Amino Acids
Secret Research on Glycine
Glycine is considered an antidote to fructose. A groundbreaking new study shows that DT-109, a tripeptide composed of glycine and leucine, reverses fatty liver and inhibits liver inflammation.
Amino Acids
Glycine is considered an antidote to fructose. A groundbreaking new study shows that DT-109, a tripeptide composed of glycine and leucine, reverses fatty liver and inhibits liver inflammation.
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Glycine. The smallest and in the truest sense of the word sweet amino acid.
State of Affairs: Glycine as an "antidote to fructose"?
Many of us know it as an essential component of collagen. That is, the structural protein that makes up our bones, connective tissue, skin, and other structure-forming tissues. Glycine plays an important role here because, as the smallest amino acid, it enables the typical twists of long collagen strands.
Anyone who needs a 1x1 crash course on this can find [source no longer available].
Among the list of glycine's functions, there is also the point that "glycine could be the antidote to fructose." We didn't make up this phrase. It was the title of a work published in 2014 by Mark F. McCarty and James J. DiNicolantonio in a scientific journal [source no longer available].
James DiNicolantonio was a nobody back then. Today he's well-known to many. He has published not only scientific papers but also works in popular science and operates [source no longer available] with nearly 1.4 million followers. Mark F. McCarty is especially known to people who concern themselves with micronutrient hypotheses.
Back to the content: Fructose in drinking water makes the liver fatty and causes the metabolic health of animals to spiral out of control. In modern food, it mainly comes in the form of household sugar (sucrose) on the menu. Important advice, therefore, is always: avoid household sugar!
Could glycine additionally serve as an antidote here? The two authors summarized in their work: "Of particular interest are studies showing that high glycine intake can counteract many of the negative effects of a sugar-rich diet on the liver, fat mass, and vascular function in rats." Fascinating.
Because we have been closely following the importance of glycine for many, many years, we decided early on to use glycine as a functional amino acid in our products. It appears, for example, in our [source no longer available], but also in [source no longer available] or in [source no longer available]. You can also [source no longer available] and stir 5 g of it as a "sweetener" into your tea. It doesn't get easier!
Brand New: "DT-109" Reverses Fatty Liver and Inhibits Liver Inflammation
Very recently, [source no longer available] appeared in the prestigious journal Cell Metabolism, introducing a mysterious substance: DT-109. Sounds a bit fancy like Area 51. But behind it is quite simply a so-called tripeptide, that is, three amino acids linked together: Glycine-Glycine-Leucine. That's 2/3 glycine and 1/3 leucine.
Now it gets fancy again. The authors describe the "magical" effects of DT-109 as follows:
"Using a multiomics approach combining transcriptomics, proteomics, metabolomics, and metagenomics, we found that DT-109 reverses hepatic steatosis and prevents the progression of fibrosis in nonhuman primates, not only by stimulating fatty acid oxidation and glutathione production, as was the case in mice, but also by modulating microbial bile acid metabolism."
Wow! A simple tripeptide reverses (non-alcoholic) fatty liver in mice and apes and even inhibits (inflammatory) liver fibrosis, a consequence of fatty liver and precursor to fatal cirrhosis. Groundbreaking.
Through apparently considerable effort, the researchers found that DT-109 stimulates fat oxidation, drives glutathione production (the body's most important antioxidant), and influences gut bacteria. The latter, of course, also metabolize breakdown products that the liver releases via bile—which in turn has effects on the health of the host.
The researchers explain the action of DT-109, namely Glycine-Glycine-Leucine, partly by the fact that recent studies show that impaired glycine metabolism is a causative factor in non-alcoholic fatty liver disease (NASH) and thus qualifies as a therapeutic target for NASH and cardiometabolic disease. DT-109 reverses this.
Indeed, this also applies to "other glycine-based treatments, including dietary supplementation with glycine or its precursor serine. According to studies, fatty liver is reduced in patients and mice with non-alcoholic fatty liver disease, and indices of fat oxidation are increased in rats fed sucrose (household sugar)."
Fascinating, isn't it? The researchers even provide us with a dose for DT-109, namely 24–83 mg per kg of body weight. For an 80 kg man, that would be 1920 to 6640 mg total for DT-109, of which approximately 1000 mg and 3300 mg would be glycine (mass basis 1.15:1 glycine:leucine). Of course, it currently cannot be ruled out that DT-109 as a tripeptide has its own effects that are not covered by glycine or leucine alone.
A teaspoon of glycine in tea or coffee would already be 5 g (5000 mg) of glycine.
Background
For those who finally wonder who comes up with such clever Area 51-style names for compounds or where DT-109 suddenly comes from: we live in the era of GLP-1 agonists, the incretin mimetics. GLP-1 is an intestinal hormone that is stimulated upon food intake—or, as it later turned out, [source no longer available]—and significantly enhances insulin secretion.
This phenomenon was dubbed the incretin effect in the 1960s. Nowadays, in the field of (pre-)diabetes, there are the GLP-1 analogs exenatide, liraglutide, and dulaglutide. They bind to the GLP-1 receptor and thus mimic the action of GLP-1—this lowers blood sugar levels by increasing insulin secretion.
DT-109 was discovered by the biotech company Diapin and described as "the most active of the investigated peptides," which in animal studies dose-dependently lowers blood sugar levels and raises GLP-1. Exactly what [source no longer available]. Because glycine itself can also stimulate GLP-1 secretion.
Learned something new, haven't we?
