Body’s fat metabolism wards off sugar's effects and promotes healthy ageing: Study

By Emma Cash

- Last updated on GMT

©iStock/wgmbh
©iStock/wgmbh

Related tags Metabolism

The chemical link between a low-carbohydrate diet and healthy ageing could be explained by new scientific evidence showing that the body’s own fat-metabolism protects against sugar’s harmful effects.

Researchers from Aarhus University, Denmark, have discovered a detoxification system in the body which scientists were previously not aware of, according to their paper published in Cell Chemical Biology.

This new information has shed light on why a diet low in carbohydrates can prevent a range of age-related diseases, such as diabetes, Alzheimer’s and cancer.

According to the researchers, it was found that fat-metabolism in the cells takes place simultaneously with a detoxification of the harmful substances from the blood sugar, indicating our bodies have a detoxification system previously unknown about.

This chemical process could researchers better understand prevention techniques for age-related diseases.

Sugar detox

“Previous research partly based on animal experiments using mice and monkeys shows that a diet with less sugar and more fat protects against diseases such as diabetes, Alzheimer’s and cancer. At the same time, it has also been known that methylglyoxal causes age-related diseases,” ​said Mogens Johannsen, study lead and professor of chemical biology at the Department of Forensic Medicine, Aarhus University.

“We have found a new metabolite that demonstrates an alternative chemical detoxification of methylglyoxal when we burn fat. It is a surprising discovery, as ketones in themselves can lead to the harmful sugar metabolite methylglyoxal,”

“The explanation may be a delicate balance between creation and detoxification. In any case, this illustrates that biological systems are enormously complex.”

This detoxification occurs without the involvement of the enzymes that scientists have previously looked at in relation to fat-metabolism and the breaking down of sugar.

Instead, the process involves ketone acetoacetate - a type of metabolite originating from the body’s fat-metabolism – capturing and inhibiting another metabolite, methylglyoxal, which originates from the body’s sugar metabolism.

Methylglyoxal is toxic to cells and plays crucial roles in age-related diseases, especially diabetes as untreated diabetics have higher concentrations of methylglyoxal in their blood.

The researchers say this is what makes the process so important.

When the two metabolites meet, a third metabolite, which does not have the harmful effects of methylglyoxal, emerges. The third metabolite is called 3-HHD.

Although 3-HHD was first discussed in the 1930s, this group of researchers are the first to find 3-HHD in the blood of people who lacked insulin and/or had fasted the night before – a condition known to give ketosis.

Ketosis is caused when the body does not have enough fuel in the form of carbohydrates and so the liver forms ketone from the body’s fat to use as fuel.

Increased concentrations of ketones are usually found in the blood of people who ingest too many proteins, who are on a low calorie or low-carbohydrate diet, or who have untreated diabetes.

Johannsen says this research can help with understanding the role of ketones and reactive metabolites in biological ageing.

'Fewer carbohydrates and more fat'

“Now we have evidence for saying that ketones can minimise the amount of harmful methylglyoxal in living organisms, and that is a discovery that gets noticed, as it involves two of the most debated substances within biological aging and late diabetic complications. Moreover, these substances react with each other,”​ he said.

Furthermore, the discovery could lead to treatments for diabetic complications being developed.

One perspective could be to follow a diet with fewer carbohydrates and more fat. The fat helps to encapsulate and destroy the sugars that cause the pain ​[of neuropathy]”.

The research team say more research and clinical trials will be needed to further establish this.

Source: Cell Chemical Biology

Published online, DOI:10.1016/j.chembiol.2017.07.012

Study: “Ketone Body Acetoacetate Buffers Methylglyoxal via a Non-enzymatic Conversion during Diabetic and Dietary Ketosis”

Authors: Trine Salomón et al.

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