce obesity-related disease.

The study is published in Cell Reports.

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