Fat metabolism protects the body against toxins from sugar
When the body burns fat it creates compounds that counteract some of the harmful effects of sugar.
Scientists have long known that when the body metabolises sugar it creates a toxic substance, which can play an important role in the development of age and lifestyle related diseases such as diabetes, cancer, and Alzheimer’s.
But new research shows that when the body burns fat, it creates compounds that counteract these harmful sugar by-products.
“You can remove some of the toxic by-products from the sugar metabolism by eating fats or following a low-calorie or low-carbohydrate diet, which makes the body burn its own fat,” says co-author Mogens Johannsen, a professor in forensic medicine at Aarhus University, Denmark.
The study is based on in-vitro experiments and blood samples, and is published in the scientific journal, Cell Chemical Biology.
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Explains the positive effects of the Keto Diet
The results could explain why high-fat, low-sugar diets have proven effective at preventing diabetes, Alzheimer’s, and cancer in animal trials.
Animals that eat a diet rich in fat—a so-called ketogenic diet, or keto diet—also live significantly longer.
But the results are also surprising as previous research suggested the opposite: That fat burning created these same harmful substances.
It appears that a healthy diet is dependent on a hair-thin balance between the formation of toxic substances and the subsequent detoxification of sugar combustion, but too much sugar can tip the balance, such that this detoxification does not occur.
“It illustrates that biological systems are immensely complex and we still do not understand them completely,” says Johannsen.
Could reduce pain in diabetes patients
The study could potentially lead to new treatments for diabetes patients.
Neuropathy is a very painful complication in diabetic patients, which occurs due to damaged nerves.
The damage is, among other things, the result of the accumulation of the toxic substances and so the new insights could lead to a new type of diet that could ease the symptoms.
“We could perhaps develop diets with fewer carbohydrates and more fat. Such a diet could possibly help the body create more metabolites to neutralise the toxins and ease pain among neuropathy patients,” says Johannson.
More research needed
As with all research, there is a “but:” Johannsen and colleagues have not yet quantified the chemical reaction between the two substances.
“We don’t yet know how much this process actually detoxifies,” says co-author Thomas B. Poulsen, associate professor from the Department of Chemistry at Aarhus University.
“It’s an explosive topic, because it touches on some of the most discussed substances in biological ageing and late-complications for diabetic patients,” says Johannsen, who will continue the research.
They plan to conduct another study where they administer the detoxifying metabolite to patients to see whether it effects the amount of toxic substances in their blood and helps relieve pain.
“We are, however, still in the very early stages,” says Johannsen.
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Tricky to know how significant the results are
Professor Henrik Enghusen Poulsen from Bispebjerg-Frederiksberg Hospital in Denmark has the same reservations.
Whether the toxic substances are especially significant for ageing and the risk of developing type 2 diabetes is an ongoing discussion among scientists, says Poulsen, who was not involved in the study.
“It’s interesting that they have discovered this spontaneous chemical reaction, but it is far too early to say whether it has clinical significance,” he says.
“It’s possible that in some years someone will look back and say that they led the way to something, but only time will tell. Before we know the quantified, clinical significance, it’s difficult to say what it will lead to,” says Poulsen.
Read more in the Danish version of this story on Videnskab.dk
Translated by: Catherine Jex
- Ketone Body Acetoacetate Buffers Methylglyoxal via a Non-enzymatic Conversion during Diabetic and Dietary Ketosis, Cell Chemical Biology (2017), doi:10.1016/j.chembiol.2017.07.012